---
_id: '15160'
abstract:
- lang: eng
text: The circadian clock orchestrates global changes in transcriptional regulation
on a daily basis via the bHLH-PAS transcription factor CLOCK:BMAL1. Pathways driven
by other bHLH-PAS transcription factors have a homologous repressor that modulates
activity on a tissue-specific basis, but none have been identified for CLOCK:BMAL1.
We show here that the cancer/testis antigen PASD1 fulfills this role to suppress
circadian rhythms. PASD1 is evolutionarily related to CLOCK and interacts with
the CLOCK:BMAL1 complex to repress transcriptional activation. Expression of PASD1
is restricted to germline tissues in healthy individuals but can be induced in
cells of somatic origin upon oncogenic transformation. Reducing PASD1 in human
cancer cells significantly increases the amplitude of transcriptional oscillations
to generate more robust circadian rhythms. Our results describe a function for
a germline-specific protein in regulation of the circadian clock and provide a
molecular link from oncogenic transformation to suppression of circadian rhythms.
article_processing_charge: No
article_type: original
author:
- first_name: Alicia Kathleen
full_name: Michael, Alicia Kathleen
id: 6437c950-2a03-11ee-914d-d6476dd7b75c
last_name: Michael
- first_name: Stacy L.
full_name: Harvey, Stacy L.
last_name: Harvey
- first_name: Patrick J.
full_name: Sammons, Patrick J.
last_name: Sammons
- first_name: Amanda P.
full_name: Anderson, Amanda P.
last_name: Anderson
- first_name: Hema M.
full_name: Kopalle, Hema M.
last_name: Kopalle
- first_name: Alison H.
full_name: Banham, Alison H.
last_name: Banham
- first_name: Carrie L.
full_name: Partch, Carrie L.
last_name: Partch
citation:
ama: Michael AK, Harvey SL, Sammons PJ, et al. Cancer/Testis antigen PASD1 silences
the circadian clock. Molecular Cell. 2015;58(5):743-754. doi:10.1016/j.molcel.2015.03.031
apa: Michael, A. K., Harvey, S. L., Sammons, P. J., Anderson, A. P., Kopalle, H.
M., Banham, A. H., & Partch, C. L. (2015). Cancer/Testis antigen PASD1 silences
the circadian clock. Molecular Cell. Elsevier. https://doi.org/10.1016/j.molcel.2015.03.031
chicago: Michael, Alicia K., Stacy L. Harvey, Patrick J. Sammons, Amanda P. Anderson,
Hema M. Kopalle, Alison H. Banham, and Carrie L. Partch. “Cancer/Testis Antigen
PASD1 Silences the Circadian Clock.” Molecular Cell. Elsevier, 2015. https://doi.org/10.1016/j.molcel.2015.03.031.
ieee: A. K. Michael et al., “Cancer/Testis antigen PASD1 silences the circadian
clock,” Molecular Cell, vol. 58, no. 5. Elsevier, pp. 743–754, 2015.
ista: Michael AK, Harvey SL, Sammons PJ, Anderson AP, Kopalle HM, Banham AH, Partch
CL. 2015. Cancer/Testis antigen PASD1 silences the circadian clock. Molecular
Cell. 58(5), 743–754.
mla: Michael, Alicia K., et al. “Cancer/Testis Antigen PASD1 Silences the Circadian
Clock.” Molecular Cell, vol. 58, no. 5, Elsevier, 2015, pp. 743–54, doi:10.1016/j.molcel.2015.03.031.
short: A.K. Michael, S.L. Harvey, P.J. Sammons, A.P. Anderson, H.M. Kopalle, A.H.
Banham, C.L. Partch, Molecular Cell 58 (2015) 743–754.
date_created: 2024-03-21T07:58:08Z
date_published: 2015-06-04T00:00:00Z
date_updated: 2024-03-25T11:52:26Z
day: '04'
doi: 10.1016/j.molcel.2015.03.031
extern: '1'
intvolume: ' 58'
issue: '5'
keyword:
- Cell Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.molcel.2015.03.031
month: '06'
oa: 1
oa_version: Published Version
page: 743-754
publication: Molecular Cell
publication_identifier:
issn:
- 1097-2765
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cancer/Testis antigen PASD1 silences the circadian clock
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 58
year: '2015'
...
---
_id: '15159'
abstract:
- lang: eng
text: It is widely recognized that BMAL1 is an essential subunit of the primary
transcription factor that drives rhythmic circadian transcription in the nucleus.
In a surprising turn, Lipton et al. now show that BMAL1 rhythmically interacts
with translational machinery in the cytosol to stimulate protein synthesis in
response to mTOR signaling.
article_processing_charge: No
article_type: original
author:
- first_name: Alicia Kathleen
full_name: Michael, Alicia Kathleen
id: 6437c950-2a03-11ee-914d-d6476dd7b75c
last_name: Michael
- first_name: Hande
full_name: Asimgil, Hande
last_name: Asimgil
- first_name: Carrie L.
full_name: Partch, Carrie L.
last_name: Partch
citation:
ama: Michael AK, Asimgil H, Partch CL. Cytosolic BMAL1 moonlights as a translation
factor. Trends in Biochemical Sciences. 2015;40(9):489-490. doi:10.1016/j.tibs.2015.07.006
apa: Michael, A. K., Asimgil, H., & Partch, C. L. (2015). Cytosolic BMAL1 moonlights
as a translation factor. Trends in Biochemical Sciences. Elsevier. https://doi.org/10.1016/j.tibs.2015.07.006
chicago: Michael, Alicia K., Hande Asimgil, and Carrie L. Partch. “Cytosolic BMAL1
Moonlights as a Translation Factor.” Trends in Biochemical Sciences. Elsevier,
2015. https://doi.org/10.1016/j.tibs.2015.07.006.
ieee: A. K. Michael, H. Asimgil, and C. L. Partch, “Cytosolic BMAL1 moonlights as
a translation factor,” Trends in Biochemical Sciences, vol. 40, no. 9.
Elsevier, pp. 489–490, 2015.
ista: Michael AK, Asimgil H, Partch CL. 2015. Cytosolic BMAL1 moonlights as a translation
factor. Trends in Biochemical Sciences. 40(9), 489–490.
mla: Michael, Alicia K., et al. “Cytosolic BMAL1 Moonlights as a Translation Factor.”
Trends in Biochemical Sciences, vol. 40, no. 9, Elsevier, 2015, pp. 489–90,
doi:10.1016/j.tibs.2015.07.006.
short: A.K. Michael, H. Asimgil, C.L. Partch, Trends in Biochemical Sciences 40
(2015) 489–490.
date_created: 2024-03-21T07:57:44Z
date_published: 2015-09-01T00:00:00Z
date_updated: 2024-03-25T11:53:58Z
day: '01'
doi: 10.1016/j.tibs.2015.07.006
extern: '1'
intvolume: ' 40'
issue: '9'
keyword:
- Molecular Biology
- Biochemistry
language:
- iso: eng
month: '09'
oa_version: None
page: 489-490
publication: Trends in Biochemical Sciences
publication_identifier:
issn:
- 0968-0004
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cytosolic BMAL1 moonlights as a translation factor
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 40
year: '2015'
...
---
_id: '1619'
abstract:
- lang: eng
text: The emergence of drug resistant pathogens is a serious public health problem.
It is a long-standing goal to predict rates of resistance evolution and design
optimal treatment strategies accordingly. To this end, it is crucial to reveal
the underlying causes of drug-specific differences in the evolutionary dynamics
leading to resistance. However, it remains largely unknown why the rates of resistance
evolution via spontaneous mutations and the diversity of mutational paths vary
substantially between drugs. Here we comprehensively quantify the distribution
of fitness effects (DFE) of mutations, a key determinant of evolutionary dynamics,
in the presence of eight antibiotics representing the main modes of action. Using
precise high-throughput fitness measurements for genome-wide Escherichia coli
gene deletion strains, we find that the width of the DFE varies dramatically between
antibiotics and, contrary to conventional wisdom, for some drugs the DFE width
is lower than in the absence of stress. We show that this previously underappreciated
divergence in DFE width among antibiotics is largely caused by their distinct
drug-specific dose-response characteristics. Unlike the DFE, the magnitude of
the changes in tolerated drug concentration resulting from genome-wide mutations
is similar for most drugs but exceptionally small for the antibiotic nitrofurantoin,
i.e., mutations generally have considerably smaller resistance effects for nitrofurantoin
than for other drugs. A population genetics model predicts that resistance evolution
for drugs with this property is severely limited and confined to reproducible
mutational paths. We tested this prediction in laboratory evolution experiments
using the “morbidostat”, a device for evolving bacteria in well-controlled drug
environments. Nitrofurantoin resistance indeed evolved extremely slowly via reproducible
mutations—an almost paradoxical behavior since this drug causes DNA damage and
increases the mutation rate. Overall, we identified novel quantitative characteristics
of the evolutionary landscape that provide the conceptual foundation for predicting
the dynamics of drug resistance evolution.
article_number: e1002299
author:
- first_name: Guillaume
full_name: Chevereau, Guillaume
id: 424D78A0-F248-11E8-B48F-1D18A9856A87
last_name: Chevereau
- first_name: Marta
full_name: Dravecka, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Dravecka
orcid: 0000-0002-2519-8004
- first_name: Tugce
full_name: Batur, Tugce
last_name: Batur
- first_name: Aysegul
full_name: Guvenek, Aysegul
last_name: Guvenek
- first_name: Dilay
full_name: Ayhan, Dilay
last_name: Ayhan
- first_name: Erdal
full_name: Toprak, Erdal
last_name: Toprak
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Chevereau G, Lukacisinova M, Batur T, et al. Quantifying the determinants of
evolutionary dynamics leading to drug resistance. PLoS Biology. 2015;13(11).
doi:10.1371/journal.pbio.1002299
apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D., Toprak,
E., & Bollenbach, M. T. (2015). Quantifying the determinants of evolutionary
dynamics leading to drug resistance. PLoS Biology. Public Library of Science.
https://doi.org/10.1371/journal.pbio.1002299
chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek,
Dilay Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Quantifying the Determinants
of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology. Public
Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.
ieee: G. Chevereau et al., “Quantifying the determinants of evolutionary
dynamics leading to drug resistance,” PLoS Biology, vol. 13, no. 11. Public
Library of Science, 2015.
ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan D, Toprak E, Bollenbach
MT. 2015. Quantifying the determinants of evolutionary dynamics leading to drug
resistance. PLoS Biology. 13(11), e1002299.
mla: Chevereau, Guillaume, et al. “Quantifying the Determinants of Evolutionary
Dynamics Leading to Drug Resistance.” PLoS Biology, vol. 13, no. 11, e1002299,
Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.
short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D. Ayhan, E. Toprak,
M.T. Bollenbach, PLoS Biology 13 (2015).
date_created: 2018-12-11T11:53:04Z
date_published: 2015-11-18T00:00:00Z
date_updated: 2024-03-27T23:30:28Z
day: '18'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.1371/journal.pbio.1002299
ec_funded: 1
file:
- access_level: open_access
checksum: 0e82e3279f50b15c6c170c042627802b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:00Z
date_updated: 2020-07-14T12:45:07Z
file_id: '4723'
file_name: IST-2016-468-v1+1_journal.pbio.1002299.pdf
file_size: 1387760
relation: main_file
file_date_updated: 2020-07-14T12:45:07Z
has_accepted_license: '1'
intvolume: ' 13'
issue: '11'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303507'
name: Optimality principles in responses to antibiotics
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '5547'
pubrep_id: '468'
quality_controlled: '1'
related_material:
record:
- id: '9711'
relation: research_data
status: public
- id: '9765'
relation: research_data
status: public
- id: '6263'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Quantifying the determinants of evolutionary dynamics leading to drug resistance
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: 13
year: '2015'
...
---
_id: '10382'
abstract:
- lang: eng
text: 'Protein oligomers have been implicated as toxic agents in a wide range of
amyloid-related diseases. However, it has remained unsolved whether the oligomers
are a necessary step in the formation of amyloid fibrils or just a dangerous byproduct.
Analogously, it has not been resolved if the amyloid nucleation process is a classical
one-step nucleation process or a two-step process involving prenucleation clusters.
We use coarse-grained computer simulations to study the effect of nonspecific
attractions between peptides on the primary nucleation process underlying amyloid
fibrillization. We find that, for peptides that do not attract, the classical
one-step nucleation mechanism is possible but only at nonphysiologically high
peptide concentrations. At low peptide concentrations, which mimic the physiologically
relevant regime, attractive interpeptide interactions are essential for fibril
formation. Nucleation then inevitably takes place through a two-step mechanism
involving prefibrillar oligomers. We show that oligomers not only help peptides
meet each other but also, create an environment that facilitates the conversion
of monomers into the β-sheet–rich form characteristic of fibrils. Nucleation typically
does not proceed through the most prevalent oligomers but through an oligomer
size that is only observed in rare fluctuations, which is why such aggregates
might be hard to capture experimentally. Finally, we find that the nucleation
of amyloid fibrils cannot be described by classical nucleation theory: in the
two-step mechanism, the critical nucleus size increases with increases in both
concentration and interpeptide interactions, which is in direct contrast with
predictions from classical nucleation theory.'
acknowledgement: We thank Michele Vendruscolo, Iskra Staneva, and William M. Jacobs,
for helpful discussions. A.Š. acknowledges support from the Human Frontier Science
Program and Emmanuel College. Y.C.C. and D.F. are supported by Engineering and Physical
Sciences Research Council Programme Grant EP/I001352/1. T.P.J.K. acknowledges the
Frances and Augustus Newman Foundation, the European Research Council, and the Biotechnology
and Biological Sciences Research Council. D.F. acknowledges European Research Council
Advanced Grant 227758.
article_processing_charge: No
article_type: original
author:
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Yassmine C.
full_name: Chebaro, Yassmine C.
last_name: Chebaro
- first_name: Tuomas P. J.
full_name: Knowles, Tuomas P. J.
last_name: Knowles
- first_name: Daan
full_name: Frenkel, Daan
last_name: Frenkel
citation:
ama: Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. Crucial role of nonspecific interactions
in amyloid nucleation. Proceedings of the National Academy of Sciences.
2014;111(50):17869-17874. doi:10.1073/pnas.1410159111
apa: Šarić, A., Chebaro, Y. C., Knowles, T. P. J., & Frenkel, D. (2014). Crucial
role of nonspecific interactions in amyloid nucleation. Proceedings of the
National Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1410159111
chicago: Šarić, Anđela, Yassmine C. Chebaro, Tuomas P. J. Knowles, and Daan Frenkel.
“Crucial Role of Nonspecific Interactions in Amyloid Nucleation.” Proceedings
of the National Academy of Sciences. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1410159111.
ieee: A. Šarić, Y. C. Chebaro, T. P. J. Knowles, and D. Frenkel, “Crucial role of
nonspecific interactions in amyloid nucleation,” Proceedings of the National
Academy of Sciences, vol. 111, no. 50. National Academy of Sciences, pp. 17869–17874,
2014.
ista: Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. 2014. Crucial role of nonspecific
interactions in amyloid nucleation. Proceedings of the National Academy of Sciences.
111(50), 17869–17874.
mla: Šarić, Anđela, et al. “Crucial Role of Nonspecific Interactions in Amyloid
Nucleation.” Proceedings of the National Academy of Sciences, vol. 111,
no. 50, National Academy of Sciences, 2014, pp. 17869–74, doi:10.1073/pnas.1410159111.
short: A. Šarić, Y.C. Chebaro, T.P.J. Knowles, D. Frenkel, Proceedings of the National
Academy of Sciences 111 (2014) 17869–17874.
date_created: 2021-11-29T13:09:53Z
date_published: 2014-12-01T00:00:00Z
date_updated: 2021-11-29T13:29:05Z
day: '01'
doi: 10.1073/pnas.1410159111
extern: '1'
external_id:
arxiv:
- '1412.0897'
pmid:
- '25453085'
intvolume: ' 111'
issue: '50'
keyword:
- multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.pnas.org/content/111/50/17869
month: '12'
oa: 1
oa_version: Published Version
page: 17869-17874
pmid: 1
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
scopus_import: '1'
status: public
title: Crucial role of nonspecific interactions in amyloid nucleation
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 111
year: '2014'
...
---
_id: '10383'
abstract:
- lang: eng
text: We use numerical simulations to compute the equation of state of a suspension
of spherical self-propelled nanoparticles in two and three dimensions. We study
in detail the effect of excluded volume interactions and confinement as a function
of the system's temperature, concentration, and strength of the propulsion. We
find a striking nonmonotonic dependence of the pressure on the temperature and
provide simple scaling arguments to predict and explain the occurrence of such
anomalous behavior. We explicitly show how our results have important implications
for the effective forces on passive components suspended in a bath of active particles.
article_number: '052303'
article_processing_charge: No
article_type: original
author:
- first_name: S. A.
full_name: Mallory, S. A.
last_name: Mallory
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: C.
full_name: Valeriani, C.
last_name: Valeriani
- first_name: A.
full_name: Cacciuto, A.
last_name: Cacciuto
citation:
ama: Mallory SA, Šarić A, Valeriani C, Cacciuto A. Anomalous thermomechanical properties
of a self-propelled colloidal fluid. Physical Review E. 2014;89(5). doi:10.1103/physreve.89.052303
apa: Mallory, S. A., Šarić, A., Valeriani, C., & Cacciuto, A. (2014). Anomalous
thermomechanical properties of a self-propelled colloidal fluid. Physical Review
E. American Physical Society. https://doi.org/10.1103/physreve.89.052303
chicago: Mallory, S. A., Anđela Šarić, C. Valeriani, and A. Cacciuto. “Anomalous
Thermomechanical Properties of a Self-Propelled Colloidal Fluid.” Physical
Review E. American Physical Society, 2014. https://doi.org/10.1103/physreve.89.052303.
ieee: S. A. Mallory, A. Šarić, C. Valeriani, and A. Cacciuto, “Anomalous thermomechanical
properties of a self-propelled colloidal fluid,” Physical Review E, vol.
89, no. 5. American Physical Society, 2014.
ista: Mallory SA, Šarić A, Valeriani C, Cacciuto A. 2014. Anomalous thermomechanical
properties of a self-propelled colloidal fluid. Physical Review E. 89(5), 052303.
mla: Mallory, S. A., et al. “Anomalous Thermomechanical Properties of a Self-Propelled
Colloidal Fluid.” Physical Review E, vol. 89, no. 5, 052303, American Physical
Society, 2014, doi:10.1103/physreve.89.052303.
short: S.A. Mallory, A. Šarić, C. Valeriani, A. Cacciuto, Physical Review E 89 (2014).
date_created: 2021-11-29T13:10:33Z
date_published: 2014-05-06T00:00:00Z
date_updated: 2021-11-29T13:29:01Z
day: '06'
doi: 10.1103/physreve.89.052303
extern: '1'
external_id:
arxiv:
- '1310.0826'
pmid:
- '25353796'
intvolume: ' 89'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1310.0826
month: '05'
oa: 1
oa_version: Preprint
pmid: 1
publication: Physical Review E
publication_identifier:
eissn:
- 1550-2376
issn:
- 1539-3755
publication_status: published
publisher: American Physical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Anomalous thermomechanical properties of a self-propelled colloidal fluid
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 89
year: '2014'
...
---
_id: '1058'
abstract:
- lang: eng
text: Diffraction-unlimited far-field super-resolution fluorescence (nanoscopy)
methods typically rely on transiently transferring fluorophores between two states,
whereby this transfer is usually laid out as a switch. However, depending on whether
this is induced in a spatially controlled manner using a pattern of light (coordinate-targeted)
or stochastically on a single-molecule basis, specific requirements on the fluorophores
are imposed. Therefore, the fluorophores are usually utilized just for one class
of methods only. In this study we demonstrate that the reversibly switchable fluorescent
protein Dreiklang enables live-cell recordings in both spatially controlled and
stochastic modes. We show that the Dreiklang chromophore entails three different
light-induced switching mechanisms, namely a reversible photochemical one, off-switching
by stimulated emission, and a reversible transfer to a long-lived dark state from
the S1 state, all of which can be utilized to overcome the diffraction barrier.
We also find that for the single-molecule- based stochastic GSDIM approach (ground-state
depletion followed by individual molecule return), Dreiklang provides a larger
number of on-off localization events as compared to its progenitor Citrine. Altogether,
Dreiklang is a versatile probe for essentially all popular forms of live-cell
fluorescence nanoscopy.
article_processing_charge: No
author:
- first_name: Nickels
full_name: Jensen, Nickels
last_name: Jensen
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
- first_name: Katrin
full_name: Willig, Katrin
last_name: Willig
- first_name: Flavie
full_name: Lavoie Cardinal, Flavie
last_name: Lavoie Cardinal
- first_name: Tanja
full_name: Brakemann, Tanja
last_name: Brakemann
- first_name: Stefan
full_name: Hell, Stefan
last_name: Hell
- first_name: Stefan
full_name: Jakobs, Stefan
last_name: Jakobs
citation:
ama: Jensen N, Danzl JG, Willig K, et al. Coordinate-targeted and coordinate-stochastic
super-resolution microscopy with the reversibly switchable fluorescent protein
dreiklang. ChemPhysChem. 2014;15(4):756-762. doi:10.1002/cphc.201301034
apa: Jensen, N., Danzl, J. G., Willig, K., Lavoie Cardinal, F., Brakemann, T., Hell,
S., & Jakobs, S. (2014). Coordinate-targeted and coordinate-stochastic super-resolution
microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem.
Wiley-Blackwell. https://doi.org/10.1002/cphc.201301034
chicago: Jensen, Nickels, Johann G Danzl, Katrin Willig, Flavie Lavoie Cardinal,
Tanja Brakemann, Stefan Hell, and Stefan Jakobs. “Coordinate-Targeted and Coordinate-Stochastic
Super-Resolution Microscopy with the Reversibly Switchable Fluorescent Protein
Dreiklang.” ChemPhysChem. Wiley-Blackwell, 2014. https://doi.org/10.1002/cphc.201301034.
ieee: N. Jensen et al., “Coordinate-targeted and coordinate-stochastic super-resolution
microscopy with the reversibly switchable fluorescent protein dreiklang,” ChemPhysChem,
vol. 15, no. 4. Wiley-Blackwell, pp. 756–762, 2014.
ista: Jensen N, Danzl JG, Willig K, Lavoie Cardinal F, Brakemann T, Hell S, Jakobs
S. 2014. Coordinate-targeted and coordinate-stochastic super-resolution microscopy
with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. 15(4),
756–762.
mla: Jensen, Nickels, et al. “Coordinate-Targeted and Coordinate-Stochastic Super-Resolution
Microscopy with the Reversibly Switchable Fluorescent Protein Dreiklang.” ChemPhysChem,
vol. 15, no. 4, Wiley-Blackwell, 2014, pp. 756–62, doi:10.1002/cphc.201301034.
short: N. Jensen, J.G. Danzl, K. Willig, F. Lavoie Cardinal, T. Brakemann, S. Hell,
S. Jakobs, ChemPhysChem 15 (2014) 756–762.
date_created: 2018-12-11T11:49:55Z
date_published: 2014-03-17T00:00:00Z
date_updated: 2021-01-12T06:47:58Z
day: '17'
doi: 10.1002/cphc.201301034
extern: '1'
intvolume: ' 15'
issue: '4'
language:
- iso: eng
month: '03'
oa_version: None
page: 756 - 762
publication: ChemPhysChem
publication_status: published
publisher: Wiley-Blackwell
publist_id: '6332'
status: public
title: Coordinate-targeted and coordinate-stochastic super-resolution microscopy with
the reversibly switchable fluorescent protein dreiklang
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2014'
...
---
_id: '10815'
abstract:
- lang: eng
text: In the last several decades, developmental biology has clarified the molecular
mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated
that the “tool-kit genes” essential for regulating developmental processes are
not only highly conserved among species, but are also used as systems at various
times and places in an organism to control distinct developmental events. Therefore,
mutations in many of these tool-kit genes may cause congenital diseases involving
morphological abnormalities. This link between genes and abnormal morphological
phenotypes underscores the importance of understanding how cells behave and contribute
to morphogenesis as a result of gene function. Recent improvements in live imaging
and in quantitative analyses of cellular dynamics will advance our understanding
of the cellular pathogenesis of congenital diseases associated with aberrant morphologies.
In these studies, it is critical to select an appropriate model organism for the
particular phenomenon of interest.
acknowledgement: The authors thank all the members of the Division of Morphogenesis,
National Institute for Basic Biology, for their contributions to the research, their
encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical
reading of the manuscript. We also thank the Model Animal Research and Spectrography
and Bioimaging Facilities, NIBB Core Research Facilities, for technical support.
M.H. was supported by a research fellowship from the Japan Society for the Promotion
of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid
for Scientific Research on Innovative Areas from the Ministry of Education, Culture,
Sports, Science, and Technology (MEXT), Japan, to N.U.
article_processing_charge: No
article_type: original
author:
- first_name: Masakazu
full_name: Hashimoto, Masakazu
last_name: Hashimoto
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Naoto
full_name: Ueno, Naoto
last_name: Ueno
citation:
ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development
underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039
apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms
of development underlying congenital diseases. Congenital Anomalies. Wiley.
https://doi.org/10.1111/cga.12039
chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular
Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies.
Wiley, 2014. https://doi.org/10.1111/cga.12039.
ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of
development underlying congenital diseases,” Congenital Anomalies, vol.
54, no. 1. Wiley, pp. 1–7, 2014.
ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of
development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.
mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development
Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1,
Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039.
short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.
date_created: 2022-03-04T08:17:25Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2022-03-04T08:26:05Z
day: '01'
department:
- _id: CaHe
doi: 10.1111/cga.12039
external_id:
pmid:
- '24666178'
intvolume: ' 54'
issue: '1'
keyword:
- Developmental Biology
- Embryology
- General Medicine
- Pediatrics
- Perinatology
- and Child Health
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/cga.12039
month: '02'
oa: 1
oa_version: None
page: 1-7
pmid: 1
publication: Congenital Anomalies
publication_identifier:
issn:
- 0914-3505
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular and cellular mechanisms of development underlying congenital diseases
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2014'
...
---
_id: '10811'
abstract:
- lang: eng
text: Auxin is an important signaling compound in plants and vital for plant development
and growth. The present book, Auxin and its Role in Plant Development, provides
the reader with detailed and comprehensive insight into the functioning of the
molecule on the whole and specifically in plant development. In the first part,
the functioning, metabolism and signaling pathways of auxin in plants are explained,
the second part depicts the specific role of auxin in plant development and the
third part describes the interaction and functioning of the signaling compound upon
stimuli of the environment. Each chapter is written by international experts in
the respective field and designed for scientists and researchers in plant biology,
plant development and cell biology to summarize the recent progress in understanding
the role of auxin and suggest future perspectives for auxin research.
article_processing_charge: No
citation:
ama: 'Zažímalová E, Petrášek J, Benková E, eds. Auxin and Its Role in Plant Development.
1st ed. Vienna: Springer Nature; 2014. doi:10.1007/978-3-7091-1526-8'
apa: 'Zažímalová, E., Petrášek, J., & Benková, E. (Eds.). (2014). Auxin and
Its Role in Plant Development (1st ed.). Vienna: Springer Nature. https://doi.org/10.1007/978-3-7091-1526-8'
chicago: 'Zažímalová, Eva, Jan Petrášek, and Eva Benková, eds. Auxin and Its
Role in Plant Development. 1st ed. Vienna: Springer Nature, 2014. https://doi.org/10.1007/978-3-7091-1526-8.'
ieee: 'E. Zažímalová, J. Petrášek, and E. Benková, Eds., Auxin and Its Role in
Plant Development, 1st ed. Vienna: Springer Nature, 2014.'
ista: 'Zažímalová E, Petrášek J, Benková E eds. 2014. Auxin and Its Role in Plant
Development 1st ed., Vienna: Springer Nature, 444p.'
mla: Zažímalová, Eva, et al., editors. Auxin and Its Role in Plant Development.
1st ed., Springer Nature, 2014, doi:10.1007/978-3-7091-1526-8.
short: E. Zažímalová, J. Petrášek, E. Benková, eds., Auxin and Its Role in Plant
Development, 1st ed., Springer Nature, Vienna, 2014.
date_created: 2022-03-03T11:52:44Z
date_published: 2014-04-01T00:00:00Z
date_updated: 2022-03-04T07:38:15Z
day: '01'
department:
- _id: EvBe
doi: 10.1007/978-3-7091-1526-8
edition: '1'
editor:
- first_name: Eva
full_name: Zažímalová, Eva
last_name: Zažímalová
- first_name: Jan
full_name: Petrášek, Jan
last_name: Petrášek
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
language:
- iso: eng
month: '04'
oa_version: None
page: '444'
place: Vienna
publication_identifier:
eisbn:
- '9783709115268'
isbn:
- '9783709115251'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Auxin and Its Role in Plant Development
type: book_editor
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2014'
...
---
_id: '10884'
abstract:
- lang: eng
text: "We revisit the parameterized model checking problem for token-passing systems
and specifications in indexed CTL ∗ \\X. Emerson and Namjoshi (1995, 2003) have
shown that parameterized model checking of indexed CTL ∗ \\X in uni-directional
token rings can be reduced to checking rings up to some cutoff size. Clarke et
al. (2004) have shown a similar result for general topologies and indexed LTL
\\X, provided processes cannot choose the directions for sending or receiving
the token.\r\nWe unify and substantially extend these results by systematically
exploring fragments of indexed CTL ∗ \\X with respect to general topologies.
For each fragment we establish whether a cutoff exists, and for some concrete
topologies, such as rings, cliques and stars, we infer small cutoffs. Finally,
we show that the problem becomes undecidable, and thus no cutoffs exist, if processes
are allowed to choose the directions in which they send or from which they receive
the token."
acknowledgement: "This work was supported by the Austrian Science Fund through grant
P23499-N23\r\nand through the RiSE network (S11403, S11405, S11406, S11407-N23);
ERC Starting Grant (279307: Graph Games); Vienna Science and Technology Fund (WWTF)\r\ngrants
PROSEED, ICT12-059, and VRG11-005."
alternative_title:
- LNCS
article_processing_charge: No
author:
- first_name: Benjamin
full_name: Aminof, Benjamin
id: 4A55BD00-F248-11E8-B48F-1D18A9856A87
last_name: Aminof
- first_name: Swen
full_name: Jacobs, Swen
last_name: Jacobs
- first_name: Ayrat
full_name: Khalimov, Ayrat
last_name: Khalimov
- first_name: Sasha
full_name: Rubin, Sasha
id: 2EC51194-F248-11E8-B48F-1D18A9856A87
last_name: Rubin
citation:
ama: 'Aminof B, Jacobs S, Khalimov A, Rubin S. Parameterized model checking of token-passing
systems. In: Verification, Model Checking, and Abstract Interpretation.
Vol 8318. Springer Nature; 2014:262-281. doi:10.1007/978-3-642-54013-4_15'
apa: 'Aminof, B., Jacobs, S., Khalimov, A., & Rubin, S. (2014). Parameterized
model checking of token-passing systems. In Verification, Model Checking, and
Abstract Interpretation (Vol. 8318, pp. 262–281). San Diego, CA, United States:
Springer Nature. https://doi.org/10.1007/978-3-642-54013-4_15'
chicago: Aminof, Benjamin, Swen Jacobs, Ayrat Khalimov, and Sasha Rubin. “Parameterized
Model Checking of Token-Passing Systems.” In Verification, Model Checking,
and Abstract Interpretation, 8318:262–81. Springer Nature, 2014. https://doi.org/10.1007/978-3-642-54013-4_15.
ieee: B. Aminof, S. Jacobs, A. Khalimov, and S. Rubin, “Parameterized model checking
of token-passing systems,” in Verification, Model Checking, and Abstract Interpretation,
San Diego, CA, United States, 2014, vol. 8318, pp. 262–281.
ista: 'Aminof B, Jacobs S, Khalimov A, Rubin S. 2014. Parameterized model checking
of token-passing systems. Verification, Model Checking, and Abstract Interpretation.
VMCAI: Verifcation, Model Checking, and Abstract Interpretation, LNCS, vol. 8318,
262–281.'
mla: Aminof, Benjamin, et al. “Parameterized Model Checking of Token-Passing Systems.”
Verification, Model Checking, and Abstract Interpretation, vol. 8318, Springer
Nature, 2014, pp. 262–81, doi:10.1007/978-3-642-54013-4_15.
short: B. Aminof, S. Jacobs, A. Khalimov, S. Rubin, in:, Verification, Model Checking,
and Abstract Interpretation, Springer Nature, 2014, pp. 262–281.
conference:
end_date: 2014-01-21
location: San Diego, CA, United States
name: 'VMCAI: Verifcation, Model Checking, and Abstract Interpretation'
start_date: 2014-01-19
date_created: 2022-03-18T13:01:22Z
date_published: 2014-01-30T00:00:00Z
date_updated: 2022-05-17T08:36:01Z
day: '30'
department:
- _id: KrCh
doi: 10.1007/978-3-642-54013-4_15
ec_funded: 1
external_id:
arxiv:
- '1311.4425'
intvolume: ' 8318'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: ' https://doi.org/10.48550/arXiv.1311.4425'
month: '01'
oa: 1
oa_version: Preprint
page: 262-281
project:
- _id: 2584A770-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P 23499-N23
name: Modern Graph Algorithmic Techniques in Formal Verification
- _id: 25863FF4-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: S11407
name: Game Theory
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '279307'
name: 'Quantitative Graph Games: Theory and Applications'
publication: Verification, Model Checking, and Abstract Interpretation
publication_identifier:
eisbn:
- '9783642540134'
eissn:
- 1611-3349
isbn:
- '9783642540127'
issn:
- 0302-9743
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Parameterized model checking of token-passing systems
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8318
year: '2014'
...
---
_id: '10893'
abstract:
- lang: eng
text: Saddle periodic orbits are an essential and stable part of the topological
skeleton of a 3D vector field. Nevertheless, there is currently no efficient algorithm
to robustly extract these features. In this chapter, we present a novel technique
to extract saddle periodic orbits. Exploiting the analytic properties of such
an orbit, we propose a scalar measure based on the finite-time Lyapunov exponent
(FTLE) that indicates its presence. Using persistent homology, we can then extract
the robust cycles of this field. These cycles thereby represent the saddle periodic
orbits of the given vector field. We discuss the different existing FTLE approximation
schemes regarding their applicability to this specific problem and propose an
adapted version of FTLE called Normalized Velocity Separation. Finally, we evaluate
our method using simple analytic vector field data.
acknowledgement: First, we thank the reviewers of this paper for their ideas and critical
comments. In addition, we thank Ronny Peikert and Filip Sadlo for a fruitful discussions.
This research is supported by the European Commission under the TOPOSYS project
FP7-ICT-318493-STREP, the European Social Fund (ESF App. No. 100098251), and the
European Science Foundation under the ACAT Research Network Program.
article_processing_charge: No
author:
- first_name: Jens
full_name: Kasten, Jens
last_name: Kasten
- first_name: Jan
full_name: Reininghaus, Jan
id: 4505473A-F248-11E8-B48F-1D18A9856A87
last_name: Reininghaus
- first_name: Wieland
full_name: Reich, Wieland
last_name: Reich
- first_name: Gerik
full_name: Scheuermann, Gerik
last_name: Scheuermann
citation:
ama: 'Kasten J, Reininghaus J, Reich W, Scheuermann G. Toward the extraction of
saddle periodic orbits. In: Bremer P-T, Hotz I, Pascucci V, Peikert R, eds. Topological
Methods in Data Analysis and Visualization III . Vol 1. Mathematics and Visualization.
Cham: Springer; 2014:55-69. doi:10.1007/978-3-319-04099-8_4'
apa: 'Kasten, J., Reininghaus, J., Reich, W., & Scheuermann, G. (2014). Toward
the extraction of saddle periodic orbits. In P.-T. Bremer, I. Hotz, V. Pascucci,
& R. Peikert (Eds.), Topological Methods in Data Analysis and Visualization
III (Vol. 1, pp. 55–69). Cham: Springer. https://doi.org/10.1007/978-3-319-04099-8_4'
chicago: 'Kasten, Jens, Jan Reininghaus, Wieland Reich, and Gerik Scheuermann. “Toward
the Extraction of Saddle Periodic Orbits.” In Topological Methods in Data Analysis
and Visualization III , edited by Peer-Timo Bremer, Ingrid Hotz, Valerio Pascucci,
and Ronald Peikert, 1:55–69. Mathematics and Visualization. Cham: Springer, 2014.
https://doi.org/10.1007/978-3-319-04099-8_4.'
ieee: 'J. Kasten, J. Reininghaus, W. Reich, and G. Scheuermann, “Toward the extraction
of saddle periodic orbits,” in Topological Methods in Data Analysis and Visualization
III , vol. 1, P.-T. Bremer, I. Hotz, V. Pascucci, and R. Peikert, Eds. Cham:
Springer, 2014, pp. 55–69.'
ista: 'Kasten J, Reininghaus J, Reich W, Scheuermann G. 2014.Toward the extraction
of saddle periodic orbits. In: Topological Methods in Data Analysis and Visualization
III . vol. 1, 55–69.'
mla: Kasten, Jens, et al. “Toward the Extraction of Saddle Periodic Orbits.” Topological
Methods in Data Analysis and Visualization III , edited by Peer-Timo Bremer
et al., vol. 1, Springer, 2014, pp. 55–69, doi:10.1007/978-3-319-04099-8_4.
short: J. Kasten, J. Reininghaus, W. Reich, G. Scheuermann, in:, P.-T. Bremer, I.
Hotz, V. Pascucci, R. Peikert (Eds.), Topological Methods in Data Analysis and
Visualization III , Springer, Cham, 2014, pp. 55–69.
date_created: 2022-03-21T07:11:23Z
date_published: 2014-03-19T00:00:00Z
date_updated: 2022-06-21T12:01:47Z
day: '19'
department:
- _id: HeEd
doi: 10.1007/978-3-319-04099-8_4
ec_funded: 1
editor:
- first_name: Peer-Timo
full_name: Bremer, Peer-Timo
last_name: Bremer
- first_name: Ingrid
full_name: Hotz, Ingrid
last_name: Hotz
- first_name: Valerio
full_name: Pascucci, Valerio
last_name: Pascucci
- first_name: Ronald
full_name: Peikert, Ronald
last_name: Peikert
intvolume: ' 1'
language:
- iso: eng
month: '03'
oa_version: None
page: 55-69
place: Cham
project:
- _id: 255D761E-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '318493'
name: Topological Complex Systems
publication: 'Topological Methods in Data Analysis and Visualization III '
publication_identifier:
eisbn:
- '9783319040998'
eissn:
- 2197-666X
isbn:
- '9783319040981'
issn:
- 1612-3786
publication_status: published
publisher: Springer
quality_controlled: '1'
scopus_import: '1'
series_title: Mathematics and Visualization
status: public
title: Toward the extraction of saddle periodic orbits
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2014'
...