---
_id: '5984'
abstract:
- lang: eng
text: G-protein-coupled receptors (GPCRs) form the largest receptor family, relay
environmental stimuli to changes in cell behavior and represent prime drug targets.
Many GPCRs are classified as orphan receptors because of the limited knowledge
on their ligands and coupling to cellular signaling machineries. Here, we engineer
a library of 63 chimeric receptors that contain the signaling domains of human
orphan and understudied GPCRs functionally linked to the light-sensing domain
of rhodopsin. Upon stimulation with visible light, we identify activation of canonical
cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent
pathways, downstream of the engineered receptors. For the human pseudogene GPR33,
we resurrect a signaling function that supports its hypothesized role as a pathogen
entry site. These results demonstrate that substituting unknown chemical activators
with a light switch can reveal information about protein function and provide
an optically controlled protein library for exploring the physiology and therapeutic
potential of understudied GPCRs.
article_number: '1950'
article_processing_charge: No
author:
- first_name: Maurizio
full_name: Morri, Maurizio
id: 4863116E-F248-11E8-B48F-1D18A9856A87
last_name: Morri
- first_name: Inmaculada
full_name: Sanchez-Romero, Inmaculada
id: 3D9C5D30-F248-11E8-B48F-1D18A9856A87
last_name: Sanchez-Romero
- first_name: Alexandra-Madelaine
full_name: Tichy, Alexandra-Madelaine
id: 29D8BB2C-F248-11E8-B48F-1D18A9856A87
last_name: Tichy
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
- first_name: Elliot J.
full_name: Gerrard, Elliot J.
last_name: Gerrard
- first_name: Priscila
full_name: Hirschfeld, Priscila
id: 435ACB3A-F248-11E8-B48F-1D18A9856A87
last_name: Hirschfeld
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
citation:
ama: Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human
class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1).
doi:10.1038/s41467-018-04342-1
apa: Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J.,
Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class
A orphan G-protein-coupled receptors. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-018-04342-1
chicago: Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy,
Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald
L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled
Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1.
ieee: M. Morri et al., “Optical functionalization of human class A orphan
G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer
Nature, 2018.
ista: Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P,
Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan
G-protein-coupled receptors. Nature Communications. 9(1), 1950.
mla: Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan
G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950,
Springer Nature, 2018, doi:10.1038/s41467-018-04342-1.
short: M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld,
J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).
date_created: 2019-02-14T10:50:24Z
date_published: 2018-12-01T00:00:00Z
date_updated: 2023-09-19T14:29:32Z
day: '01'
ddc:
- '570'
department:
- _id: HaJa
- _id: CaGu
- _id: MiSi
doi: 10.1038/s41467-018-04342-1
ec_funded: 1
external_id:
isi:
- '000432280000006'
file:
- access_level: open_access
checksum: 8325fcc194264af4749e662a73bf66b5
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T10:58:29Z
date_updated: 2020-07-14T12:47:14Z
file_id: '5985'
file_name: 2018_Springer_Morri.pdf
file_size: 1349914
relation: main_file
file_date_updated: 2020-07-14T12:47:14Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303564'
name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 255A6082-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optical functionalization of human class A orphan G-protein-coupled receptors
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '5992'
abstract:
- lang: eng
text: Lamellipodia are flat membrane protrusions formed during mesenchymal motion.
Polymerization at the leading edge assembles the actin filament network and generates
protrusion force. How this force is supported by the network and how the assembly
rate is shared between protrusion and network retrograde flow determines the protrusion
rate. We use mathematical modeling to understand experiments changing the F-actin
density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex
activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction
of density with a decrease of protrusion velocity, an increase in the ratio of
force to filament number, but constant network assembly rate. The relation between
protrusion force and tension gradient in the F-actin network and the density dependency
of friction, elasticity, and viscosity of the network explain the experimental
observations. The formins act as filament nucleators and elongators with differential
rates. Modulation of their activity suggests an effect on network assembly rate.
Contrary to these expectations, the effect of changes in elongator composition
is much weaker than the consequences of the density change. We conclude that the
force acting on the leading edge membrane is the force required to drive F-actin
network retrograde flow.
article_processing_charge: No
author:
- first_name: Setareh
full_name: Dolati, Setareh
last_name: Dolati
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Mathias
full_name: Müsken, Mathias
last_name: Müsken
- first_name: Marieluise
full_name: Kirchner, Marieluise
last_name: Kirchner
- first_name: Gunnar
full_name: Dittmar, Gunnar
last_name: Dittmar
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
citation:
ama: Dolati S, Kage F, Mueller J, et al. On the relation between filament density,
force generation, and protrusion rate in mesenchymal cell motility. Molecular
Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082
apa: Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., …
Falcke, M. (2018). On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the
Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082
chicago: Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner,
Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation
between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal
Cell Motility.” Molecular Biology of the Cell. American Society for Cell
Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082.
ieee: S. Dolati et al., “On the relation between filament density, force
generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology
of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686,
2018.
ista: Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner
K, Falcke M. 2018. On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell.
29(22), 2674–2686.
mla: Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation,
and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the
Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86,
doi:10.1091/mbc.e18-02-0082.
short: S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K.
Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686.
date_created: 2019-02-14T12:25:47Z
date_published: 2018-11-01T00:00:00Z
date_updated: 2023-09-19T14:30:23Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1091/mbc.e18-02-0082
external_id:
isi:
- '000455641000011'
pmid:
- '30156465'
file:
- access_level: open_access
checksum: e98465b4416b3e804c47f40086932af2
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T12:34:29Z
date_updated: 2020-07-14T12:47:15Z
file_id: '5994'
file_name: 2018_ASCB_Dolati.pdf
file_size: 6668971
relation: main_file
file_date_updated: 2020-07-14T12:47:15Z
has_accepted_license: '1'
intvolume: ' 29'
isi: 1
issue: '22'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '11'
oa: 1
oa_version: Published Version
page: 2674-2686
pmid: 1
publication: Molecular Biology of the Cell
publication_identifier:
eissn:
- 1939-4586
publication_status: published
publisher: 'American Society for Cell Biology '
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the relation between filament density, force generation, and protrusion
rate in mesenchymal cell motility
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 29
year: '2018'
...
---
_id: '6497'
abstract:
- lang: eng
text: T cells are actively scanning pMHC-presenting cells in lymphoid organs and
nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the
T cell actomyosin cytoskeleton facilitates this task in distinct environments
is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative
regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface
stiffness in primary T cells. Nonetheless, intravital imaging revealed robust
motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and
differentiation during immune responses. In contrast, accumulation of Myo9b−/−
CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for
T cell crossing of basement membranes, such as those which are present between
dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control
of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell
adaptation from lymphoid to NLT surveillance and the establishment of protective
tissue–resident T cell populations.
article_processing_charge: No
author:
- first_name: Federica
full_name: Moalli, Federica
last_name: Moalli
- first_name: Xenia
full_name: Ficht, Xenia
last_name: Ficht
- first_name: Philipp
full_name: Germann, Philipp
last_name: Germann
- first_name: Mykhailo
full_name: Vladymyrov, Mykhailo
last_name: Vladymyrov
- first_name: Bettina
full_name: Stolp, Bettina
last_name: Stolp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Ruth
full_name: Lyck, Ruth
last_name: Lyck
- first_name: Jasmin
full_name: Balmer, Jasmin
last_name: Balmer
- first_name: Amleto
full_name: Fiocchi, Amleto
last_name: Fiocchi
- first_name: Mario
full_name: Kreutzfeldt, Mario
last_name: Kreutzfeldt
- first_name: Doron
full_name: Merkler, Doron
last_name: Merkler
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Akitaka
full_name: Ariga, Akitaka
last_name: Ariga
- first_name: Michael H.
full_name: Stoffel, Michael H.
last_name: Stoffel
- first_name: James
full_name: Sharpe, James
last_name: Sharpe
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Alba
full_name: Diz-Muñoz, Alba
last_name: Diz-Muñoz
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
citation:
ama: Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine.
2018;2015(7):1869–1890. doi:10.1084/jem.20170896
apa: Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I.,
… Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue
seeding of protective CD8+T cells. The Journal of Experimental Medicine.
Rockefeller University Press. https://doi.org/10.1084/jem.20170896
chicago: Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina
Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables
Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental
Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896.
ieee: F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine,
vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.
ista: Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer
J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe
J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb
enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental
Medicine. 2015(7), 1869–1890.
mla: Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid
Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine,
vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896.
short: F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R.
Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga,
M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal
of Experimental Medicine 2015 (2018) 1869–1890.
date_created: 2019-05-28T12:36:47Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2023-09-19T14:52:08Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20170896
external_id:
isi:
- '000440822900011'
file:
- access_level: open_access
checksum: 86ae5331f9bfced9a6358a790a04bef4
content_type: application/pdf
creator: kschuh
date_created: 2019-05-28T12:40:05Z
date_updated: 2020-07-14T12:47:32Z
file_id: '6498'
file_name: 2018_rupress_Moalli.pdf
file_size: 3841660
relation: main_file
file_date_updated: 2020-07-14T12:47:32Z
has_accepted_license: '1'
intvolume: ' 2015'
isi: 1
issue: '7'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 1869–1890
publication: The Journal of Experimental Medicine
publication_identifier:
eissn:
- 1540-9538
issn:
- 0022-1007
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective
CD8+T cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2015
year: '2018'
...
---
_id: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2024-03-28T23:30:09Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
text: 'In the here presented thesis, we explore the role of branched actin networks
in cell migration and antigen presentation, the two most relevant processes in
dendritic cell biology. Branched actin networks construct lamellipodial protrusions
at the leading edge of migrating cells. These are typically seen as adhesive structures,
which mediate force transduction to the extracellular matrix that leads to forward
locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
that the resulting cells lack lamellipodial protrusions. Instead, depending on
the maturation state, one or multiple filopodia were formed. By challenging these
cells in a variety of migration assays we found that lamellipodial protrusions
are dispensable for the locomotion of leukocytes and actually dampen the speed
of migration. However, lamellipodia are critically required to negotiate complex
environments that DCs experience while they travel to the next draining lymph
node. Taken together our results suggest that leukocyte lamellipodia have rather
a sensory- than a force transducing function. Furthermore, we show for the first
time structure and dynamics of dendritic cell F-actin at the immunological synapse
with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
leading to an altered ultrastructure of the immunological synapse and severe T
cell priming defects. These results point towards a previously unappreciated role
of the cellular mechanics of dendritic cells in T cell activation. Additionally,
we present a novel cell culture based system for the differentiation of dendritic
cells from conditionally immortalized hematopoietic precursors. These precursor
cells are genetically tractable via the CRISPR/Cas9 system while they retain their
ability to differentiate into highly migratory dendritic cells and other immune
cells. This will foster the study of all aspects of dendritic cell biology and
beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
opportunity to work in \r\nhis group and for his support throughout the years. He
is a truly inspiring person and \r\nthe best boss one can imagine. I would
\ also like to thank all current and past \r\nmembers of the Sixt group for
their help and the great working atmosphere in the lab. \r\nIt is a true privilege
to work with such a bright, funny and friendly group of people and \r\nI’m proud
\ that I could be part of it. Furthermore, I would like to say ‘thank
\ you’ to Daria Siekhaus for all the meetings and discussion we had throughout
the years \r\nand to Federica Benvenuti for being part of my committee.
\ I am also grateful to Jack \r\nMerrin in the nanofabrication facility
\ and all the people working in the bioimaging-\r\n, the electron microscopy-
and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998
apa: Leithner, A. F. (2018). Branched actin networks in dendritic cell biology.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998
chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.
ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute
of Science and Technology Austria, 2018.
ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute
of Science and Technology Austria.
mla: Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology.
Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.
short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-07T12:39:44Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
file:
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checksum: d5e3edbac548c26c1fa43a4b37a54a4c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T23:30:17Z
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file_id: '6219'
file_name: PhD_thesis_AlexLeithner_final_version.docx
file_size: 29027671
relation: source_file
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checksum: 071f7476db29e41146824ebd0697cb10
content_type: application/pdf
creator: dernst
date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T11:17:16Z
embargo: 2019-04-15
file_id: '6220'
file_name: PhD_thesis_AlexLeithner.pdf
file_size: 66045341
relation: main_file
file_date_updated: 2021-02-11T23:30:17Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
record:
- id: '1321'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '15'
abstract:
- lang: eng
text: Although much is known about the physiological framework of T cell motility,
and numerous rate-limiting molecules have been identified through loss-of-function
approaches, an integrated functional concept of T cell motility is lacking. Here,
we used in vivo precision morphometry together with analysis of cytoskeletal dynamics
in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic
organs. We show that the contributions of the integrin LFA-1 and the chemokine
receptor CCR7 are complementary rather than positioned in a linear pathway, as
they are during leukocyte extravasation from the blood vasculature. Our data demonstrate
that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction
that is sufficient to drive locomotion in the absence of considerable surface
adhesions and plasma membrane flux.
acknowledged_ssus:
- _id: SSU
acknowledgement: This work was funded by grants from the European Research Council
(ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S.
and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457
and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).
article_processing_charge: No
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently
tune actin flow and substrate friction during intranodal migration of T cells.
Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z
apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J.,
… Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and
substrate friction during intranodal migration of T cells. Nature Immunology.
Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z
chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian
R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines
and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal
Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018.
https://doi.org/10.1038/s41590-018-0109-z.
ieee: M. Hons et al., “Chemokines and integrins independently tune actin
flow and substrate friction during intranodal migration of T cells,” Nature
Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.
ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J,
Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow
and substrate friction during intranodal migration of T cells. Nature Immunology.
19(6), 606–616.
mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow
and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology,
vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.
short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz,
J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.
date_created: 2018-12-11T11:44:10Z
date_published: 2018-05-18T00:00:00Z
date_updated: 2024-03-28T23:30:40Z
day: '18'
department:
- _id: MiSi
- _id: Bio
doi: 10.1038/s41590-018-0109-z
ec_funded: 1
external_id:
isi:
- '000433041500026'
pmid:
- '29777221'
intvolume: ' 19'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29777221
month: '05'
oa: 1
oa_version: Published Version
page: 606 - 616
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '8040'
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Chemokines and integrins independently tune actin flow and substrate friction
during intranodal migration of T cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 19
year: '2018'
...
---
_id: '569'
abstract:
- lang: eng
text: The actomyosin ring generates force to ingress the cytokinetic cleavage furrow
in animal cells, yet its filament organization and the mechanism of contractility
is not well understood. We quantified actin filament order in human cells using
fluorescence polarization microscopy and found that cleavage furrow ingression
initiates by contraction of an equatorial actin network with randomly oriented
filaments. The network subsequently gradually reoriented actin filaments along
the cell equator. This strictly depended on myosin II activity, suggesting local
network reorganization by mechanical forces. Cortical laser microsurgery revealed
that during cytokinesis progression, mechanical tension increased substantially
along the direction of the cell equator, while the network contracted laterally
along the pole-to-pole axis without a detectable increase in tension. Our data
suggest that an asymmetric increase in cortical tension promotes filament reorientation
along the cytokinetic cleavage furrow, which might have implications for diverse
other biological processes involving actomyosin rings.
article_number: e30867
author:
- first_name: Felix
full_name: Spira, Felix
last_name: Spira
- first_name: Sara
full_name: Cuylen Haering, Sara
last_name: Cuylen Haering
- first_name: Shalin
full_name: Mehta, Shalin
last_name: Mehta
- first_name: Matthias
full_name: Samwer, Matthias
last_name: Samwer
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Amitabh
full_name: Verma, Amitabh
last_name: Verma
- first_name: Rudolf
full_name: Oldenbourg, Rudolf
last_name: Oldenbourg
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Daniel
full_name: Gerlich, Daniel
last_name: Gerlich
citation:
ama: Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells
initiates by contraction of an equatorial actomyosin network composed of randomly
oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867
apa: Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma,
A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.30867
chicago: Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne
Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich.
“Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin
Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences
Publications, 2017. https://doi.org/10.7554/eLife.30867.
ieee: F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments,”
eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg
R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. eLife.
6, e30867.
mla: Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction
of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.”
ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867.
short: F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma,
R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-06T00:00:00Z
date_updated: 2023-02-23T12:30:29Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.30867
file:
- access_level: open_access
checksum: ba09c1451153d39e4f4b7cee013e314c
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:40Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4829'
file_name: IST-2017-919-v1+1_elife-30867-figures-v1.pdf
file_size: 9666973
relation: main_file
- access_level: open_access
checksum: 01eb51f1d6ad679947415a51c988e137
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:41Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4830'
file_name: IST-2017-919-v1+2_elife-30867-v1.pdf
file_size: 5951246
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7245'
pubrep_id: '919'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin
network composed of randomly oriented filaments
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '571'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis and play diverse
roles during immune responses. Despite these versatile tasks in mammalian biology,
their skills on a cellular level are deemed limited, mainly consisting in rolling,
adhesion, and aggregate formation. Here, we identify an unappreciated asset of
platelets and show that adherent platelets use adhesion receptors to mechanically
probe the adhesive substrate in their local microenvironment. When actomyosin-dependent
traction forces overcome substrate resistance, platelets migrate and pile up the
adhesive substrate together with any bound particulate material. They use this
ability to act as cellular scavengers, scanning the vascular surface for potential
invaders and collecting deposited bacteria. Microbe collection by migrating platelets
boosts the activity of professional phagocytes, exacerbating inflammatory tissue
injury in sepsis. This assigns platelets a central role in innate immune responses
and identifies them as potential targets to dampen inflammatory tissue damage
in clinical scenarios of severe systemic infection. In addition to their role
in thrombosis and hemostasis, platelets can also migrate to sites of infection
to help trap bacteria and clear the vascular surface.
author:
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Zerkah
full_name: Ahmad, Zerkah
last_name: Ahmad
- first_name: Gerhild
full_name: Rosenberger, Gerhild
last_name: Rosenberger
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Benjamin
full_name: Busch, Benjamin
last_name: Busch
- first_name: Gökce
full_name: Yavuz, Gökce
last_name: Yavuz
- first_name: Manja
full_name: Luckner, Manja
last_name: Luckner
- first_name: Hellen
full_name: Ishikawa Ankerhold, Hellen
last_name: Ishikawa Ankerhold
- first_name: Roman
full_name: Hennel, Roman
last_name: Hennel
- first_name: Alexandre
full_name: Benechet, Alexandre
last_name: Benechet
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Sue
full_name: Chandraratne, Sue
last_name: Chandraratne
- first_name: Irene
full_name: Schubert, Irene
last_name: Schubert
- first_name: Sebastian
full_name: Helmer, Sebastian
last_name: Helmer
- first_name: Bianca
full_name: Striednig, Bianca
last_name: Striednig
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Marek
full_name: Janko, Marek
last_name: Janko
- first_name: Ralph
full_name: Böttcher, Ralph
last_name: Böttcher
- first_name: Admar
full_name: Verschoor, Admar
last_name: Verschoor
- first_name: Catherine
full_name: Leon, Catherine
last_name: Leon
- first_name: Christian
full_name: Gachet, Christian
last_name: Gachet
- first_name: Thomas
full_name: Gudermann, Thomas
last_name: Gudermann
- first_name: Michael
full_name: Mederos Y Schnitzler, Michael
last_name: Mederos Y Schnitzler
- first_name: Zachary
full_name: Pincus, Zachary
last_name: Pincus
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Rainer
full_name: Haas, Rainer
last_name: Haas
- first_name: Gerhard
full_name: Wanner, Gerhard
last_name: Wanner
- first_name: Kirsten
full_name: Lauber, Kirsten
last_name: Lauber
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano
scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382.
doi:10.1016/j.cell.2017.11.001
apa: Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B.,
… Massberg, S. (2017). Migrating platelets are mechano scavengers that collect
and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001
chicago: Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo
Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano
Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017.
https://doi.org/10.1016/j.cell.2017.11.001.
ieee: F. R. Gärtner et al., “Migrating platelets are mechano scavengers that
collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press,
pp. 1368–1382, 2017.
ista: Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner
M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert
I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet
C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner
G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers
that collect and bundle bacteria. Cell Press. 171(6), 1368–1382.
mla: Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That
Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press,
2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001.
short: F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G.
Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S.
Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher,
A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus,
M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press
171 (2017) 1368–1382.
date_created: 2018-12-11T11:47:15Z
date_published: 2017-11-30T00:00:00Z
date_updated: 2021-01-12T08:03:15Z
day: '30'
department:
- _id: MiSi
doi: 10.1016/j.cell.2017.11.001
ec_funded: 1
intvolume: ' 171'
issue: '6'
language:
- iso: eng
month: '11'
oa_version: None
page: 1368 - 1382
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Cell Press
publication_identifier:
issn:
- '00928674'
publication_status: published
publisher: Cell Press
publist_id: '7243'
quality_controlled: '1'
scopus_import: 1
status: public
title: Migrating platelets are mechano scavengers that collect and bundle bacteria
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 171
year: '2017'
...
---
_id: '659'
abstract:
- lang: eng
text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed
by Arp2/3 complex-dependent branching thought to be crucial for force generation
and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors
targeting to the lamellipodium tip and shown here to nucleate and elongate actin
filaments with complementary activities in vitro. In migrating B16-F1 melanoma
cells, both formins contribute to the velocity of lamellipodium protrusion. Loss
of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width,
actin filament density and -bundling, without changing patterns of Arp2/3 complex
incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost
completely abolishes protrusion forces exerted by lamellipodia and modifies their
ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3
in fibroblasts reduces both migration and capability of cells to move against
viscous media. Together, we conclude that force generation in lamellipodia strongly
depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent
filament branching.
article_number: '14832'
article_processing_charge: No
author:
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Moritz
full_name: Winterhoff, Moritz
last_name: Winterhoff
- first_name: Vanessa
full_name: Dimchev, Vanessa
last_name: Dimchev
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Tobias
full_name: Thalheim, Tobias
last_name: Thalheim
- first_name: Anika
full_name: Freise, Anika
last_name: Freise
- first_name: Stefan
full_name: Brühmann, Stefan
last_name: Brühmann
- first_name: Jana
full_name: Kollasser, Jana
last_name: Kollasser
- first_name: Jennifer
full_name: Block, Jennifer
last_name: Block
- first_name: Georgi A
full_name: Dimchev, Georgi A
last_name: Dimchev
- first_name: Matthias
full_name: Geyer, Matthias
last_name: Geyer
- first_name: Hams
full_name: Schnittler, Hams
last_name: Schnittler
- first_name: Cord
full_name: Brakebusch, Cord
last_name: Brakebusch
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Marie
full_name: Carlier, Marie
last_name: Carlier
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Josef
full_name: Käs, Josef
last_name: Käs
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
citation:
ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force
generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832
apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A.,
… Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832
chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim,
Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force
Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832.
ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,”
Nature Communications, vol. 8. Nature Publishing Group, 2017.
ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann
S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal
T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial
force generation. Nature Communications. 8, 14832.
mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature
Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832.
short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S.
Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch,
T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications
8 (2017).
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-22T00:00:00Z
date_updated: 2021-01-12T08:08:06Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms14832
file:
- access_level: open_access
checksum: dae30190291c3630e8102d8714a8d23e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:21Z
date_updated: 2020-07-14T12:47:34Z
file_id: '5072'
file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf
file_size: 9523746
relation: main_file
file_date_updated: 2020-07-14T12:47:34Z
has_accepted_license: '1'
intvolume: ' 8'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7075'
pubrep_id: '902'
quality_controlled: '1'
scopus_import: 1
status: public
title: FMNL formins boost lamellipodial force generation
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '668'
abstract:
- lang: eng
text: Macrophage filopodia, finger-like membrane protrusions, were first implicated
in phagocytosis more than 100 years ago, but little is still known about the involvement
of these actin-dependent structures in particle clearance. Using spinning disk
confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP
macrophages, we show that filopodia, or filopodia-like structures, support pathogen
clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial
(Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing
toward the cell body, the most common mode of capture; (ii) capturing via the
tip followed by retraction; (iii) combinations of surfing and retraction; or (iv)
sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces
cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and
filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii)
the rapid growth of new protrusions. To explore the role of filopodia-inducing
Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages
exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which
could be explained by the marked rounded-up morphology of these cells. Macrophages
lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility,
and phagocytic cup formation, but displayed markedly reduced filopodia formation.
In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage
filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia
or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial
spreading.
article_type: original
author:
- first_name: Markus
full_name: Horsthemke, Markus
last_name: Horsthemke
- first_name: Anne
full_name: Bachg, Anne
last_name: Bachg
- first_name: Katharina
full_name: Groll, Katharina
last_name: Groll
- first_name: Sven
full_name: Moyzio, Sven
last_name: Moyzio
- first_name: Barbara
full_name: Müther, Barbara
last_name: Müther
- first_name: Sandra
full_name: Hemkemeyer, Sandra
last_name: Hemkemeyer
- first_name: Roland
full_name: Wedlich Söldner, Roland
last_name: Wedlich Söldner
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Sebastian
full_name: Tacke, Sebastian
last_name: Tacke
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- first_name: Peter
full_name: Hanley, Peter
last_name: Hanley
citation:
ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics
in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion.
Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923
apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S.,
… Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture
and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological
Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923
chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther,
Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial
Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10
Deletion.” Journal of Biological Chemistry. American Society for Biochemistry
and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923.
ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle
capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal
of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry
and Molecular Biology, pp. 7258–7273, 2017.
ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich
Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial
dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10
deletion. Journal of Biological Chemistry. 292(17), 7258–7273.
mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle
Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal
of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry
and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923.
short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R.
Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological
Chemistry 292 (2017) 7258–7273.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-04-28T00:00:00Z
date_updated: 2021-01-12T08:08:34Z
day: '28'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1074/jbc.M116.766923
file:
- access_level: open_access
checksum: d488162874326a4bb056065fa549dc4a
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T15:25:42Z
date_updated: 2020-07-14T12:47:37Z
file_id: '6971'
file_name: 2017_JBC_Horsthemke.pdf
file_size: 5647880
relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: ' 292'
issue: '17'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 7258 - 7273
publication: Journal of Biological Chemistry
publication_identifier:
issn:
- '00219258'
publication_status: published
publisher: American Society for Biochemistry and Molecular Biology
publist_id: '7059'
quality_controlled: '1'
scopus_import: 1
status: public
title: Multiple roles of filopodial dynamics in particle capture and phagocytosis
and phenotypes of Cdc42 and Myo10 deletion
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 292
year: '2017'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '5'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '674'
abstract:
- lang: eng
text: Navigation of cells along gradients of guidance cues is a determining step
in many developmental and immunological processes. Gradients can either be soluble
or immobilized to tissues as demonstrated for the haptotactic migration of dendritic
cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate
how gradient characteristics govern cellular response patterns, we here introduce
an in vitro system allowing to track migratory responses of DCs to precisely controlled
immobilized gradients of CCL21. We find that haptotactic sensing depends on the
absolute CCL21 concentration and local steepness of the gradient, consistent with
a scenario where DC directionality is governed by the signal-to-noise ratio of
CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC
guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore,
we find that CCR7 signal termination by the G-protein-coupled receptor kinase
6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient
sensing in vitro and confirm those observations in vivo. These findings suggest
that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal
guidance in vivo.
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Teresa
full_name: Tarrant, Teresa
last_name: Tarrant
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic
chemokine gradients in a manner governed by signal to noise ratio and dependent
on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004
apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries,
I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients
in a manner governed by signal to noise ratio and dependent on GRK6. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004
chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus
Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret
Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio
and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.
ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine
gradients in a manner governed by signal to noise ratio and dependent on GRK6,”
Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.
ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner
AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells
interpret haptotactic chemokine gradients in a manner governed by signal to noise
ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.
mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients
in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current
Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.
short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries,
A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt,
Current Biology 27 (2017) 1314–1325.
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2023-02-23T12:50:44Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
intvolume: ' 27'
issue: '9'
language:
- iso: eng
month: '05'
oa_version: None
page: 1314 - 1325
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '7050'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed
by signal to noise ratio and dependent on GRK6
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...
---
_id: '677'
abstract:
- lang: eng
text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler
that acts in transcription, replication, and genome stability. It is required
for resistance against genotoxic agents and is involved in the repair of DNA double-strand
breaks (DSBs) by homologous recombination (HR). However, the causes of the HR
defect in INO80-C mutant cells are controversial. Here, we unite previous findings
using a system to study HR with high spatial resolution in budding yeast. We find
that INO80-C has at least two distinct functions during HR—DNA end resection and
presynaptic filament formation. Importantly, the second function is linked to
the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation
and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic
filament formation is the crucial INO80-C function during HR.
author:
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Boris
full_name: Pfander, Boris
last_name: Pfander
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z
to promote presynaptic filament formation during homologous recombination. Cell
Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051
apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80
complex removes H2A.Z to promote presynaptic filament formation during homologous
recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051
chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.
ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.
ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes
H2A.Z to promote presynaptic filament formation during homologous recombination.
Cell Reports. 19(7), 1294–1303.
mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic
Filament Formation during Homologous Recombination.” Cell Reports, vol.
19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.
short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017)
1294–1303.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-16T00:00:00Z
date_updated: 2021-01-12T08:08:57Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
file:
- access_level: open_access
checksum: efc7287d9c6354983cb151880e9ad72a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:48Z
date_updated: 2020-07-14T12:47:40Z
file_id: '5171'
file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf
file_size: 3005610
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7046'
pubrep_id: '899'
quality_controlled: '1'
scopus_import: 1
status: public
title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during
homologous recombination
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '694'
abstract:
- lang: eng
text: A change regarding the extent of adhesion - hereafter referred to as adhesion
plasticity - between adhesive and less-adhesive states of mammalian cells is important
for their behavior. To investigate adhesion plasticity, we have selected a stable
isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension.
These suspension cells are unable to re-adhere to various matrices or to contract
three-dimensional collagen lattices. By using transcriptome analysis, we identified
the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity.
Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore,
by transiently challenging breast cancer cells to grow under non-adherent conditions
markedly reduces Tns3 protein expression, which is regained upon re-adhesion.
Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion,
spreading and migration. Tns3-knockdown cells display impaired structure and dynamics
of focal adhesion complexes as determined by immunostaining. Restoration of Tns3
protein expression in suspension cells partially rescues adhesion and focal contact
composition. Our work identifies Tns3 as a crucial focal adhesion component regulated
by, and functionally contributing to, the switch between adhesive and non-adhesive
states in MDA-MB-468 cancer cells.
article_type: original
author:
- first_name: Astrid
full_name: Veß, Astrid
last_name: Veß
- first_name: Ulrich
full_name: Blache, Ulrich
last_name: Blache
- first_name: Laura
full_name: Leitner, Laura
last_name: Leitner
- first_name: Angela
full_name: Kurz, Angela
last_name: Kurz
- first_name: Anja
full_name: Ehrenpfordt, Anja
last_name: Ehrenpfordt
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Guido
full_name: Posern, Guido
last_name: Posern
citation:
ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells
reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell
Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899
apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., &
Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual
regulation of tensin3 and adhesion plasticity. Journal of Cell Science.
Company of Biologists. https://doi.org/10.1242/jcs.200899
chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt,
Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells
Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell
Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899.
ieee: A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals
mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science,
vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.
ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017.
A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184.
mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual
Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science,
vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.
short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern,
Journal of Cell Science 130 (2017) 2172–2184.
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:41Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1242/jcs.200899
external_id:
pmid:
- '28515231'
file:
- access_level: open_access
checksum: 42c81a0a4fc3128883b391c3af3f74bc
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T09:43:56Z
date_updated: 2020-07-14T12:47:45Z
file_id: '6966'
file_name: 2017_CellScience_Vess.pdf
file_size: 10847596
relation: main_file
file_date_updated: 2020-07-14T12:47:45Z
has_accepted_license: '1'
intvolume: ' 130'
issue: '13'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 2172 - 2184
pmid: 1
publication: Journal of Cell Science
publication_identifier:
issn:
- '00219533'
publication_status: published
publisher: Company of Biologists
publist_id: '7008'
quality_controlled: '1'
scopus_import: 1
status: public
title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 130
year: '2017'
...
---
_id: '1161'
abstract:
- lang: eng
text: Coordinated changes of cell shape are often the result of the excitable, wave-like
dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion
waves arise from mechanochemical crosstalk between adhesion sites, membrane tension
and the actin protrusive machinery.
article_processing_charge: No
author:
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology.
2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035'
apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035'
chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current
Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.'
ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current
Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.'
ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology.
27(1), R24–R25.'
mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current
Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.'
short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.
date_created: 2018-12-11T11:50:29Z
date_published: 2017-01-09T00:00:00Z
date_updated: 2023-09-20T11:28:19Z
day: '09'
department:
- _id: MiSi
doi: 10.1016/j.cub.2016.11.035
external_id:
isi:
- '000391902500010'
intvolume: ' 27'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: R24 - R25
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '6197'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: Making the waves'
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 27
year: '2017'
...
---
_id: '727'
abstract:
- lang: eng
text: 'Actin filaments polymerizing against membranes power endocytosis, vesicular
traffic, and cell motility. In vitro reconstitution studies suggest that the structure
and the dynamics of actin networks respond to mechanical forces. We demonstrate
that lamellipodial actin of migrating cells responds to mechanical load when membrane
tension is modulated. In a steady state, migrating cell filaments assume the canonical
dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension
triggers a dense network with a broadened range of angles, whereas decreased tension
causes a shift to a sparse configuration dominated by filaments growing perpendicularly
to the plasma membrane. We show that these responses emerge from the geometry
of branched actin: when load per filament decreases, elongation speed increases
and perpendicular filaments gradually outcompete others because they polymerize
the shortest distance to the membrane, where they are protected from capping.
This network-intrinsic geometrical adaptation mechanism tunes protrusive force
in response to mechanical load.'
acknowledged_ssus:
- _id: ScienComp
article_processing_charge: No
author:
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Gregory
full_name: Szep, Gregory
id: 4BFB7762-F248-11E8-B48F-1D18A9856A87
last_name: Szep
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Arnon
full_name: Lieber, Arnon
last_name: Lieber
- first_name: Christoph
full_name: Winkler, Christoph
last_name: Winkler
- first_name: Karsten
full_name: Kruse, Karsten
last_name: Kruse
- first_name: John
full_name: Small, John
last_name: Small
- first_name: Christian
full_name: Schmeiser, Christian
last_name: Schmeiser
- first_name: Kinneret
full_name: Keren, Kinneret
last_name: Keren
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin
networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051
apa: Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C.,
… Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2017.07.051
chicago: Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber,
Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin
Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051.
ieee: J. Mueller et al., “Load adaptation of lamellipodial actin networks,”
Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.
ista: Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K,
Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of
lamellipodial actin networks. Cell. 171(1), 188–200.
mla: Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell,
vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051.
short: J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K.
Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017)
188–200.
date_created: 2018-12-11T11:48:10Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2023-09-28T11:33:49Z
day: '21'
department:
- _id: MiSi
- _id: Bio
doi: 10.1016/j.cell.2017.07.051
ec_funded: 1
external_id:
isi:
- '000411331800020'
intvolume: ' 171'
isi: 1
issue: '1'
language:
- iso: eng
month: '09'
oa_version: None
page: 188 - 200
project:
- _id: 25AD6156-B435-11E9-9278-68D0E5697425
grant_number: LS13-029
name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Cell
publication_identifier:
issn:
- '00928674'
publication_status: published
publisher: Cell Press
publist_id: '6951'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Load adaptation of lamellipodial actin networks
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 171
year: '2017'
...
---
_id: '5567'
abstract:
- lang: eng
text: Immunological synapse DC-Tcells
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Immunological synapse DC-Tcells. 2017. doi:10.15479/AT:ISTA:71
apa: Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science
and Technology Austria. https://doi.org/10.15479/AT:ISTA:71
chicago: Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of
Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:71.
ieee: A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and
Technology Austria, 2017.
ista: Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and
Technology Austria, 10.15479/AT:ISTA:71.
mla: Leithner, Alexander F. Immunological Synapse DC-Tcells. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:71.
short: A.F. Leithner, (2017).
datarep_id: '71'
date_created: 2018-12-12T12:31:34Z
date_published: 2017-08-09T00:00:00Z
date_updated: 2024-02-21T13:47:00Z
day: '09'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:71
file:
- access_level: open_access
checksum: 3d6942d47d0737d064706b5728c4d8c8
content_type: video/x-msvideo
creator: system
date_created: 2018-12-12T13:02:47Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5612'
file_name: IST-2017-71-v1+1_Synapse_1.avi
file_size: 236204020
relation: main_file
- access_level: open_access
checksum: 4850006c047b0147a9e85b3c2f6f0af4
content_type: video/x-msvideo
creator: system
date_created: 2018-12-12T13:02:51Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5613'
file_name: IST-2017-71-v1+2_Synapse_2.avi
file_size: 226232496
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
has_accepted_license: '1'
keyword:
- Immunological synapse
license: https://creativecommons.org/publicdomain/zero/1.0/
month: '08'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Immunological synapse DC-Tcells
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '664'
abstract:
- lang: eng
text: Immune cells communicate using cytokine signals, but the quantitative rules
of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et
al. (2017) suggest that the distribution of a cytokine within a lymphatic organ
is primarily governed by the local density of cells consuming it.
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520.
doi:10.1016/j.immuni.2017.04.006
apa: Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity.
Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006
chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity.
Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006.
ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity,
vol. 46, no. 4. Cell Press, pp. 519–520, 2017.
ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.
mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity,
vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006.
short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2024-03-28T23:30:09Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
intvolume: ' 46'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 519 - 520
publication: Immunity
publication_identifier:
issn:
- '10747613'
publication_status: published
publisher: Cell Press
publist_id: '7065'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: The dynamic cytokine niche
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 46
year: '2017'
...
---
_id: '679'
abstract:
- lang: eng
text: Protective responses against pathogens require a rapid mobilization of resting
neutrophils and the timely removal of activated ones. Neutrophils are exceptionally
short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged
neutrophils is regulated differently from that in the circulating steady-state
pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing
protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated
infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient
neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection
site. In the context of myeloid-specific deletion of Ttp, the potentiation of
neutrophil deployment protected mice against lethal soft tissue infection with
Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome
analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically
associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not
other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher
Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP.
The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable
to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates
that posttranscriptional gene regulation by TTP schedules the termination of the
antimicrobial engagement of neutrophils. The balancing role of TTP comes at the
cost of an increased risk of bacterial infections.
acknowledgement: This work was supported by grants from the Austrian Science Fund
(FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union
Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN)
for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement
PITN-GA-2012-316682; and by a joint research cluster initiative of the University
of Vienna and the Medical University of Vienna.
author:
- first_name: Florian
full_name: Ebner, Florian
last_name: Ebner
- first_name: Vitaly
full_name: Sedlyarov, Vitaly
last_name: Sedlyarov
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Masa
full_name: Ivin, Masa
last_name: Ivin
- first_name: Franz
full_name: Kratochvill, Franz
last_name: Kratochvill
- first_name: Nina
full_name: Gratz, Nina
last_name: Gratz
- first_name: Lukas
full_name: Kenner, Lukas
last_name: Kenner
- first_name: Andreas
full_name: Villunger, Andreas
last_name: Villunger
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Pavel
full_name: Kovarik, Pavel
last_name: Kovarik
citation:
ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin
schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631
apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N.,
… Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis
of pathogen-engaged neutrophils during bacterial infection. The Journal of
Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631
chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill,
Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik.
“The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged
Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation.
American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631.
ieee: F. Ebner et al., “The RNA-binding protein tristetraprolin schedules
apoptosis of pathogen-engaged neutrophils during bacterial infection,” The
Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical
Investigation, pp. 2051–2065, 2017.
ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L,
Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin
schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
The Journal of Clinical Investigation. 127(6), 2051–2065.
mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis
of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of
Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation,
2017, pp. 2051–65, doi:10.1172/JCI80631.
short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L.
Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation
127 (2017) 2051–2065.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2024-03-28T23:30:23Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
pmid:
- '28504646'
intvolume: ' 127'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/
month: '06'
oa: 1
oa_version: Submitted Version
page: 2051 - 2065
pmid: 1
project:
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
publication: The Journal of Clinical Investigation
publication_identifier:
issn:
- '00219738'
publication_status: published
publisher: American Society for Clinical Investigation
publist_id: '7038'
quality_controlled: '1'
related_material:
record:
- id: '12401'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged
neutrophils during bacterial infection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 127
year: '2017'
...
---
_id: '1137'
abstract:
- lang: eng
text: RASGRP1 is an important guanine nucleotide exchange factor and activator of
the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences
of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial
and viral infections, born to healthy consanguineous parents, we used homozygosity
mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1.
This variant segregated perfectly with the disease and has not been reported in
genetic databases. RASGRP1 deficiency was associated in T cells and B cells with
decreased phosphorylation of the extracellular-signal-regulated serine kinase
ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency
also resulted in defective proliferation, activation and motility of T cells and
B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity
with defective granule convergence and actin accumulation. Interaction proteomics
identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links
RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation
of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed
the migration and activation defects of RASGRP1-deficient lymphocytes.
article_processing_charge: No
article_type: original
author:
- first_name: Elisabeth
full_name: Salzer, Elisabeth
last_name: Salzer
- first_name: Deniz
full_name: Çaǧdaş, Deniz
last_name: Çaǧdaş
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Emily
full_name: Mace, Emily
last_name: Mace
- first_name: Wojciech
full_name: Garncarz, Wojciech
last_name: Garncarz
- first_name: Oezlem
full_name: Petronczki, Oezlem
last_name: Petronczki
- first_name: René
full_name: Platzer, René
last_name: Platzer
- first_name: Laurène
full_name: Pfajfer, Laurène
last_name: Pfajfer
- first_name: Ivan
full_name: Bilic, Ivan
last_name: Bilic
- first_name: Sol
full_name: Ban, Sol
last_name: Ban
- first_name: Katharina
full_name: Willmann, Katharina
last_name: Willmann
- first_name: Malini
full_name: Mukherjee, Malini
last_name: Mukherjee
- first_name: Verena
full_name: Supper, Verena
last_name: Supper
- first_name: Hsiangting
full_name: Hsu, Hsiangting
last_name: Hsu
- first_name: Pinaki
full_name: Banerjee, Pinaki
last_name: Banerjee
- first_name: Papiya
full_name: Sinha, Papiya
last_name: Sinha
- first_name: Fabienne
full_name: Mcclanahan, Fabienne
last_name: Mcclanahan
- first_name: Gerhard
full_name: Zlabinger, Gerhard
last_name: Zlabinger
- first_name: Winfried
full_name: Pickl, Winfried
last_name: Pickl
- first_name: John
full_name: Gribben, John
last_name: Gribben
- first_name: Hannes
full_name: Stockinger, Hannes
last_name: Stockinger
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Johannes
full_name: Huppa, Johannes
last_name: Huppa
- first_name: Loï̈C
full_name: Dupré, Loï̈C
last_name: Dupré
- first_name: Özden
full_name: Sanal, Özden
last_name: Sanal
- first_name: Ulrich
full_name: Jäger, Ulrich
last_name: Jäger
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Ilhan
full_name: Tezcan, Ilhan
last_name: Tezcan
- first_name: Jordan
full_name: Orange, Jordan
last_name: Orange
- first_name: Kaan
full_name: Boztug, Kaan
last_name: Boztug
citation:
ama: Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency
with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360.
doi:10.1038/ni.3575
apa: Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., …
Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal
dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575
chicago: Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz,
Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency
with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing
Group, 2016. https://doi.org/10.1038/ni.3575.
ieee: E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with
impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature
Publishing Group, pp. 1352–1360, 2016.
ista: Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer
L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha
P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa
J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1
deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature
Immunology. 17(12), 1352–1360.
mla: Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with
Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature
Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575.
short: E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer,
L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P.
Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger,
K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange,
K. Boztug, Nature Immunology 17 (2016) 1352–1360.
date_created: 2018-12-11T11:50:21Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:33Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/ni.3575
external_id:
pmid:
- '27776107'
intvolume: ' 17'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263
month: '12'
oa: 1
oa_version: Submitted Version
page: 1352 - 1360
pmid: 1
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6221'
quality_controlled: '1'
scopus_import: 1
status: public
title: RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2016'
...
---
_id: '1142'
abstract:
- lang: eng
text: Hemolysis drives susceptibility to bacterial infections and predicts poor
outcome from sepsis. These detrimental effects are commonly considered to be a
consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative
sepsis model and found that elevated heme levels impaired the control of bacterial
proliferation independently of heme-iron acquisition by pathogens. Heme strongly
inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting
actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein
Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach
revealed that quinine effectively prevented heme effects on the cytoskeleton,
restored phagocytosis and improved survival in sepsis. These mechanistic insights
provide potential therapeutic targets for patients with sepsis or hemolytic disorders.
acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University)
and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for
providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s
Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct.
pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of
Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns
Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding
retrovirus was kindly provided by A. Leithner (Institute of Science and Technology
Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research,
National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent
technical support (Core imaging facility, Medical University of Vienna). We thank
D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was
supported by the Austrian Academy of Sciences, the Science Fund of the Austrian
National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA
framework (to S.Knapp).'
author:
- first_name: Rui
full_name: Martins, Rui
last_name: Martins
- first_name: Julia
full_name: Maier, Julia
last_name: Maier
- first_name: Anna
full_name: Gorki, Anna
last_name: Gorki
- first_name: Kilian
full_name: Huber, Kilian
last_name: Huber
- first_name: Omar
full_name: Sharif, Omar
last_name: Sharif
- first_name: Philipp
full_name: Starkl, Philipp
last_name: Starkl
- first_name: Simona
full_name: Saluzzo, Simona
last_name: Saluzzo
- first_name: Federica
full_name: Quattrone, Federica
last_name: Quattrone
- first_name: Riem
full_name: Gawish, Riem
last_name: Gawish
- first_name: Karin
full_name: Lakovits, Karin
last_name: Lakovits
- first_name: Michael
full_name: Aichinger, Michael
last_name: Aichinger
- first_name: Branka
full_name: Radic Sarikas, Branka
last_name: Radic Sarikas
- first_name: Charles
full_name: Lardeau, Charles
last_name: Lardeau
- first_name: Anastasiya
full_name: Hladik, Anastasiya
last_name: Hladik
- first_name: Ana
full_name: Korosec, Ana
last_name: Korosec
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Michelle
full_name: Duggan, Michelle
id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87
last_name: Duggan
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Harald
full_name: Esterbauer, Harald
last_name: Esterbauer
- first_name: Jacques
full_name: Colinge, Jacques
last_name: Colinge
- first_name: Stephanie
full_name: Eisenbarth, Stephanie
last_name: Eisenbarth
- first_name: Thomas
full_name: Decker, Thomas
last_name: Decker
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Stefan
full_name: Kubicek, Stefan
last_name: Kubicek
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Giulio
full_name: Superti Furga, Giulio
last_name: Superti Furga
- first_name: Sylvia
full_name: Knapp, Sylvia
last_name: Knapp
citation:
ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility
to infection via disruption of phagocyte functions. Nature Immunology.
2016;17(12):1361-1372. doi:10.1038/ni.3590
apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp,
S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption
of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590
chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp
Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to
Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature
Publishing Group, 2016. https://doi.org/10.1038/ni.3590.
ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to
infection via disruption of phagocyte functions,” Nature Immunology, vol.
17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.
ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone
F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec
A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth
S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme
drives hemolysis-induced susceptibility to infection via disruption of phagocyte
functions. Nature Immunology. 17(12), 1361–1372.
mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection
via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no.
12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590.
short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo,
F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau,
A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer,
J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti
Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.
date_created: 2018-12-11T11:50:22Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:48:36Z
day: '01'
department:
- _id: MiSi
- _id: PeJo
doi: 10.1038/ni.3590
intvolume: ' 17'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d
month: '12'
oa: 1
oa_version: Submitted Version
page: 1361 - 1372
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6216'
quality_controlled: '1'
scopus_import: 1
status: public
title: Heme drives hemolysis-induced susceptibility to infection via disruption of
phagocyte functions
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 17
year: '2016'
...
---
_id: '1150'
abstract:
- lang: eng
text: When neutrophils infiltrate a site of inflammation, they have to stop at the
right place to exert their effector function. In this issue of Developmental Cell,
Wang et al. (2016) show that neutrophils sense reactive oxygen species via the
TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental
Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017
apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil
Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017
chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017.
ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,”
Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.
ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration.
Developmental Cell. 38(5), 448–450.
mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50,
doi:10.1016/j.devcel.2016.08.017.
short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.
date_created: 2018-12-11T11:50:25Z
date_published: 2016-09-12T00:00:00Z
date_updated: 2021-01-12T06:48:39Z
day: '12'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2016.08.017
intvolume: ' 38'
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 448 - 450
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '6208'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Radical Break Restraining Neutrophil Migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2016'
...
---
_id: '1154'
abstract:
- lang: eng
text: "Cellular locomotion is a central hallmark of eukaryotic life. It is governed
by cell-extrinsic molecular factors, which can either emerge in the soluble phase
or as immobilized, often adhesive ligands. To encode for direction, every cue
must be present as a spatial or temporal gradient. Here, we developed a microfluidic
chamber that allows measurement of cell migration in combined response to surface
immobilized and soluble molecular gradients. As a proof of principle we study
the response of dendritic cells to their major guidance cues, chemokines. The
majority of data on chemokine gradient sensing is based on in vitro studies employing
soluble gradients. Despite evidence suggesting that in vivo chemokines are often
immobilized to sugar residues, limited information is available how cells respond
to immobilized chemokines. We tracked migration of dendritic cells towards immobilized
gradients of the chemokine CCL21 and varying superimposed soluble gradients of
CCL19. Differential migratory patterns illustrate the potential of our setup to
quantitatively study the competitive response to both types of gradients. Beyond
chemokines our approach is broadly applicable to alternative systems of chemo-
and haptotaxis such as cells migrating along gradients of adhesion receptor ligands
vs. any soluble cue. \r\n"
acknowledgement: 'This work was supported by the Swiss National Science Foundation
(Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society
(research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF)
to J.S., the European Research Council (grant ERC GA 281556) and a START award from
the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility'
article_number: '36440'
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Tino
full_name: Frank, Tino
last_name: Frank
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Savaş
full_name: Tay, Savaş
last_name: Tay
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
citation:
ama: Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring
cell migration towards substrate bound and soluble chemokine gradients. Scientific
Reports. 2016;6. doi:10.1038/srep36440
apa: Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach,
M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports.
Nature Publishing Group. https://doi.org/10.1038/srep36440
chicago: Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild,
Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic
Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine
Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440.
ieee: J. Schwarz et al., “A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients,” Scientific Reports,
vol. 6. Nature Publishing Group, 2016.
ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay
S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports. 6,
36440.
mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards
Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol.
6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440.
short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach,
S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016).
date_created: 2018-12-11T11:50:27Z
date_published: 2016-11-07T00:00:00Z
date_updated: 2021-01-12T06:48:41Z
day: '07'
ddc:
- '579'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
- _id: ToBo
doi: 10.1038/srep36440
ec_funded: 1
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:32Z
date_updated: 2018-12-12T10:09:32Z
file_id: '4756'
file_name: IST-2017-744-v1+1_srep36440.pdf
file_size: 2353456
relation: main_file
file_date_updated: 2018-12-12T10:09:32Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '6204'
pubrep_id: '744'
quality_controlled: '1'
scopus_import: 1
status: public
title: A microfluidic device for measuring cell migration towards substrate bound
and soluble chemokine gradients
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2016'
...
---
_id: '1201'
abstract:
- lang: eng
text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear
actin cytoskeleton that protects the nucleus and its genomic content of migrating
cells squeezing through small spaces.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449.
doi:10.1016/j.cell.2016.11.024
apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2016.11.024
chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell.
Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024.
ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell,
vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.
ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.
mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell,
vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024.
short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.
date_created: 2018-12-11T11:50:41Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:49:03Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.cell.2016.11.024
intvolume: ' 167'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1448 - 1449
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '6149'
quality_controlled: '1'
scopus_import: 1
status: public
title: Formin’ a nuclear protection
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 167
year: '2016'
...
---
_id: '1217'
abstract:
- lang: eng
text: Understanding the regulation of T-cell responses during inflammation and auto-immunity
is fundamental for designing efficient therapeutic strategies against immune diseases.
In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived
immunosuppressive molecule. We describe for the first time that T cells secrete
PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine
PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation
in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation.
PGE 2 was found to provide additive co-stimulatory signaling through AKT activation.
Intravital multiphoton microscopy showed that triggering EP receptors in T cells
is also essential for the stability of T cell-dendritic cell (DC) interactions
and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We
further demonstrated that blocking EP receptors in T cells during the initial
phase of collagen-induced arthritis in mice resulted in a reduction of clinical
arthritis. This could be attributable to defective T-cell activation, accompanied
by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining
LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations
of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T
cells to attain a favorable activation threshold. PGE 2 signaling in T cells is
also required for maintaining long and stable interactions with DCs within LNs.
Blockade of EP receptors in vivo impairs T-cell activation and development of
T cell-mediated inflammatory responses. This may have implications in various
pathophysiological settings.
acknowledgement: This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006
awarded by the Spanish Ministry of Science and Education and the Community of Madrid
to Dr M Fresno.
author:
- first_name: Vinatha
full_name: Sreeramkumar, Vinatha
last_name: Sreeramkumar
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Carmen
full_name: Punzón, Carmen
last_name: Punzón
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: David
full_name: Sancho, David
last_name: Sancho
- first_name: Manuel
full_name: Fresno Forcelledo, Manuel
last_name: Fresno Forcelledo
- first_name: Natalia
full_name: Cuesta, Natalia
last_name: Cuesta
citation:
ama: Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation
requires signaling through prostaglandin E2 (EP) receptors. Immunology and
Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62
apa: Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo,
M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/icb.2015.62
chicago: Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David
Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming
and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology
and Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/icb.2015.62.
ieee: V. Sreeramkumar et al., “Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors,” Immunology and Cell Biology,
vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016.
ista: Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M,
Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through
prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51.
mla: Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires
Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology,
vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:10.1038/icb.2015.62.
short: V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo,
N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.
date_created: 2018-12-11T11:50:46Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:49:09Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/icb.2015.62
intvolume: ' 94'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 39 - 51
publication: Immunology and Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6116'
quality_controlled: '1'
scopus_import: 1
status: public
title: Efficient T-cell priming and activation requires signaling through prostaglandin
E2 (EP) receptors
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 94
year: '2016'
...
---
_id: '1285'
abstract:
- lang: eng
text: Cell migration is central to a multitude of physiological processes, including
embryonic development, immune surveillance, and wound healing, and deregulated
migration is key to cancer dissemination. Decades of investigations have uncovered
many of the molecular and physical mechanisms underlying cell migration. Together
with protrusion extension and cell body retraction, adhesion to the substrate
via specific focal adhesion points has long been considered an essential step
in cell migration. Although this is true for cells moving on two-dimensional substrates,
recent studies have demonstrated that focal adhesions are not required for cells
moving in three dimensions, in which confinement is sufficient to maintain a cell
in contact with its substrate. Here, we review the investigations that have led
to challenging the requirement of specific adhesions for migration, discuss the
physical mechanisms proposed for cell body translocation during focal adhesion-independent
migration, and highlight the remaining open questions for the future.
acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript
and Guillaume Salbreux for discussions. The authors are supported by the United
Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the
MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC
GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian
Science Foundation (M.S.).
author:
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Irene
full_name: Aspalter, Irene
last_name: Aspalter
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual
Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341
apa: Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent
cell migration. Annual Review of Cell and Developmental Biology. Annual
Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341
chicago: Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent
Cell Migration.” Annual Review of Cell and Developmental Biology. Annual
Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341.
ieee: E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,”
Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews,
pp. 469–490, 2016.
ista: Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration.
Annual Review of Cell and Developmental Biology. 32, 469–490.
mla: Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual
Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp.
469–90, doi:10.1146/annurev-cellbio-111315-125341.
short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental
Biology 32 (2016) 469–490.
date_created: 2018-12-11T11:51:08Z
date_published: 2016-10-06T00:00:00Z
date_updated: 2021-01-12T06:49:37Z
day: '06'
department:
- _id: MiSi
doi: 10.1146/annurev-cellbio-111315-125341
ec_funded: 1
intvolume: ' 32'
language:
- iso: eng
month: '10'
oa_version: None
page: 469 - 490
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Annual Review of Cell and Developmental Biology
publication_status: published
publisher: Annual Reviews
publist_id: '6031'
quality_controlled: '1'
scopus_import: 1
status: public
title: Focal adhesion-independent cell migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2016'
...
---
_id: '1490'
abstract:
- lang: eng
text: To induce adaptive immunity, dendritic cells (DCs) migrate through afferent
lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in
several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively
crawl into downstream collecting vessels. From there, they are next passively
and rapidly transported to the dLN by lymph flow. Here, we describe a role for
the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging
in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely
abolished DC migration from capillaries toward collecting vessels and reduced
the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that
in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial
monolayers, thereby inducing downstream-directed DC migration. These findings
reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through
the formation of a flow-induced gradient.
author:
- first_name: Erica
full_name: Russo, Erica
last_name: Russo
- first_name: Alvaro
full_name: Teijeira, Alvaro
last_name: Teijeira
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Ann
full_name: Willrodt, Ann
last_name: Willrodt
- first_name: Joël
full_name: Bloch, Joël
last_name: Bloch
- first_name: Maximilian
full_name: Nitschké, Maximilian
last_name: Nitschké
- first_name: Laura
full_name: Santambrogio, Laura
last_name: Santambrogio
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Cornelia
full_name: Halin, Cornelia
last_name: Halin
citation:
ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports.
2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048
apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké,
M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048
chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch,
Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt,
and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016.
https://doi.org/10.1016/j.celrep.2016.01.048.
ieee: E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7.
Cell Press, pp. 1723–1734, 2016.
ista: Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio
L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7),
1723–1734.
mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7,
Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048.
short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké,
L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734.
date_created: 2018-12-11T11:52:19Z
date_published: 2016-02-23T00:00:00Z
date_updated: 2021-01-12T06:51:07Z
day: '23'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2016.01.048
file:
- access_level: open_access
checksum: c98c1151d5f1e5ce1643a83d8d7f3c29
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:30Z
date_updated: 2020-07-14T12:44:58Z
file_id: '4948'
file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf
file_size: 5489897
relation: main_file
file_date_updated: 2020-07-14T12:44:58Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '7'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1723 - 1734
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '5697'
pubrep_id: '515'
quality_controlled: '1'
scopus_import: 1
status: public
title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent
lymphatic vessels
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2016'
...
---
_id: '1599'
abstract:
- lang: eng
text: "The addition of polysialic acid to N- and/or O-linked glycans, referred to
as polysialylation, is a rare posttranslational modification that is mainly known
to control the developmental plasticity of the nervous system. Here we show that
CCR7, the central chemokine receptor controlling immune cell trafficking to secondary
lymphatic organs, carries polysialic acid. This modification is essential for
the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking
is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed
lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function
analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited
conformation, which is released upon interaction with polysialic acid. Thus, we
describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic
basis.\r\n"
acknowledged_ssus:
- _id: SSU
acknowledgement: 'We thank S. Schüchner and E. Ogris for kindly providing the antibody
to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific
Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for
critically reading the manuscript. '
article_processing_charge: No
article_type: original
author:
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Christine
full_name: Moussion, Christine
id: 3356F664-F248-11E8-B48F-1D18A9856A87
last_name: Moussion
- first_name: Christopher
full_name: Veldkamp, Christopher
last_name: Veldkamp
- first_name: Rita
full_name: Gerardy Schahn, Rita
last_name: Gerardy Schahn
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Larry
full_name: Williams, Larry
last_name: Williams
- first_name: Gary
full_name: Chaffee, Gary
last_name: Chaffee
- first_name: Andrew
full_name: Phillips, Andrew
last_name: Phillips
- first_name: Friedrich
full_name: Freiberger, Friedrich
last_name: Freiberger
- first_name: Richard
full_name: Imre, Richard
last_name: Imre
- first_name: Deni
full_name: Taleski, Deni
last_name: Taleski
- first_name: Richard
full_name: Payne, Richard
last_name: Payne
- first_name: Asolina
full_name: Braun, Asolina
last_name: Braun
- first_name: Reinhold
full_name: Förster, Reinhold
last_name: Förster
- first_name: Karl
full_name: Mechtler, Karl
last_name: Mechtler
- first_name: Martina
full_name: Mühlenhoff, Martina
last_name: Mühlenhoff
- first_name: Brian
full_name: Volkman, Brian
last_name: Volkman
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic
cell trafficking by regulating chemokine recognition. Science. 2016;351(6269):186-190.
doi:10.1126/science.aad0512
apa: Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy Schahn, R., de Vries, I.,
Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking
by regulating chemokine recognition. Science. American Association for
the Advancement of Science. https://doi.org/10.1126/science.aad0512
chicago: Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy
Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation
Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science.
American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aad0512.
ieee: E. Kiermaier et al., “Polysialylation controls dendritic cell trafficking
by regulating chemokine recognition,” Science, vol. 351, no. 6269. American
Association for the Advancement of Science, pp. 186–190, 2016.
ista: Kiermaier E, Moussion C, Veldkamp C, Gerardy Schahn R, de Vries I, Williams
L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster
R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls
dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269),
186–190.
mla: Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking
by Regulating Chemokine Recognition.” Science, vol. 351, no. 6269, American
Association for the Advancement of Science, 2016, pp. 186–90, doi:10.1126/science.aad0512.
short: E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy Schahn, I. de Vries,
L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne,
A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science
351 (2016) 186–190.
date_created: 2018-12-11T11:52:57Z
date_published: 2016-01-08T00:00:00Z
date_updated: 2021-01-12T06:51:52Z
day: '08'
department:
- _id: MiSi
doi: 10.1126/science.aad0512
ec_funded: 1
external_id:
pmid:
- '26657283'
intvolume: ' 351'
issue: '6269'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/
month: '01'
oa: 1
oa_version: Submitted Version
page: 186 - 190
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A76F58-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '289720'
name: Stromal Cell-immune Cell Interactions in Health and Disease
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5570'
quality_controlled: '1'
scopus_import: 1
status: public
title: Polysialylation controls dendritic cell trafficking by regulating chemokine
recognition
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 351
year: '2016'
...
---
_id: '1597'
abstract:
- lang: eng
text: Chemokines are the main guidance cues directing leukocyte migration. Opposed
to early assumptions, chemokines do not necessarily act as soluble cues but are
often immobilized within tissues, e.g., dendritic cell migration toward lymphatic
vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled
assay systems to quantitatively study haptotaxis in vitro are still missing. In
this chapter, we describe an in vitro haptotaxis assay optimized for the unique
properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive
state, using laser-assisted protein adsorption by photobleaching. The cells follow
this immobilized CCL21 gradient in a haptotaxis chamber, which provides three
dimensionally confined migration conditions.
acknowledged_ssus:
- _id: Bio
acknowledgement: This work was supported by the Boehringer Ingelheim Fonds, the European
Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation
(FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input
and the Imaging Facility of IST Austria for excellent support.
article_processing_charge: No
article_type: original
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. Methods
in Enzymology. 2016;570:567-581. doi:10.1016/bs.mie.2015.11.004
apa: Schwarz, J., & Sixt, M. K. (2016). Quantitative analysis of dendritic cell
haptotaxis. Methods in Enzymology. Elsevier. https://doi.org/10.1016/bs.mie.2015.11.004
chicago: Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell
Haptotaxis.” Methods in Enzymology. Elsevier, 2016. https://doi.org/10.1016/bs.mie.2015.11.004.
ieee: J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,”
Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016.
ista: Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis.
Methods in Enzymology. 570, 567–581.
mla: Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell
Haptotaxis.” Methods in Enzymology, vol. 570, Elsevier, 2016, pp. 567–81,
doi:10.1016/bs.mie.2015.11.004.
short: J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581.
date_created: 2018-12-11T11:52:56Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:51:51Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/bs.mie.2015.11.004
ec_funded: 1
external_id:
pmid:
- '26921962'
intvolume: ' 570'
language:
- iso: eng
month: '01'
oa_version: None
page: 567 - 581
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Methods in Enzymology
publication_status: published
publisher: Elsevier
publist_id: '5573'
quality_controlled: '1'
scopus_import: 1
status: public
title: Quantitative analysis of dendritic cell haptotaxis
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 570
year: '2016'
...
---
_id: '1129'
abstract:
- lang: eng
text: "Directed cell migration is a hallmark feature, present in almost all multi-cellular\r\norganisms.
Despite its importance, basic questions regarding force transduction\r\nor directional
sensing are still heavily investigated. Directed migration of cells\r\nguided
by immobilized guidance cues - haptotaxis - occurs in key-processes,\r\nsuch as
embryonic development and immunity (Middleton et al., 1997; Nguyen\r\net al.,
2000; Thiery, 1984; Weber et al., 2013). Immobilized guidance cues\r\ncomprise
adhesive ligands, such as collagen and fibronectin (Barczyk et al.,\r\n2009),
or chemokines - the main guidance cues for migratory leukocytes\r\n(Middleton
et al., 1997; Weber et al., 2013). While adhesive ligands serve as\r\nattachment
sites guiding cell migration (Carter, 1965), chemokines instruct\r\nhaptotactic
migration by inducing adhesion to adhesive ligands and directional\r\nguidance
(Rot and Andrian, 2004; Schumann et al., 2010). Quantitative analysis\r\nof the
cellular response to immobilized guidance cues requires in vitro assays\r\nthat
foster cell migration, offer accurate control of the immobilized cues on a\r\nsubcellular
scale and in the ideal case closely reproduce in vivo conditions. The\r\nexploration
of haptotactic cell migration through design and employment of such\r\nassays
represents the main focus of this work.\r\nDendritic cells (DCs) are leukocytes,
which after encountering danger\r\nsignals such as pathogens in peripheral organs
instruct naïve T-cells and\r\nconsequently the adaptive immune response in the
lymph node (Mellman and\r\nSteinman, 2001). To reach the lymph node from the periphery,
DCs follow\r\nhaptotactic gradients of the chemokine CCL21 towards lymphatic vessels\r\n(Weber
et al., 2013). Questions about how DCs interpret haptotactic CCL21\r\ngradients
have not yet been addressed. The main reason for this is the lack of\r\nan assay
that offers diverse haptotactic environments, hence allowing the study\r\nof DC
migration as a response to different signals of immobilized guidance cue.\r\nIn
this work, we developed an in vitro assay that enables us to\r\nquantitatively
assess DC haptotaxis, by combining precisely controllable\r\nchemokine photo-patterning
with physically confining migration conditions. With this tool at hand, we studied
the influence of CCL21 gradient properties and\r\nconcentration on DC haptotaxis.
We found that haptotactic gradient sensing\r\ndepends on the absolute CCL21 concentration
in combination with the local\r\nsteepness of the gradient. Our analysis suggests
that the directionality of\r\nmigrating DCs is governed by the signal-to-noise
ratio of CCL21 binding to its\r\nreceptor CCR7. Moreover, the haptotactic CCL21
gradient formed in vivo\r\nprovides an optimal shape for DCs to recognize haptotactic
guidance cue.\r\nBy reconstitution of the CCL21 gradient in vitro we were also
able to\r\nstudy the influence of CCR7 signal termination on DC haptotaxis. To
this end,\r\nwe used DCs lacking the G-protein coupled receptor kinase GRK6, which
is\r\nresponsible for CCL21 induced CCR7 receptor phosphorylation and\r\ndesensitization
(Zidar et al., 2009). We found that CCR7 desensitization by\r\nGRK6 is crucial
for maintenance of haptotactic CCL21 gradient sensing in vitro\r\nand confirm
those observations in vivo.\r\nIn the context of the organism, immobilized haptotactic
guidance cues\r\noften coincide and compete with soluble chemotactic guidance
cues. During\r\nwound healing, fibroblasts are exposed and influenced by adhesive
cues and\r\nsoluble factors at the same time (Wu et al., 2012; Wynn, 2008). Similarly,\r\nmigrating
DCs are exposed to both, soluble chemokines (CCL19 and truncated\r\nCCL21) inducing
chemotactic behavior as well as the immobilized CCL21. To\r\nquantitatively assess
these complex coinciding immobilized and soluble\r\nguidance cues, we implemented
our chemokine photo-patterning technique in a\r\nmicrofluidic system allowing
for chemotactic gradient generation. To validate\r\nthe assay, we observed DC
migration in competing CCL19/CCL21\r\nenvironments.\r\nAdhesiveness guided haptotaxis
has been studied intensively over the\r\nlast century. However, quantitative studies
leading to conceptual models are\r\nlargely missing, again due to the lack of
a precisely controllable in vitro assay. A\r\nrequirement for such an in vitro
assay is that it must prevent any uncontrolled\r\ncell adhesion. This can be accomplished
by stable passivation of the surface. In\r\naddition, controlled adhesion must
be sustainable, quantifiable and dose\r\ndependent in order to create homogenous
gradients. Therefore, we developed a novel covalent photo-patterning technique
satisfying all these needs. In\r\ncombination with a sustainable poly-vinyl alcohol
(PVA) surface coating we\r\nwere able to generate gradients of adhesive cue to
direct cell migration. This\r\napproach allowed us to characterize the haptotactic
migratory behavior of\r\nzebrafish keratocytes in vitro. Furthermore, defined
patterns of adhesive cue\r\nallowed us to control for cell shape and growth on
a subcellular scale."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: LifeSc
acknowledgement: "First, I would like to thank Michael Sixt for being a great supervisor,
mentor and\r\nscientist. I highly appreciate his guidance and continued support.
Furthermore, I\r\nam very grateful that he gave me the exceptional opportunity to
pursue many\r\nideas of which some managed to be included in this thesis.\r\nI owe
sincere thanks to the members of my PhD thesis committee, Daria\r\nSiekhaus, Daniel
Legler and Harald Janovjak. Especially I would like to thank\r\nDaria for her advice
and encouragement during our regular progress meetings.\r\nI also want to thank
the team and fellows of the Boehringer Ingelheim Fond\r\n(BIF) PhD Fellowship for
amazing and inspiring meetings and the BIF for\r\nfinancial support.\r\nImportant
factors for the success of this thesis were the warm, creative\r\nand helpful atmosphere
as well as the team spirit of the whole Sixt Lab.\r\nTherefore I would like to thank
my current and former colleagues Frank Assen,\r\nMarkus Brown, Ingrid de Vries,
Michelle Duggan, Alexander Eichner, Miroslav\r\nHons, Eva Kiermaier, Aglaja Kopf,
Alexander Leithner, Christine Moussion, Jan\r\nMüller, Maria Nemethova, Jörg Renkawitz,
Anne Reversat, Kari Vaahtomeri,\r\nMichele Weber and Stefan Wieser. We had an amazing
time with many\r\nlegendary evenings and events. Along these lines I want to thank
the in vitro\r\ncrew of the lab, Jörg, Anne and Alex, for lots of ideas and productive\r\ndiscussions.
I am sure, some day we will reveal the secret of the ‘splodge’.\r\nI want to thank
the members of the Heisenberg Lab for a great time and\r\nthrilling kicker matches.
In this regard I especially want to thank Maurizio\r\n‘Gnocci’ Monti, Gabriel Krens,
Alex Eichner, Martin Behrndt, Vanessa Barone,Philipp Schmalhorst, Michael Smutny,
Daniel Capek, Anne Reversat, Eva\r\nKiermaier, Frank Assen and Jan Müller for wonderful
after-lunch matches.\r\nI would not have been able to analyze the thousands of cell
trajectories\r\nand probably hundreds of thousands of mouse clicks without the productive\r\ncollaboration
with Veronika Bierbaum and Tobias Bollenbach. Thanks Vroni for\r\ncountless meetings,
discussions and graphs and of course for proofreading and\r\nadvice for this thesis.
For proofreading I also want to thank Evi, Jörg, Jack and\r\nAnne.\r\nI would like
to acknowledge Matthias Mehling for a very productive\r\ncollaboration and for introducing
me into the wild world of microfluidics. Jack\r\nMerrin, for countless wafers, PDMS
coated coverslips and help with anything\r\nmicro-fabrication related. And Maria
Nemethova for establishing the ‘click’\r\npatterning approach with me. Without her
it still would be just one of the ideas…\r\nMany thanks to Ekaterina Papusheva,
Robert Hauschild, Doreen Milius\r\nand Nasser Darwish from the Bioimaging Facility
as well as the Preclinical and\r\nthe Life Science facilities of IST Austria for
excellent technical support. At this\r\npoint I especially want to thank Robert
for countless image analyses and\r\ntechnical ideas. Always interested and creative
he played an essential role in all\r\nof my projects.\r\nAdditionally I want to
thank Ingrid and Gabby for welcoming me warmly\r\nwhen I first started at IST, for
scientific and especially mental support in all\r\nthose years, countless coffee
sessions and Heurigen evenings. #BioimagingFacility #LifeScienceFacility #PreClinicalFacility"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
citation:
ama: Schwarz J. Quantitative analysis of haptotactic cell migration. 2016.
apa: Schwarz, J. (2016). Quantitative analysis of haptotactic cell migration.
Institute of Science and Technology Austria.
chicago: Schwarz, Jan. “Quantitative Analysis of Haptotactic Cell Migration.” Institute
of Science and Technology Austria, 2016.
ieee: J. Schwarz, “Quantitative analysis of haptotactic cell migration,” Institute
of Science and Technology Austria, 2016.
ista: Schwarz J. 2016. Quantitative analysis of haptotactic cell migration. Institute
of Science and Technology Austria.
mla: Schwarz, Jan. Quantitative Analysis of Haptotactic Cell Migration. Institute
of Science and Technology Austria, 2016.
short: J. Schwarz, Quantitative Analysis of Haptotactic Cell Migration, Institute
of Science and Technology Austria, 2016.
date_created: 2018-12-11T11:50:18Z
date_published: 2016-07-01T00:00:00Z
date_updated: 2023-09-07T11:54:33Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
file:
- access_level: closed
checksum: e3cd6b28f9c5cccb8891855565a2dade
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date_created: 2019-08-13T10:55:35Z
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creator: dernst
date_created: 2021-02-22T11:43:14Z
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file_name: 2016_Thesis_JSchwarz.pdf
file_size: 8396717
relation: main_file
success: 1
file_date_updated: 2021-02-22T11:43:14Z
has_accepted_license: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '178'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '6231'
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Quantitative analysis of haptotactic cell migration
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2016'
...
---
_id: '1321'
abstract:
- lang: eng
text: Most migrating cells extrude their front by the force of actin polymerization.
Polymerization requires an initial nucleation step, which is mediated by factors
establishing either parallel filaments in the case of filopodia or branched filaments
that form the branched lamellipodial network. Branches are considered essential
for regular cell motility and are initiated by the Arp2/3 complex, which in turn
is activated by nucleation-promoting factors of the WASP and WAVE families. Here
we employed rapid amoeboid crawling leukocytes and found that deletion of the
WAVE complex eliminated actin branching and thus lamellipodia formation. The cells
were left with parallel filaments at the leading edge, which translated, depending
on the differentiation status of the cell, into a unipolar pointed cell shape
or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased
speed and enormous directional persistence, while they were unable to turn towards
chemotactic gradients. Cells with multiple filopodia retained chemotactic activity
but their migration was progressively impaired with increasing geometrical complexity
of the extracellular environment. These findings establish that diversified leading
edge protrusions serve as explorative structures while they slow down actual locomotion.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by the German Research Foundation (DFG)
Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC
GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria
for excellent technical support."
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: David
full_name: De Gorter, David
last_name: De Gorter
- first_name: Florian
full_name: Schur, Florian
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Jonathan
full_name: Bayerl, Jonathan
last_name: Bayerl
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Frank
full_name: Lai, Frank
last_name: Lai
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Victor
full_name: Small, Victor
last_name: Small
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote
environmental exploration but are dispensable for locomotion of leukocytes. Nature
Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426
apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz,
J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/ncb3426
chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus
Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote
Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature
Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.
ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes,” Nature Cell
Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.
ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J,
De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser
M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin
protrusions promote environmental exploration but are dispensable for locomotion
of leukocytes. Nature Cell Biology. 18, 1253–1259.
mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental
Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell
Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426.
short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz,
J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild,
F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt,
Nature Cell Biology 18 (2016) 1253–1259.
date_created: 2018-12-11T11:51:21Z
date_published: 2016-10-24T00:00:00Z
date_updated: 2024-03-28T23:30:16Z
day: '24'
ddc:
- '570'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/ncb3426
ec_funded: 1
file:
- access_level: open_access
checksum: e1411cb7c99a2d9089c178a6abef25e7
content_type: application/pdf
creator: dernst
date_created: 2020-05-14T16:33:46Z
date_updated: 2020-07-14T12:44:43Z
file_id: '7844'
file_name: 2018_NatureCell_Leithner.pdf
file_size: 4433280
relation: main_file
file_date_updated: 2020-07-14T12:44:43Z
has_accepted_license: '1'
intvolume: ' 18'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Submitted Version
page: 1253 - 1259
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5949'
quality_controlled: '1'
related_material:
record:
- id: '323'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Diversified actin protrusions promote environmental exploration but are dispensable
for locomotion of leukocytes
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2016'
...
---
_id: '1530'
abstract:
- lang: eng
text: In growing cells, protein synthesis and cell growth are typically not synchronous,
and, thus, protein concentrations vary over the cell division cycle. We have developed
a theoretical description of genetic regulatory systems in bacteria that explicitly
considers the cell division cycle to investigate its impact on gene expression.
We calculate the cell-to-cell variations arising from cells being at different
stages in the division cycle for unregulated genes and for basic regulatory mechanisms.
These variations contribute to the extrinsic noise observed in single-cell experiments,
and are most significant for proteins with short lifetimes. Negative autoregulation
buffers against variation of protein concentration over the division cycle, but
the effect is found to be relatively weak. Stronger buffering is achieved by an
increased protein lifetime. Positive autoregulation can strongly amplify such
variation if the parameters are set to values that lead to resonance-like behaviour.
For cooperative positive autoregulation, the concentration variation over the
division cycle diminishes the parameter region of bistability and modulates the
switching times between the two stable states. The same effects are seen for a
two-gene mutual-repression toggle switch. By contrast, an oscillatory circuit,
the repressilator, is only weakly affected by the division cycle.
article_number: '066003'
author:
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Stefan
full_name: Klumpp, Stefan
last_name: Klumpp
citation:
ama: Bierbaum V, Klumpp S. Impact of the cell division cycle on gene circuits. Physical
Biology. 2015;12(6). doi:10.1088/1478-3975/12/6/066003
apa: Bierbaum, V., & Klumpp, S. (2015). Impact of the cell division cycle on
gene circuits. Physical Biology. IOP Publishing Ltd. https://doi.org/10.1088/1478-3975/12/6/066003
chicago: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle
on Gene Circuits.” Physical Biology. IOP Publishing Ltd., 2015. https://doi.org/10.1088/1478-3975/12/6/066003.
ieee: V. Bierbaum and S. Klumpp, “Impact of the cell division cycle on gene circuits,”
Physical Biology, vol. 12, no. 6. IOP Publishing Ltd., 2015.
ista: Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits.
Physical Biology. 12(6), 066003.
mla: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on
Gene Circuits.” Physical Biology, vol. 12, no. 6, 066003, IOP Publishing
Ltd., 2015, doi:10.1088/1478-3975/12/6/066003.
short: V. Bierbaum, S. Klumpp, Physical Biology 12 (2015).
date_created: 2018-12-11T11:52:33Z
date_published: 2015-09-25T00:00:00Z
date_updated: 2021-01-12T06:51:25Z
day: '25'
department:
- _id: MiSi
doi: 10.1088/1478-3975/12/6/066003
intvolume: ' 12'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
publication: Physical Biology
publication_status: published
publisher: IOP Publishing Ltd.
publist_id: '5641'
quality_controlled: '1'
scopus_import: 1
status: public
title: Impact of the cell division cycle on gene circuits
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2015'
...
---
_id: '1553'
abstract:
- lang: eng
text: Cell movement has essential functions in development, immunity, and cancer.
Various cell migration patterns have been reported, but no general rule has emerged
so far. Here, we show on the basis of experimental data in vitro and in vivo that
cell persistence, which quantifies the straightness of trajectories, is robustly
coupled to cell migration speed. We suggest that this universal coupling constitutes
a generic law of cell migration, which originates in the advection of polarity
cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis
relies on a theoretical model that we validate by measuring the persistence of
cells upon modulation of actin flow speeds and upon optogenetic manipulation of
the binding of an actin regulator to actin filaments. Beyond the quantitative
prediction of the coupling, the model yields a generic phase diagram of cellular
trajectories, which recapitulates the full range of observed migration patterns.
author:
- first_name: Paolo
full_name: Maiuri, Paolo
last_name: Maiuri
- first_name: Jean
full_name: Rupprecht, Jean
last_name: Rupprecht
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Olivier
full_name: Bénichou, Olivier
last_name: Bénichou
- first_name: Nicolas
full_name: Carpi, Nicolas
last_name: Carpi
- first_name: Mathieu
full_name: Coppey, Mathieu
last_name: Coppey
- first_name: Simon
full_name: De Beco, Simon
last_name: De Beco
- first_name: Nir
full_name: Gov, Nir
last_name: Gov
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Carolina
full_name: Lage Crespo, Carolina
last_name: Lage Crespo
- first_name: Franziska
full_name: Lautenschlaeger, Franziska
last_name: Lautenschlaeger
- first_name: Maël
full_name: Le Berre, Maël
last_name: Le Berre
- first_name: Ana
full_name: Lennon Duménil, Ana
last_name: Lennon Duménil
- first_name: Matthew
full_name: Raab, Matthew
last_name: Raab
- first_name: Hawa
full_name: Thiam, Hawa
last_name: Thiam
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
citation:
ama: Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling
between cell speed and cell persistence. Cell. 2015;161(2):374-386. doi:10.1016/j.cell.2015.01.056
apa: Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N.,
… Voituriez, R. (2015). Actin flows mediate a universal coupling between cell
speed and cell persistence. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.056
chicago: Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier
Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal
Coupling between Cell Speed and Cell Persistence.” Cell. Cell Press, 2015.
https://doi.org/10.1016/j.cell.2015.01.056.
ieee: P. Maiuri et al., “Actin flows mediate a universal coupling between
cell speed and cell persistence,” Cell, vol. 161, no. 2. Cell Press, pp.
374–386, 2015.
ista: Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M,
De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre
M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin
flows mediate a universal coupling between cell speed and cell persistence. Cell.
161(2), 374–386.
mla: Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell
Speed and Cell Persistence.” Cell, vol. 161, no. 2, Cell Press, 2015, pp.
374–86, doi:10.1016/j.cell.2015.01.056.
short: P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M.
Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger,
M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez,
Cell 161 (2015) 374–386.
date_created: 2018-12-11T11:52:41Z
date_published: 2015-04-09T00:00:00Z
date_updated: 2021-01-12T06:51:33Z
day: '09'
department:
- _id: MiSi
- _id: CaHe
doi: 10.1016/j.cell.2015.01.056
ec_funded: 1
intvolume: ' 161'
issue: '2'
language:
- iso: eng
month: '04'
oa_version: None
page: 374 - 386
project:
- _id: 2529486C-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T 560-B17
name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25ABD200-B435-11E9-9278-68D0E5697425
grant_number: RGP0058/2011
name: 'Cell migration in complex environments: from in vivo experiments to theoretical
models'
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5618'
quality_controlled: '1'
scopus_import: 1
status: public
title: Actin flows mediate a universal coupling between cell speed and cell persistence
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 161
year: '2015'
...
---
_id: '1561'
abstract:
- lang: eng
text: Replication-deficient recombinant adenoviruses are potent vectors for the
efficient transient expression of exogenous genes in resting immune cells. However,
most leukocytes are refractory to efficient adenoviral transduction as they lack
expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle,
we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early
enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring
of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously,
CARΔ1 expression permits selective and highly efficient adenoviral transduction
of immune cell populations, such as mast cells or T cells, directly ex vivo in
bulk cultures without prior cell purification or activation. Furthermore, we show
that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated
conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as
well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function
mouse strain will hence be a valuable tool to rapidly dissect the function of
specific genes in leukocyte physiology.
author:
- first_name: Klaus
full_name: Heger, Klaus
last_name: Heger
- first_name: Maike
full_name: Kober, Maike
last_name: Kober
- first_name: David
full_name: Rieß, David
last_name: Rieß
- first_name: Christoph
full_name: Drees, Christoph
last_name: Drees
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Arianna
full_name: Bertossi, Arianna
last_name: Bertossi
- first_name: Axel
full_name: Roers, Axel
last_name: Roers
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Marc
full_name: Schmidt Supprian, Marc
last_name: Schmidt Supprian
citation:
ama: Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain
facilitates selective and efficient infection of primary immune cells with adenoviral
vectors. European Journal of Immunology. 2015;45(6):1614-1620. doi:10.1002/eji.201545457
apa: Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt
Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors.
European Journal of Immunology. Wiley. https://doi.org/10.1002/eji.201545457
chicago: Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries,
Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel
Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection
of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology.
Wiley, 2015. https://doi.org/10.1002/eji.201545457.
ieee: K. Heger et al., “A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors,”
European Journal of Immunology, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015.
ista: Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK,
Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates
selective and efficient infection of primary immune cells with adenoviral vectors.
European Journal of Immunology. 45(6), 1614–1620.
mla: Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates
Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.”
European Journal of Immunology, vol. 45, no. 6, Wiley, 2015, pp. 1614–20,
doi:10.1002/eji.201545457.
short: K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers,
M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620.
date_created: 2018-12-11T11:52:44Z
date_published: 2015-06-01T00:00:00Z
date_updated: 2021-01-12T06:51:36Z
day: '01'
department:
- _id: MiSi
doi: 10.1002/eji.201545457
intvolume: ' 45'
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 1614 - 1620
publication: European Journal of Immunology
publication_status: published
publisher: Wiley
publist_id: '5610'
quality_controlled: '1'
scopus_import: 1
status: public
title: A novel Cre recombinase reporter mouse strain facilitates selective and efficient
infection of primary immune cells with adenoviral vectors
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 45
year: '2015'
...
---
_id: '1560'
abstract:
- lang: eng
text: Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells
and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP
is a crucial component of this selector function.
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology.
2015;16(4):338-340. doi:10.1038/ni.3126
apa: Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature
Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126
chicago: Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” Nature
Immunology. Nature Publishing Group, 2015. https://doi.org/10.1038/ni.3126.
ieee: M. Hons and M. K. Sixt, “The lymph node filter revealed,” Nature Immunology,
vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015.
ista: Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology.
16(4), 338–340.
mla: Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” Nature
Immunology, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:10.1038/ni.3126.
short: M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340.
date_created: 2018-12-11T11:52:43Z
date_published: 2015-03-19T00:00:00Z
date_updated: 2021-01-12T06:51:36Z
day: '19'
department:
- _id: MiSi
doi: 10.1038/ni.3126
intvolume: ' 16'
issue: '4'
language:
- iso: eng
month: '03'
oa_version: None
page: 338 - 340
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5611'
quality_controlled: '1'
scopus_import: 1
status: public
title: The lymph node filter revealed
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2015'
...
---
_id: '1575'
abstract:
- lang: eng
text: The immune response relies on the migration of leukocytes and on their ability
to stop in precise anatomical locations to fulfil their task. How leukocyte migration
and function are coordinated is unknown. Here we show that in immature dendritic
cells, which patrol their environment by engulfing extracellular material, cell
migration and antigen capture are antagonistic. This antagonism results from transient
enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient
of the motor protein, slowing down locomotion but promoting antigen capture. We
further highlight that myosin IIA enrichment at the cell front requires the MHC
class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization,
Ii imposes on dendritic cells an intermittent antigen capture behaviour that might
facilitate environment patrolling. We propose that the requirement for myosin
II in both cell migration and specific cell functions may provide a general mechanism
for their coordination in time and space.
acknowledgement: M.C. and M.L.H. were supported by fellowships from the Fondation
pour la Recherche Médicale and the Association pour la Recherche contre le Cancer,
respectively. This work was funded by grants from the City of Paris and the European
Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour
la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico)
to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL*
and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an
ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934,
Institut Curie).
article_number: '7526'
author:
- first_name: Mélanie
full_name: Chabaud, Mélanie
last_name: Chabaud
- first_name: Mélina
full_name: Heuzé, Mélina
last_name: Heuzé
- first_name: Marine
full_name: Bretou, Marine
last_name: Bretou
- first_name: Pablo
full_name: Vargas, Pablo
last_name: Vargas
- first_name: Paolo
full_name: Maiuri, Paolo
last_name: Maiuri
- first_name: Paola
full_name: Solanes, Paola
last_name: Solanes
- first_name: Mathieu
full_name: Maurin, Mathieu
last_name: Maurin
- first_name: Emmanuel
full_name: Terriac, Emmanuel
last_name: Terriac
- first_name: Maël
full_name: Le Berre, Maël
last_name: Le Berre
- first_name: Danielle
full_name: Lankar, Danielle
last_name: Lankar
- first_name: Tristan
full_name: Piolot, Tristan
last_name: Piolot
- first_name: Robert
full_name: Adelstein, Robert
last_name: Adelstein
- first_name: Yingfan
full_name: Zhang, Yingfan
last_name: Zhang
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Jordan
full_name: Jacobelli, Jordan
last_name: Jacobelli
- first_name: Olivier
full_name: Bénichou, Olivier
last_name: Bénichou
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Ana
full_name: Lennon Duménil, Ana
last_name: Lennon Duménil
citation:
ama: Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are
antagonistic processes coupled by myosin II in dendritic cells. Nature Communications.
2015;6. doi:10.1038/ncomms8526
apa: Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., …
Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic
processes coupled by myosin II in dendritic cells. Nature Communications.
Nature Publishing Group. https://doi.org/10.1038/ncomms8526
chicago: Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri,
Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are
Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications.
Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526.
ieee: M. Chabaud et al., “Cell migration and antigen capture are antagonistic
processes coupled by myosin II in dendritic cells,” Nature Communications,
vol. 6. Nature Publishing Group, 2015.
ista: Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac
E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J,
Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen
capture are antagonistic processes coupled by myosin II in dendritic cells. Nature
Communications. 6, 7526.
mla: Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic
Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications,
vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526.
short: M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin,
E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt,
J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications
6 (2015).
date_created: 2018-12-11T11:52:48Z
date_published: 2015-06-25T00:00:00Z
date_updated: 2021-01-12T06:51:42Z
day: '25'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms8526
file:
- access_level: open_access
checksum: bae12e86be2adb28253f890b8bba8315
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:58Z
date_updated: 2020-07-14T12:45:02Z
file_id: '4915'
file_name: IST-2016-476-v1+1_ncomms8526.pdf
file_size: 4530215
relation: main_file
file_date_updated: 2020-07-14T12:45:02Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5596'
pubrep_id: '476'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cell migration and antigen capture are antagonistic processes coupled by myosin
II in dendritic cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2015'
...
---
_id: '1676'
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Erez
full_name: Raz, Erez
last_name: Raz
citation:
ama: 'Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current
Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004'
apa: 'Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration.
Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004'
chicago: 'Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and
Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.'
ieee: 'M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,”
Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.'
ista: 'Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current
Opinion in Cell Biology. 36(10), 4–6.'
mla: 'Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.”
Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6,
doi:10.1016/j.ceb.2015.09.004.'
short: M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6.
date_created: 2018-12-11T11:53:25Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2021-01-12T06:52:27Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.ceb.2015.09.004
intvolume: ' 36'
issue: '10'
language:
- iso: eng
month: '10'
oa_version: None
page: 4 - 6
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '5473'
scopus_import: 1
status: public
title: 'Editorial overview: Cell adhesion and migration'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2015'
...
---
_id: '1687'
abstract:
- lang: eng
text: Guided cell movement is essential for development and integrity of animals
and crucially involved in cellular immune responses. Leukocytes are professional
migratory cells that can navigate through most types of tissues and sense a wide
range of directional cues. The responses of these cells to attractants have been
mainly explored in tissue culture settings. How leukocytes make directional decisions
in situ, within the challenging environment of a tissue maze, is less understood.
Here we review recent advances in how leukocytes sense chemical cues in complex
tissue settings and make links with paradigms of directed migration in development
and Dictyostelium discoideum amoebae.
author:
- first_name: Milka
full_name: Sarris, Milka
last_name: Sarris
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation
in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102.
doi:10.1016/j.ceb.2015.08.001'
apa: 'Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant
interpretation in complex environments. Current Opinion in Cell Biology.
Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001'
chicago: 'Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant
Interpretation in Complex Environments.” Current Opinion in Cell Biology.
Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001.'
ieee: 'M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation
in complex environments,” Current Opinion in Cell Biology, vol. 36, no.
10. Elsevier, pp. 93–102, 2015.'
ista: 'Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation
in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.'
mla: 'Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant
Interpretation in Complex Environments.” Current Opinion in Cell Biology,
vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.'
short: M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102.
date_created: 2018-12-11T11:53:28Z
date_published: 2015-10-01T00:00:00Z
date_updated: 2021-01-12T06:52:31Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.ceb.2015.08.001
ec_funded: 1
file:
- access_level: open_access
checksum: c29973924b790aab02fdd91857759cfb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:21Z
date_updated: 2020-07-14T12:45:12Z
file_id: '4875'
file_name: IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf
file_size: 797964
relation: main_file
file_date_updated: 2020-07-14T12:45:12Z
has_accepted_license: '1'
intvolume: ' 36'
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 93 - 102
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '5458'
pubrep_id: '445'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Navigating in tissue mazes: Chemoattractant interpretation in complex environments'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2015'
...
---
_id: '1686'
author:
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils
blaze a trail with migratory cues for T cells to follow to sites of infection.
Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867'
apa: 'Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between
immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow
to sites of infection. Science. American Association for the Advancement
of Science. https://doi.org/10.1126/science.aad0867'
chicago: 'Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between
Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow
to Sites of Infection.” Science. American Association for the Advancement
of Science, 2015. https://doi.org/10.1126/science.aad0867.'
ieee: 'E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells:
Neutrophils blaze a trail with migratory cues for T cells to follow to sites of
infection,” Science, vol. 349, no. 6252. American Association for the Advancement
of Science, pp. 1055–1056, 2015.'
ista: 'Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells:
Neutrophils blaze a trail with migratory cues for T cells to follow to sites of
infection. Science. 349(6252), 1055–1056.'
mla: 'Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune
Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to
Sites of Infection.” Science, vol. 349, no. 6252, American Association
for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.'
short: E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056.
date_created: 2018-12-11T11:53:28Z
date_published: 2015-09-04T00:00:00Z
date_updated: 2021-01-12T06:52:31Z
day: '04'
department:
- _id: MiSi
doi: 10.1126/science.aad0867
intvolume: ' 349'
issue: '6252'
language:
- iso: eng
month: '09'
oa_version: None
page: 1055 - 1056
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5459'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Fragmented communication between immune cells: Neutrophils blaze a trail with
migratory cues for T cells to follow to sites of infection'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 349
year: '2015'
...
---
_id: '477'
abstract:
- lang: eng
text: Dendritic cells are potent antigen-presenting cells endowed with the unique
ability to initiate adaptive immune responses upon inflammation. Inflammatory
processes are often associated with an increased production of serotonin, which
operates by activating specific receptors. However, the functional role of serotonin
receptors in regulation of dendritic cell functions is poorly understood. Here,
we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as
its downstream effector Cdc42 is upregulated in dendritic cells upon maturation.
Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation
affected dendritic cell morphology through Cdc42-mediated signaling. In addition,
basal activity of 5-HT7TR was required for the proper expression of the chemokine
receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent
with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic
cells in vitro by modulating their directionality and migration velocity. Accordingly,
migration of dendritic cells in murine colon explants was abolished after pharmacological
receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated
signaling in the regulation of dendritic cell morphology and motility, suggesting
that 5-HT7TR could be a new target for treatment of a variety of inflammatory
and immune disorders.
author:
- first_name: Katrin
full_name: Holst, Katrin
last_name: Holst
- first_name: Daria
full_name: Guseva, Daria
last_name: Guseva
- first_name: Susann
full_name: Schindler, Susann
last_name: Schindler
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Armin
full_name: Braun, Armin
last_name: Braun
- first_name: Himpriya
full_name: Chopra, Himpriya
last_name: Chopra
- first_name: Oliver
full_name: Pabst, Oliver
last_name: Pabst
- first_name: Evgeni
full_name: Ponimaskin, Evgeni
last_name: Ponimaskin
citation:
ama: Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates
the morphology and migratory properties of dendritic cells. Journal of Cell
Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999
apa: Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., …
Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology
and migratory properties of dendritic cells. Journal of Cell Science. Company
of Biologists. https://doi.org/10.1242/jcs.167999
chicago: Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun,
Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor
5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.”
Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999.
ieee: K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology
and migratory properties of dendritic cells,” Journal of Cell Science,
vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015.
ista: Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin
E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory
properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880.
mla: Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology
and Migratory Properties of Dendritic Cells.” Journal of Cell Science,
vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999.
short: K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst,
E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880.
date_created: 2018-12-11T11:46:41Z
date_published: 2015-06-15T00:00:00Z
date_updated: 2021-01-12T08:00:54Z
day: '15'
department:
- _id: MiSi
doi: 10.1242/jcs.167999
intvolume: ' 128'
issue: '15'
language:
- iso: eng
month: '06'
oa_version: None
page: 2866 - 2880
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '7343'
quality_controlled: '1'
scopus_import: 1
status: public
title: The serotonin receptor 5-HT7R regulates the morphology and migratory properties
of dendritic cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 128
year: '2015'
...
---
_id: '1618'
abstract:
- lang: eng
text: CCL19 and CCL21 are chemokines involved in the trafficking of immune cells,
particularly within the lymphatic system, through activation of CCR7. Concurrent
expression of PSGL-1 and CCR7 in naive T-cells enhances recruitment of these cells
to secondary lymphoid organs by CCL19 and CCL21. Here the solution structure of
CCL19 is reported. It contains a canonical chemokine domain. Chemical shift mapping
shows the N-termini of PSGL-1 and CCR7 have overlapping binding sites for CCL19
and binding is competitive. Implications for the mechanism of PSGL-1's enhancement
of resting T-cell recruitment are discussed.
article_processing_charge: No
author:
- first_name: Christopher
full_name: Veldkamp, Christopher
last_name: Veldkamp
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Skylar
full_name: Gabel Eissens, Skylar
last_name: Gabel Eissens
- first_name: Miranda
full_name: Gillitzer, Miranda
last_name: Gillitzer
- first_name: David
full_name: Lippner, David
last_name: Lippner
- first_name: Frank
full_name: Disilvio, Frank
last_name: Disilvio
- first_name: Casey
full_name: Mueller, Casey
last_name: Mueller
- first_name: Paeton
full_name: Wantuch, Paeton
last_name: Wantuch
- first_name: Gary
full_name: Chaffee, Gary
last_name: Chaffee
- first_name: Michael
full_name: Famiglietti, Michael
last_name: Famiglietti
- first_name: Danielle
full_name: Zgoba, Danielle
last_name: Zgoba
- first_name: Asha
full_name: Bailey, Asha
last_name: Bailey
- first_name: Yaya
full_name: Bah, Yaya
last_name: Bah
- first_name: Samantha
full_name: Engebretson, Samantha
last_name: Engebretson
- first_name: David
full_name: Graupner, David
last_name: Graupner
- first_name: Emily
full_name: Lackner, Emily
last_name: Lackner
- first_name: Vincent
full_name: Larosa, Vincent
last_name: Larosa
- first_name: Tysha
full_name: Medeiros, Tysha
last_name: Medeiros
- first_name: Michael
full_name: Olson, Michael
last_name: Olson
- first_name: Andrew
full_name: Phillips, Andrew
last_name: Phillips
- first_name: Harley
full_name: Pyles, Harley
last_name: Pyles
- first_name: Amanda
full_name: Richard, Amanda
last_name: Richard
- first_name: Scott
full_name: Schoeller, Scott
last_name: Schoeller
- first_name: Boris
full_name: Touzeau, Boris
last_name: Touzeau
- first_name: Larry
full_name: Williams, Larry
last_name: Williams
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Francis
full_name: Peterson, Francis
last_name: Peterson
citation:
ama: Veldkamp C, Kiermaier E, Gabel Eissens S, et al. Solution structure of CCL19
and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry.
2015;54(27):4163-4166. doi:10.1021/acs.biochem.5b00560
apa: Veldkamp, C., Kiermaier, E., Gabel Eissens, S., Gillitzer, M., Lippner, D.,
Disilvio, F., … Peterson, F. (2015). Solution structure of CCL19 and identification
of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. American Chemical
Society. https://doi.org/10.1021/acs.biochem.5b00560
chicago: Veldkamp, Christopher, Eva Kiermaier, Skylar Gabel Eissens, Miranda Gillitzer,
David Lippner, Frank Disilvio, Casey Mueller, et al. “Solution Structure of CCL19
and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry.
American Chemical Society, 2015. https://doi.org/10.1021/acs.biochem.5b00560.
ieee: C. Veldkamp et al., “Solution structure of CCL19 and identification
of overlapping CCR7 and PSGL-1 binding sites,” Biochemistry, vol. 54, no.
27. American Chemical Society, pp. 4163–4166, 2015.
ista: Veldkamp C, Kiermaier E, Gabel Eissens S, Gillitzer M, Lippner D, Disilvio
F, Mueller C, Wantuch P, Chaffee G, Famiglietti M, Zgoba D, Bailey A, Bah Y, Engebretson
S, Graupner D, Lackner E, Larosa V, Medeiros T, Olson M, Phillips A, Pyles H,
Richard A, Schoeller S, Touzeau B, Williams L, Sixt MK, Peterson F. 2015. Solution
structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites.
Biochemistry. 54(27), 4163–4166.
mla: Veldkamp, Christopher, et al. “Solution Structure of CCL19 and Identification
of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry, vol. 54, no.
27, American Chemical Society, 2015, pp. 4163–66, doi:10.1021/acs.biochem.5b00560.
short: C. Veldkamp, E. Kiermaier, S. Gabel Eissens, M. Gillitzer, D. Lippner, F.
Disilvio, C. Mueller, P. Wantuch, G. Chaffee, M. Famiglietti, D. Zgoba, A. Bailey,
Y. Bah, S. Engebretson, D. Graupner, E. Lackner, V. Larosa, T. Medeiros, M. Olson,
A. Phillips, H. Pyles, A. Richard, S. Schoeller, B. Touzeau, L. Williams, M.K.
Sixt, F. Peterson, Biochemistry 54 (2015) 4163–4166.
date_created: 2018-12-11T11:53:03Z
date_published: 2015-06-26T00:00:00Z
date_updated: 2023-03-30T11:32:57Z
day: '26'
department:
- _id: MiSi
doi: 10.1021/acs.biochem.5b00560
ec_funded: 1
external_id:
pmid:
- '26115234'
intvolume: ' 54'
issue: '27'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809050/
month: '06'
oa: 1
oa_version: Submitted Version
page: 4163 - 4166
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Biochemistry
publication_status: published
publisher: American Chemical Society
publist_id: '5548'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1
binding sites
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2015'
...
---
_id: '1537'
abstract:
- lang: eng
text: 3D amoeboid cell migration is central to many developmental and disease-related
processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid
cell migration mode in early zebrafish embryos, termed stable-bleb migration.
Stable-bleb cells display an invariant polarized balloon-like shape with exceptional
migration speed and persistence. Progenitor cells can be reversibly transformed
into stable-bleb cells irrespective of their primary fate and motile characteristics
by increasing myosin II activity through biochemical or mechanical stimuli. Using
a combination of theory and experiments, we show that, in stable-bleb cells, cortical
contractility fluctuations trigger a stochastic switch into amoeboid motility,
and a positive feedback between cortical flows and gradients in contractility
maintains stable-bleb cell polarization. We further show that rearward cortical
flows drive stable-bleb cell migration in various adhesive and non-adhesive environments,
unraveling a highly versatile amoeboid migration phenotype.
acknowledged_ssus:
- _id: SSU
acknowledgement: 'We would like to thank R. Hausschild and E. Papusheva for technical
assistance and the service facilities at the IST Austria for continuous support.
The caRhoA plasmid was a kind gift of T. Kudoh and A. Takesono. We thank M. Piel
and E. Paluch for exchanging unpublished data. '
author:
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Andrew
full_name: Callan Jones, Andrew
last_name: Callan Jones
- first_name: Michael
full_name: Smutny, Michael
id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87
last_name: Smutny
orcid: 0000-0002-5920-9090
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Keisuke
full_name: Sako, Keisuke
id: 3BED66BE-F248-11E8-B48F-1D18A9856A87
last_name: Sako
orcid: 0000-0002-6453-8075
- first_name: Vanessa
full_name: Barone, Vanessa
id: 419EECCC-F248-11E8-B48F-1D18A9856A87
last_name: Barone
orcid: 0000-0003-2676-3367
- first_name: Monika
full_name: Ritsch Marte, Monika
last_name: Ritsch Marte
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Ruprecht V, Wieser S, Callan Jones A, et al. Cortical contractility triggers
a stochastic switch to fast amoeboid cell motility. Cell. 2015;160(4):673-685.
doi:10.1016/j.cell.2015.01.008
apa: Ruprecht, V., Wieser, S., Callan Jones, A., Smutny, M., Morita, H., Sako, K.,
… Heisenberg, C.-P. J. (2015). Cortical contractility triggers a stochastic switch
to fast amoeboid cell motility. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.008
chicago: Ruprecht, Verena, Stefan Wieser, Andrew Callan Jones, Michael Smutny, Hitoshi
Morita, Keisuke Sako, Vanessa Barone, et al. “Cortical Contractility Triggers
a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell. Cell Press,
2015. https://doi.org/10.1016/j.cell.2015.01.008.
ieee: V. Ruprecht et al., “Cortical contractility triggers a stochastic switch
to fast amoeboid cell motility,” Cell, vol. 160, no. 4. Cell Press, pp.
673–685, 2015.
ista: Ruprecht V, Wieser S, Callan Jones A, Smutny M, Morita H, Sako K, Barone V,
Ritsch Marte M, Sixt MK, Voituriez R, Heisenberg C-PJ. 2015. Cortical contractility
triggers a stochastic switch to fast amoeboid cell motility. Cell. 160(4), 673–685.
mla: Ruprecht, Verena, et al. “Cortical Contractility Triggers a Stochastic Switch
to Fast Amoeboid Cell Motility.” Cell, vol. 160, no. 4, Cell Press, 2015,
pp. 673–85, doi:10.1016/j.cell.2015.01.008.
short: V. Ruprecht, S. Wieser, A. Callan Jones, M. Smutny, H. Morita, K. Sako, V.
Barone, M. Ritsch Marte, M.K. Sixt, R. Voituriez, C.-P.J. Heisenberg, Cell 160
(2015) 673–685.
date_created: 2018-12-11T11:52:35Z
date_published: 2015-02-12T00:00:00Z
date_updated: 2023-09-07T12:05:08Z
day: '12'
ddc:
- '570'
department:
- _id: CaHe
- _id: MiSi
doi: 10.1016/j.cell.2015.01.008
file:
- access_level: open_access
checksum: 228d3edf40627d897b3875088a0ac51f
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:21Z
date_updated: 2020-07-14T12:45:01Z
file_id: '5003'
file_name: IST-2016-484-v1+1_1-s2.0-S0092867415000094-main.pdf
file_size: 4362653
relation: main_file
file_date_updated: 2020-07-14T12:45:01Z
has_accepted_license: '1'
intvolume: ' 160'
issue: '4'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 673 - 685
project:
- _id: 2529486C-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T 560-B17
name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation
- _id: 2527D5CC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I 812-B12
name: Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5634'
pubrep_id: '484'
quality_controlled: '1'
related_material:
record:
- id: '961'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Cortical contractility triggers a stochastic switch to fast amoeboid cell motility
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 160
year: '2015'
...
---
_id: '1877'
abstract:
- lang: eng
text: During inflammation, lymph nodes swell with an influx of immune cells. New
findings identify a signalling pathway that induces relaxation in the contractile
cells that give structure to these organs.
article_type: letter_note
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
citation:
ama: 'Sixt MK, Vaahtomeri K. Physiology: Relax and come in. Nature. 2014;514(7523):441-442.
doi:10.1038/514441a'
apa: 'Sixt, M. K., & Vaahtomeri, K. (2014). Physiology: Relax and come in. Nature.
Springer Nature. https://doi.org/10.1038/514441a'
chicago: 'Sixt, Michael K, and Kari Vaahtomeri. “Physiology: Relax and Come In.”
Nature. Springer Nature, 2014. https://doi.org/10.1038/514441a.'
ieee: 'M. K. Sixt and K. Vaahtomeri, “Physiology: Relax and come in,” Nature,
vol. 514, no. 7523. Springer Nature, pp. 441–442, 2014.'
ista: 'Sixt MK, Vaahtomeri K. 2014. Physiology: Relax and come in. Nature. 514(7523),
441–442.'
mla: 'Sixt, Michael K., and Kari Vaahtomeri. “Physiology: Relax and Come In.” Nature,
vol. 514, no. 7523, Springer Nature, 2014, pp. 441–42, doi:10.1038/514441a.'
short: M.K. Sixt, K. Vaahtomeri, Nature 514 (2014) 441–442.
date_created: 2018-12-11T11:54:30Z
date_published: 2014-10-23T00:00:00Z
date_updated: 2021-01-12T06:53:47Z
day: '23'
department:
- _id: MiSi
doi: 10.1038/514441a
intvolume: ' 514'
issue: '7523'
language:
- iso: eng
month: '10'
oa_version: None
page: 441 - 442
publication: Nature
publication_status: published
publisher: Springer Nature
publist_id: '5219'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Physiology: Relax and come in'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 514
year: '2014'
...
---
_id: '1910'
abstract:
- lang: eng
text: angerhans cells (LCs) are a unique subset of dendritic cells (DCs) that express
epithelial adhesion molecules, allowing them to form contacts with epithelial
cells and reside in epidermal/epithelial tissues. The dynamic regulation of epithelial
adhesion plays a decisive role in the life cycle of LCs. It controls whether LCs
remain immature and sessile within the epidermis or mature and egress to initiate
immune responses. So far, the molecular machinery regulating epithelial adhesion
molecules during LC maturation remains elusive. Here, we generated pure populations
of immature human LCs in vitro to systematically probe for gene-expression changes
during LC maturation. LCs down-regulate a set of epithelial genes including E-cadherin,
while they upregulate the mesenchymal marker N-cadherin known to facilitate cell
migration. In addition, N-cadherin is constitutively expressed by monocyte-derived
DCs known to exhibit characteristics of both inflammatory-type and interstitial/dermal
DCs. Moreover, the transcription factors ZEB1 and ZEB2 (ZEB is zinc-finger E-box-binding
homeobox) are upregulated in migratory LCs. ZEB1 and ZEB2 have been shown to induce
epithelial-to-mesenchymal transition (EMT) and invasive behavior in cancer cells
undergoing metastasis. Our results provide the first hint that the molecular EMT
machinery might facilitate LC mobilization. Moreover, our study suggests that
N-cadherin plays a role during DC migration.
acknowledgement: 'FWF. Grant Number: P22058-B20'
author:
- first_name: Sabine
full_name: Konradi, Sabine
last_name: Konradi
- first_name: Nighat
full_name: Yasmin, Nighat
last_name: Yasmin
- first_name: Denise
full_name: Haslwanter, Denise
last_name: Haslwanter
- first_name: Michele
full_name: Weber, Michele
id: 3A3FC708-F248-11E8-B48F-1D18A9856A87
last_name: Weber
- first_name: Bernd
full_name: Gesslbauer, Bernd
last_name: Gesslbauer
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Herbert
full_name: Strobl, Herbert
last_name: Strobl
citation:
ama: Konradi S, Yasmin N, Haslwanter D, et al. Langerhans cell maturation is accompanied
by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal
transition ZEB1/2. European Journal of Immunology. 2014;44(2):553-560.
doi:10.1002/eji.201343681
apa: Konradi, S., Yasmin, N., Haslwanter, D., Weber, M., Gesslbauer, B., Sixt, M.
K., & Strobl, H. (2014). Langerhans cell maturation is accompanied by induction
of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition
ZEB1/2. European Journal of Immunology. Wiley-Blackwell. https://doi.org/10.1002/eji.201343681
chicago: Konradi, Sabine, Nighat Yasmin, Denise Haslwanter, Michele Weber, Bernd
Gesslbauer, Michael K Sixt, and Herbert Strobl. “Langerhans Cell Maturation Is
Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal
Transition ZEB1/2.” European Journal of Immunology. Wiley-Blackwell, 2014.
https://doi.org/10.1002/eji.201343681.
ieee: S. Konradi et al., “Langerhans cell maturation is accompanied by induction
of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition
ZEB1/2,” European Journal of Immunology, vol. 44, no. 2. Wiley-Blackwell,
pp. 553–560, 2014.
ista: Konradi S, Yasmin N, Haslwanter D, Weber M, Gesslbauer B, Sixt MK, Strobl
H. 2014. Langerhans cell maturation is accompanied by induction of N-cadherin
and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2.
European Journal of Immunology. 44(2), 553–560.
mla: Konradi, Sabine, et al. “Langerhans Cell Maturation Is Accompanied by Induction
of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition
ZEB1/2.” European Journal of Immunology, vol. 44, no. 2, Wiley-Blackwell,
2014, pp. 553–60, doi:10.1002/eji.201343681.
short: S. Konradi, N. Yasmin, D. Haslwanter, M. Weber, B. Gesslbauer, M.K. Sixt,
H. Strobl, European Journal of Immunology 44 (2014) 553–560.
date_created: 2018-12-11T11:54:40Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2021-01-12T06:54:01Z
day: '01'
department:
- _id: MiSi
doi: 10.1002/eji.201343681
intvolume: ' 44'
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 553 - 560
publication: European Journal of Immunology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5185'
scopus_import: 1
status: public
title: Langerhans cell maturation is accompanied by induction of N-cadherin and the
transcriptional regulators of epithelial-mesenchymal transition ZEB1/2
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 44
year: '2014'
...
---
_id: '1925'
abstract:
- lang: eng
text: In the past decade carbon nanotubes (CNTs) have been widely studied as a potential
drug-delivery system, especially with functionality for cellular targeting. Yet,
little is known about the actual process of docking to cell receptors and transport
dynamics after internalization. Here we performed single-particle studies of folic
acid (FA) mediated CNT binding to human carcinoma cells and their transport inside
the cytosol. In particular, we employed molecular recognition force spectroscopy,
an atomic force microscopy based method, to visualize and quantify docking of
FA functionalized CNTs to FA binding receptors in terms of binding probability
and binding force. We then traced individual fluorescently labeled, FA functionalized
CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed
trajectories of directed diffusion and areas of nanotube confinement in the cytosol.
Our results demonstrate the potential of a single-molecule approach for investigation
of drug-delivery vehicles and their targeting capacity.
acknowledgement: "This work was supported by EC grant Marie Curie RTN-CT-2006-035616,
CARBIO 'Carbon nanotubes for biomedical applications' and Austrian FFG grant mnt-era.net
823980, 'IntelliTip'.\r\n"
article_number: '125704'
article_processing_charge: No
article_type: original
author:
- first_name: Constanze
full_name: Lamprecht, Constanze
last_name: Lamprecht
- first_name: Birgit
full_name: Plochberger, Birgit
last_name: Plochberger
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Christian
full_name: Rankl, Christian
last_name: Rankl
- first_name: Elena
full_name: Heister, Elena
last_name: Heister
- first_name: Barbara
full_name: Unterauer, Barbara
last_name: Unterauer
- first_name: Mario
full_name: Brameshuber, Mario
last_name: Brameshuber
- first_name: Jürgen
full_name: Danzberger, Jürgen
last_name: Danzberger
- first_name: Petar
full_name: Lukanov, Petar
last_name: Lukanov
- first_name: Emmanuel
full_name: Flahaut, Emmanuel
last_name: Flahaut
- first_name: Gerhard
full_name: Schütz, Gerhard
last_name: Schütz
- first_name: Peter
full_name: Hinterdorfer, Peter
last_name: Hinterdorfer
- first_name: Andreas
full_name: Ebner, Andreas
last_name: Ebner
citation:
ama: Lamprecht C, Plochberger B, Ruprecht V, et al. A single-molecule approach to
explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology.
2014;25(12). doi:10.1088/0957-4484/25/12/125704
apa: Lamprecht, C., Plochberger, B., Ruprecht, V., Wieser, S., Rankl, C., Heister,
E., … Ebner, A. (2014). A single-molecule approach to explore binding uptake and
transport of cancer cell targeting nanotubes. Nanotechnology. IOP Publishing.
https://doi.org/10.1088/0957-4484/25/12/125704
chicago: Lamprecht, Constanze, Birgit Plochberger, Verena Ruprecht, Stefan Wieser,
Christian Rankl, Elena Heister, Barbara Unterauer, et al. “A Single-Molecule Approach
to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology.
IOP Publishing, 2014. https://doi.org/10.1088/0957-4484/25/12/125704.
ieee: C. Lamprecht et al., “A single-molecule approach to explore binding
uptake and transport of cancer cell targeting nanotubes,” Nanotechnology,
vol. 25, no. 12. IOP Publishing, 2014.
ista: Lamprecht C, Plochberger B, Ruprecht V, Wieser S, Rankl C, Heister E, Unterauer
B, Brameshuber M, Danzberger J, Lukanov P, Flahaut E, Schütz G, Hinterdorfer P,
Ebner A. 2014. A single-molecule approach to explore binding uptake and transport
of cancer cell targeting nanotubes. Nanotechnology. 25(12), 125704.
mla: Lamprecht, Constanze, et al. “A Single-Molecule Approach to Explore Binding
Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology,
vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:10.1088/0957-4484/25/12/125704.
short: C. Lamprecht, B. Plochberger, V. Ruprecht, S. Wieser, C. Rankl, E. Heister,
B. Unterauer, M. Brameshuber, J. Danzberger, P. Lukanov, E. Flahaut, G. Schütz,
P. Hinterdorfer, A. Ebner, Nanotechnology 25 (2014).
date_created: 2018-12-11T11:54:45Z
date_published: 2014-03-28T00:00:00Z
date_updated: 2021-01-12T06:54:07Z
day: '28'
ddc:
- '570'
department:
- _id: CaHe
- _id: MiSi
doi: 10.1088/0957-4484/25/12/125704
file:
- access_level: open_access
checksum: df4e03d225a19179e7790f6d87a12332
content_type: application/pdf
creator: dernst
date_created: 2020-05-15T09:21:19Z
date_updated: 2020-07-14T12:45:21Z
file_id: '7856'
file_name: 2014_Nanotechnology_Lamprecht.pdf
file_size: 3804152
relation: main_file
file_date_updated: 2020-07-14T12:45:21Z
has_accepted_license: '1'
intvolume: ' 25'
issue: '12'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Submitted Version
publication: Nanotechnology
publication_status: published
publisher: IOP Publishing
publist_id: '5169'
scopus_import: 1
status: public
title: A single-molecule approach to explore binding uptake and transport of cancer
cell targeting nanotubes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 25
year: '2014'
...
---
_id: '2158'
abstract:
- lang: eng
text: Directional guidance of migrating cells is relatively well explored in the
reductionist setting of cell culture experiments. Here spatial gradients of chemical
cues as well as gradients of mechanical substrate characteristics prove sufficient
to attract single cells as well as their collectives. How such gradients present
and act in the context of an organism is far less clear. Here we review recent
advances in understanding how guidance cues emerge and operate in the physiological
context.
acknowledgement: This effort was supported by the Intramural Research Program of the
Center for Cancer Research, NCI, National Institutes of Health and the European
Research Council (ERC).
author:
- first_name: Ritankar
full_name: Majumdar, Ritankar
last_name: Majumdar
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Carole
full_name: Parent, Carole
last_name: Parent
citation:
ama: Majumdar R, Sixt MK, Parent C. New paradigms in the establishment and maintenance
of gradients during directed cell migration. Current Opinion in Cell Biology.
2014;30(1):33-40. doi:10.1016/j.ceb.2014.05.010
apa: Majumdar, R., Sixt, M. K., & Parent, C. (2014). New paradigms in the establishment
and maintenance of gradients during directed cell migration. Current Opinion
in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2014.05.010
chicago: Majumdar, Ritankar, Michael K Sixt, and Carole Parent. “New Paradigms in
the Establishment and Maintenance of Gradients during Directed Cell Migration.”
Current Opinion in Cell Biology. Elsevier, 2014. https://doi.org/10.1016/j.ceb.2014.05.010.
ieee: R. Majumdar, M. K. Sixt, and C. Parent, “New paradigms in the establishment
and maintenance of gradients during directed cell migration,” Current Opinion
in Cell Biology, vol. 30, no. 1. Elsevier, pp. 33–40, 2014.
ista: Majumdar R, Sixt MK, Parent C. 2014. New paradigms in the establishment and
maintenance of gradients during directed cell migration. Current Opinion in Cell
Biology. 30(1), 33–40.
mla: Majumdar, Ritankar, et al. “New Paradigms in the Establishment and Maintenance
of Gradients during Directed Cell Migration.” Current Opinion in Cell Biology,
vol. 30, no. 1, Elsevier, 2014, pp. 33–40, doi:10.1016/j.ceb.2014.05.010.
short: R. Majumdar, M.K. Sixt, C. Parent, Current Opinion in Cell Biology 30 (2014)
33–40.
date_created: 2018-12-11T11:56:03Z
date_published: 2014-10-01T00:00:00Z
date_updated: 2021-01-12T06:55:40Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.ceb.2014.05.010
external_id:
pmid:
- '24959970'
intvolume: ' 30'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177954/
month: '10'
oa: 1
oa_version: Submitted Version
page: 33 - 40
pmid: 1
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '4848'
quality_controlled: '1'
scopus_import: 1
status: public
title: New paradigms in the establishment and maintenance of gradients during directed
cell migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2014'
...
---
_id: '2214'
abstract:
- lang: eng
text: A hallmark of immune cell trafficking is directional guidance via gradients
of soluble or surface bound chemokines. Vascular endothelial cells produce, transport
and deposit either their own chemokines or chemokines produced by the underlying
stroma. Endothelial heparan sulfate (HS) was suggested to be a critical scaffold
for these chemokine pools, but it is unclear how steep chemokine gradients are
sustained between the lumenal and ablumenal aspects of blood vessels. Addressing
this question by semi-quantitative immunostaining of HS moieties around blood
vessels with a pan anti-HS IgM mAb, we found a striking HS enrichment in the basal
lamina of resting and inflamed post capillary skin venules, as well as in high
endothelial venules (HEVs) of lymph nodes. Staining of skin vessels with a glycocalyx
probe further suggested that their lumenal glycocalyx contains much lower HS density
than their basolateral extracellular matrix (ECM). This polarized HS pattern was
observed also in isolated resting and inflamed microvascular dermal cells. Notably,
progressive skin inflammation resulted in massive ECM deposition and in further
HS enrichment around skin post capillary venules and their associated pericytes.
Inflammation-dependent HS enrichment was not compromised in mice deficient in
the main HS degrading enzyme, heparanase. Our results suggest that the blood vasculature
patterns steep gradients of HS scaffolds between their lumenal and basolateral
endothelial aspects, and that inflammatory processes can further enrich the HS
content nearby inflamed vessels. We propose that chemokine gradients between the
lumenal and ablumenal sides of vessels could be favored by these sharp HS scaffold
gradients.
acknowledgement: Michael Sixt's research is supported by the European Research Council
(ERC Starting grant).
article_number: e85699
author:
- first_name: Liat
full_name: Stoler Barak, Liat
last_name: Stoler Barak
- first_name: Christine
full_name: Moussion, Christine
id: 3356F664-F248-11E8-B48F-1D18A9856A87
last_name: Moussion
- first_name: Elias
full_name: Shezen, Elias
last_name: Shezen
- first_name: Miki
full_name: Hatzav, Miki
last_name: Hatzav
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Ronen
full_name: Alon, Ronen
last_name: Alon
citation:
ama: Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. Blood vessels
pattern heparan sulfate gradients between their apical and basolateral aspects.
PLoS One. 2014;9(1). doi:10.1371/journal.pone.0085699
apa: Stoler Barak, L., Moussion, C., Shezen, E., Hatzav, M., Sixt, M. K., &
Alon, R. (2014). Blood vessels pattern heparan sulfate gradients between their
apical and basolateral aspects. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0085699
chicago: Stoler Barak, Liat, Christine Moussion, Elias Shezen, Miki Hatzav, Michael
K Sixt, and Ronen Alon. “Blood Vessels Pattern Heparan Sulfate Gradients between
Their Apical and Basolateral Aspects.” PLoS One. Public Library of Science,
2014. https://doi.org/10.1371/journal.pone.0085699.
ieee: L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M. K. Sixt, and R. Alon,
“Blood vessels pattern heparan sulfate gradients between their apical and basolateral
aspects,” PLoS One, vol. 9, no. 1. Public Library of Science, 2014.
ista: Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. 2014. Blood
vessels pattern heparan sulfate gradients between their apical and basolateral
aspects. PLoS One. 9(1), e85699.
mla: Stoler Barak, Liat, et al. “Blood Vessels Pattern Heparan Sulfate Gradients
between Their Apical and Basolateral Aspects.” PLoS One, vol. 9, no. 1,
e85699, Public Library of Science, 2014, doi:10.1371/journal.pone.0085699.
short: L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M.K. Sixt, R. Alon, PLoS
One 9 (2014).
date_created: 2018-12-11T11:56:22Z
date_published: 2014-01-22T00:00:00Z
date_updated: 2021-01-12T06:56:03Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1371/journal.pone.0085699
ec_funded: 1
file:
- access_level: open_access
checksum: 84a8033bda2e07e39405f5acc85f4eca
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:07:48Z
date_updated: 2020-07-14T12:45:33Z
file_id: '4646'
file_name: IST-2016-433-v1+1_journal.pone.0085699.pdf
file_size: 12634775
relation: main_file
file_date_updated: 2020-07-14T12:45:33Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25A76F58-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '289720'
name: Stromal Cell-immune Cell Interactions in Health and Disease
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '4756'
pubrep_id: '433'
quality_controlled: '1'
scopus_import: 1
status: public
title: Blood vessels pattern heparan sulfate gradients between their apical and basolateral
aspects
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '2215'
abstract:
- lang: eng
text: Homologous recombination is crucial for genome stability and for genetic exchange.
Although our knowledge of the principle steps in recombination and its machinery
is well advanced, homology search, the critical step of exploring the genome for
homologous sequences to enable recombination, has remained mostly enigmatic. However,
recent methodological advances have provided considerable new insights into this
fundamental step in recombination that can be integrated into a mechanistic model.
These advances emphasize the importance of genomic proximity and nuclear organization
for homology search and the critical role of homology search mediators in this
process. They also aid our understanding of how homology search might lead to
unwanted and potentially disease-promoting recombination events.
acknowledgement: J.R. was supported by a Boehringer Ingelheim Fonds PhD stipend.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Renkawitz J, Lademann C, Jentsch S. Mechanisms and principles of homology search
during recombination. Nature Reviews Molecular Cell Biology. 2014;15(6):369-383.
doi:10.1038/nrm3805
apa: Renkawitz, J., Lademann, C., & Jentsch, S. (2014). Mechanisms and principles
of homology search during recombination. Nature Reviews Molecular Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/nrm3805
chicago: Renkawitz, Jörg, Claudio Lademann, and Stefan Jentsch. “Mechanisms and
Principles of Homology Search during Recombination.” Nature Reviews Molecular
Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/nrm3805.
ieee: J. Renkawitz, C. Lademann, and S. Jentsch, “Mechanisms and principles of homology
search during recombination,” Nature Reviews Molecular Cell Biology, vol.
15, no. 6. Nature Publishing Group, pp. 369–383, 2014.
ista: Renkawitz J, Lademann C, Jentsch S. 2014. Mechanisms and principles of homology
search during recombination. Nature Reviews Molecular Cell Biology. 15(6), 369–383.
mla: Renkawitz, Jörg, et al. “Mechanisms and Principles of Homology Search during
Recombination.” Nature Reviews Molecular Cell Biology, vol. 15, no. 6,
Nature Publishing Group, 2014, pp. 369–83, doi:10.1038/nrm3805.
short: J. Renkawitz, C. Lademann, S. Jentsch, Nature Reviews Molecular Cell Biology
15 (2014) 369–383.
date_created: 2018-12-11T11:56:22Z
date_published: 2014-05-14T00:00:00Z
date_updated: 2021-01-12T06:56:03Z
day: '14'
department:
- _id: MiSi
doi: 10.1038/nrm3805
intvolume: ' 15'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 369 - 383
publication: Nature Reviews Molecular Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '4755'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mechanisms and principles of homology search during recombination
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2014'
...
---
_id: '2242'
abstract:
- lang: eng
text: MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in
many cellular pathways. MiRNAs associate with members of the Argonaute protein
family and bind to partially complementary sequences on mRNAs and induce translational
repression or mRNA decay. Using deep sequencing and Northern blotting, we characterized
miRNA expression in wild type and miR-155-deficient dendritic cells (DCs) and
macrophages. Analysis of different stimuli (LPS, LDL, eLDL, oxLDL) reveals a direct
influence of miR-155 on the expression levels of other miRNAs. For example, miR-455
is negatively regulated in miR-155-deficient cells possibly due to inhibition
of the transcription factor C/EBPbeta by miR-155. Based on our comprehensive data
sets, we propose a model of hierarchical miRNA expression dominated by miR-155
in DCs and macrophages.
author:
- first_name: Anne
full_name: Dueck, Anne
last_name: Dueck
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Dueck A, Eichner A, Sixt MK, Meister G. A miR-155-dependent microRNA hierarchy
in dendritic cell maturation and macrophage activation. FEBS Letters. 2014;588(4):632-640.
doi:10.1016/j.febslet.2014.01.009
apa: Dueck, A., Eichner, A., Sixt, M. K., & Meister, G. (2014). A miR-155-dependent
microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS
Letters. Elsevier. https://doi.org/10.1016/j.febslet.2014.01.009
chicago: Dueck, Anne, Alexander Eichner, Michael K Sixt, and Gunter Meister. “A
MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage
Activation.” FEBS Letters. Elsevier, 2014. https://doi.org/10.1016/j.febslet.2014.01.009.
ieee: A. Dueck, A. Eichner, M. K. Sixt, and G. Meister, “A miR-155-dependent microRNA
hierarchy in dendritic cell maturation and macrophage activation,” FEBS Letters,
vol. 588, no. 4. Elsevier, pp. 632–640, 2014.
ista: Dueck A, Eichner A, Sixt MK, Meister G. 2014. A miR-155-dependent microRNA
hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters.
588(4), 632–640.
mla: Dueck, Anne, et al. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell
Maturation and Macrophage Activation.” FEBS Letters, vol. 588, no. 4, Elsevier,
2014, pp. 632–40, doi:10.1016/j.febslet.2014.01.009.
short: A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640.
date_created: 2018-12-11T11:56:31Z
date_published: 2014-02-14T00:00:00Z
date_updated: 2021-01-12T06:56:14Z
day: '14'
department:
- _id: MiSi
doi: 10.1016/j.febslet.2014.01.009
intvolume: ' 588'
issue: '4'
language:
- iso: eng
month: '02'
oa_version: None
page: 632 - 640
publication: FEBS Letters
publication_identifier:
issn:
- '00145793'
publication_status: published
publisher: Elsevier
publist_id: '4714'
quality_controlled: '1'
scopus_import: 1
status: public
title: A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage
activation
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 588
year: '2014'
...
---
_id: '2830'
author:
- first_name: Christine
full_name: Moussion, Christine
id: 3356F664-F248-11E8-B48F-1D18A9856A87
last_name: Moussion
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Moussion C, Sixt MK. A conduit to amplify innate immunity. Immunity.
2013;38(5):853-854. doi:10.1016/j.immuni.2013.05.005
apa: Moussion, C., & Sixt, M. K. (2013). A conduit to amplify innate immunity.
Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2013.05.005
chicago: Moussion, Christine, and Michael K Sixt. “A Conduit to Amplify Innate Immunity.”
Immunity. Cell Press, 2013. https://doi.org/10.1016/j.immuni.2013.05.005.
ieee: C. Moussion and M. K. Sixt, “A conduit to amplify innate immunity,” Immunity,
vol. 38, no. 5. Cell Press, pp. 853–854, 2013.
ista: Moussion C, Sixt MK. 2013. A conduit to amplify innate immunity. Immunity.
38(5), 853–854.
mla: Moussion, Christine, and Michael K. Sixt. “A Conduit to Amplify Innate Immunity.”
Immunity, vol. 38, no. 5, Cell Press, 2013, pp. 853–54, doi:10.1016/j.immuni.2013.05.005.
short: C. Moussion, M.K. Sixt, Immunity 38 (2013) 853–854.
date_created: 2018-12-11T11:59:49Z
date_published: 2013-05-23T00:00:00Z
date_updated: 2021-01-12T07:00:01Z
day: '23'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2013.05.005
intvolume: ' 38'
issue: '5'
language:
- iso: eng
month: '05'
oa_version: None
page: 853 - 854
publication: Immunity
publication_status: published
publisher: Cell Press
publist_id: '3969'
quality_controlled: '1'
scopus_import: 1
status: public
title: A conduit to amplify innate immunity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2013'
...