---
_id: '3724'
abstract:
- lang: eng
text: 'Small photochromic molecules are widespread in nature and serve as switches
for a plethora of light-controlled processes. In a typical photoreceptor, the
different geometries and polarities of the photochrome isomers are tightly coupled
to functionally relevant conformational changes in the proteins. The past decade
has seen extensive efforts to mimic nature and create proteins controlled by synthetic
photochromes in the laboratory. Here, we discuss the role of molecular modeling
to gain a structural understanding of photochromes and to design light-controlled
peptides and proteins. We address several fundamental questions: What are the
molecular structures of photochromes, particularly for metastable isomers that
cannot be addressed experimentally? How are the structures of bistable photoisomers
coupled to the conformational states of peptides and proteins? Can we design light-controlled
proteins rapidly and reliably? After an introduction to the principles of molecular
modeling, we answer these questions by examining systems that range from the size
of isolated photochromes, to that of peptides and large cell surface receptors,
each from its unique computational perspective.'
author:
- first_name: Harald L
full_name: Harald Janovjak
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
- first_name: Ehud
full_name: Isacoff, Ehud Y
last_name: Isacoff
citation:
ama: 'Janovjak HL, Isacoff E. Structure-based design of light-controlled proteins.
In: Photosensitive Molecules for the Control of Biological Function. Vol
55. Springer; 2011:233-266. doi:10.1007/978-1-61779-031-7_13'
apa: Janovjak, H. L., & Isacoff, E. (2011). Structure-based design of light-controlled
proteins. In Photosensitive Molecules for the Control of Biological Function
(Vol. 55, pp. 233–266). Springer. https://doi.org/10.1007/978-1-61779-031-7_13
chicago: Janovjak, Harald L, and Ehud Isacoff. “Structure-Based Design of Light-Controlled
Proteins.” In Photosensitive Molecules for the Control of Biological Function,
55:233–66. Springer, 2011. https://doi.org/10.1007/978-1-61779-031-7_13.
ieee: H. L. Janovjak and E. Isacoff, “Structure-based design of light-controlled
proteins,” in Photosensitive Molecules for the Control of Biological Function,
vol. 55, Springer, 2011, pp. 233–266.
ista: 'Janovjak HL, Isacoff E. 2011.Structure-based design of light-controlled proteins.
In: Photosensitive Molecules for the Control of Biological Function. vol. 55,
233–266.'
mla: Janovjak, Harald L., and Ehud Isacoff. “Structure-Based Design of Light-Controlled
Proteins.” Photosensitive Molecules for the Control of Biological Function,
vol. 55, Springer, 2011, pp. 233–66, doi:10.1007/978-1-61779-031-7_13.
short: H.L. Janovjak, E. Isacoff, in:, Photosensitive Molecules for the Control
of Biological Function, Springer, 2011, pp. 233–266.
date_created: 2018-12-11T12:04:49Z
date_published: 2011-03-16T00:00:00Z
date_updated: 2021-01-12T07:51:45Z
day: '16'
doi: 10.1007/978-1-61779-031-7_13
extern: 1
intvolume: ' 55'
month: '03'
page: 233 - 266
publication: Photosensitive Molecules for the Control of Biological Function
publication_status: published
publisher: Springer
publist_id: '2504'
quality_controlled: 0
status: public
title: Structure-based design of light-controlled proteins
type: book_chapter
volume: 55
year: '2011'
...
---
_id: '3770'
abstract:
- lang: eng
text: 'The pink dolphin (Inia geoffrensis) is widely distributed along the Amazon
and Orinoco basins, covering an area of approximately 7 million km2. Previous
morphological and genetic studies have proposed the existence of at least two
evolutionary significant units: one distributed across the Orinoco and Amazon
basins and another confined to the Bolivian Amazon. The presence of barriers in
the riverine environment has been suggested to play a significant role in shaping
present-day patterns of ecological and genetic structure for this species. In
the present study, we examined the phylogeographic structure, lineage divergence
time and historical demography using mitochondrial (mt)DNA sequences in different
pink dolphin populations distributed in large and small spatial scales, including
two neighbouring Brazilian Amazon populations. mtDNA control region (CR) analysis
revealed that the Brazilian haplotypes occupy an intermediate position compared
to three previously studied geographic locations: the Colombian Amazon, the Colombian
Orinoco, and the Bolivian Amazon. On a local scale, we have identified a pattern
of maternal isolation between two neighbouring populations from Brazil. Six mtDNA
CR haplotypes were identified in Brazil with no sharing between the two populations,
as well as specific cytochrome b (cyt b) haplotypes identified in each locality.
In addition, we analyzed autosomal microsatellites to investigate male-mediated
gene flow and demographic changes within the study area in Brazil. Data analysis
of 14 microsatellite loci failed to detect significant population subdivision,
suggesting that male-mediated gene flow may maintain homogeneity between these
two locations. Moreover, both mtDNA and microsatellite data indicate a major demographic
collapse within Brazil in the late Pleistocene. Bayesian skyline plots (BSP) of
mtDNA data revealed a stable population for Colombian and Brazilian Amazon lineages
through time, whereas a population decline was demonstrated in the Colombian Orinoco
lineage. Moreover, BSP and Tajima''s D and Fu''s Fs tests revealed a recent population
expansion exclusively in the Bolivian sample. Finally, we estimated that the diversification
of the Inia sp. lineage began in the Late Pliocene (approximately 3.1 Mya) and
continued throughout the Pleistocene.'
article_processing_charge: No
author:
- first_name: Claudia
full_name: Hollatz, Claudia
last_name: Hollatz
- first_name: Sibelle
full_name: Vilaça, Sibelle
last_name: Vilaça
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
- first_name: Míriam
full_name: Marmontel, Míriam
last_name: Marmontel
- first_name: Cyndi
full_name: Baker, Cyndi
last_name: Baker
- first_name: Fabrício
full_name: Santos, Fabrício
last_name: Santos
citation:
ama: Hollatz C, Vilaça S, Fernandes Redondo RA, Marmontel M, Baker C, Santos F.
The Amazon River system as an ecological barrier driving genetic differentiation
of the pink dolphin (Inia geoffrensis). Biological Journal of the Linnean Society.
2011;102(4):812-827. doi:10.1111/j.1095-8312.2011.01616.x
apa: Hollatz, C., Vilaça, S., Fernandes Redondo, R. A., Marmontel, M., Baker, C.,
& Santos, F. (2011). The Amazon River system as an ecological barrier driving
genetic differentiation of the pink dolphin (Inia geoffrensis). Biological
Journal of the Linnean Society. Wiley. https://doi.org/10.1111/j.1095-8312.2011.01616.x
chicago: Hollatz, Claudia, Sibelle Vilaça, Rodrigo A Fernandes Redondo, Míriam Marmontel,
Cyndi Baker, and Fabrício Santos. “The Amazon River System as an Ecological Barrier
Driving Genetic Differentiation of the Pink Dolphin (Inia Geoffrensis).” Biological
Journal of the Linnean Society. Wiley, 2011. https://doi.org/10.1111/j.1095-8312.2011.01616.x.
ieee: C. Hollatz, S. Vilaça, R. A. Fernandes Redondo, M. Marmontel, C. Baker, and
F. Santos, “The Amazon River system as an ecological barrier driving genetic differentiation
of the pink dolphin (Inia geoffrensis),” Biological Journal of the Linnean
Society, vol. 102, no. 4. Wiley, pp. 812–827, 2011.
ista: Hollatz C, Vilaça S, Fernandes Redondo RA, Marmontel M, Baker C, Santos F.
2011. The Amazon River system as an ecological barrier driving genetic differentiation
of the pink dolphin (Inia geoffrensis). Biological Journal of the Linnean Society.
102(4), 812–827.
mla: Hollatz, Claudia, et al. “The Amazon River System as an Ecological Barrier
Driving Genetic Differentiation of the Pink Dolphin (Inia Geoffrensis).” Biological
Journal of the Linnean Society, vol. 102, no. 4, Wiley, 2011, pp. 812–27,
doi:10.1111/j.1095-8312.2011.01616.x.
short: C. Hollatz, S. Vilaça, R.A. Fernandes Redondo, M. Marmontel, C. Baker, F.
Santos, Biological Journal of the Linnean Society 102 (2011) 812–827.
date_created: 2018-12-11T12:05:04Z
date_published: 2011-04-01T00:00:00Z
date_updated: 2021-01-12T07:52:05Z
day: '01'
doi: 10.1111/j.1095-8312.2011.01616.x
extern: '1'
intvolume: ' 102'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 812 - 827
publication: Biological Journal of the Linnean Society
publication_status: published
publisher: Wiley
publist_id: '2457'
status: public
title: The Amazon River system as an ecological barrier driving genetic differentiation
of the pink dolphin (Inia geoffrensis)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 102
year: '2011'
...
---
_id: '3771'
abstract:
- lang: eng
text: The small-sized frugivorous bat Carollia perspicillata is an understory specialist
and occurs in a wide range of lowland habitats, tending to be more common in tropical
dry or moist forests of South and Central America. Its sister species, Carollia
brevicauda, occurs almost exclusively in the Amazon rainforest. A recent phylogeographic
study proposed a hypothesis of origin and subsequent diversification for C. perspicillata
along the Atlantic coastal forest of Brazil. Additionally, it also found two allopatric
clades for C. brevicauda separated by the Amazon Basin. We used cytochrome b gene
sequences and a more extensive sampling to test hypotheses related to the origin
and diversification of C. perspicillata plus C. brevicauda clade in South America.
The results obtained indicate that there are two sympatric evolutionary lineages
within each species. In C. perspicillata, one lineage is limited to the Southern
Atlantic Forest, whereas the other is widely distributed. Coalescent analysis
points to a simultaneous origin for C. perspicillata and C. brevicauda, although
no place for the diversification of each species can be firmly suggested. The
phylogeographic pattern shown by C. perspicillata is also congruent with the Pleistocene
refugia hypothesis as a likely vicariant phenomenon shaping the present distribution
of its intraspecific lineages.
author:
- first_name: Ana
full_name: Pavan, Ana
last_name: Pavan
- first_name: Felipe
full_name: Martins, Felipe
last_name: Martins
- first_name: Fabrício
full_name: Santos, Fabrício
last_name: Santos
- first_name: Albert
full_name: Ditchfield, Albert
last_name: Ditchfield
- first_name: Rodrigo A
full_name: Fernandes Redondo, Rodrigo A
id: 409D5C96-F248-11E8-B48F-1D18A9856A87
last_name: Fernandes Redondo
orcid: 0000-0002-5837-2793
citation:
ama: 'Pavan A, Martins F, Santos F, Ditchfield A, Fernandes Redondo RA. Patterns
of diversification in two species of short-tailed bats (Carollia Gray, 1838):
the effects of historical fragmentation of Brazilian rainforests. Biological
Journal of the Linnean Society. 2011;102(3):527-539. doi:10.1111/j.1095-8312.2010.01601.x'
apa: 'Pavan, A., Martins, F., Santos, F., Ditchfield, A., & Fernandes Redondo,
R. A. (2011). Patterns of diversification in two species of short-tailed bats
(Carollia Gray, 1838): the effects of historical fragmentation of Brazilian rainforests.
Biological Journal of the Linnean Society. Wiley-Blackwell. https://doi.org/10.1111/j.1095-8312.2010.01601.x'
chicago: 'Pavan, Ana, Felipe Martins, Fabrício Santos, Albert Ditchfield, and Rodrigo
A Fernandes Redondo. “Patterns of Diversification in Two Species of Short-Tailed
Bats (Carollia Gray, 1838): The Effects of Historical Fragmentation of Brazilian
Rainforests.” Biological Journal of the Linnean Society. Wiley-Blackwell,
2011. https://doi.org/10.1111/j.1095-8312.2010.01601.x.'
ieee: 'A. Pavan, F. Martins, F. Santos, A. Ditchfield, and R. A. Fernandes Redondo,
“Patterns of diversification in two species of short-tailed bats (Carollia Gray,
1838): the effects of historical fragmentation of Brazilian rainforests.,” Biological
Journal of the Linnean Society, vol. 102, no. 3. Wiley-Blackwell, pp. 527–539,
2011.'
ista: 'Pavan A, Martins F, Santos F, Ditchfield A, Fernandes Redondo RA. 2011. Patterns
of diversification in two species of short-tailed bats (Carollia Gray, 1838):
the effects of historical fragmentation of Brazilian rainforests. Biological Journal
of the Linnean Society. 102(3), 527–539.'
mla: 'Pavan, Ana, et al. “Patterns of Diversification in Two Species of Short-Tailed
Bats (Carollia Gray, 1838): The Effects of Historical Fragmentation of Brazilian
Rainforests.” Biological Journal of the Linnean Society, vol. 102, no.
3, Wiley-Blackwell, 2011, pp. 527–39, doi:10.1111/j.1095-8312.2010.01601.x.'
short: A. Pavan, F. Martins, F. Santos, A. Ditchfield, R.A. Fernandes Redondo, Biological
Journal of the Linnean Society 102 (2011) 527–539.
date_created: 2018-12-11T12:05:05Z
date_published: 2011-02-10T00:00:00Z
date_updated: 2021-01-12T07:52:05Z
day: '10'
department:
- _id: FyKo
doi: 10.1111/j.1095-8312.2010.01601.x
intvolume: ' 102'
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 527 - 539
publication: Biological Journal of the Linnean Society
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2456'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Patterns of diversification in two species of short-tailed bats (Carollia
Gray, 1838): the effects of historical fragmentation of Brazilian rainforests.'
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 102
year: '2011'
...
---
_id: '3778'
author:
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Barton NH. Estimating linkage disequilibria. Heredity. 2011;106(2):205-206.
doi:10.1038/hdy.2010.67
apa: Barton, N. H. (2011). Estimating linkage disequilibria. Heredity. Nature
Publishing Group. https://doi.org/10.1038/hdy.2010.67
chicago: Barton, Nicholas H. “Estimating Linkage Disequilibria.” Heredity.
Nature Publishing Group, 2011. https://doi.org/10.1038/hdy.2010.67.
ieee: N. H. Barton, “Estimating linkage disequilibria,” Heredity, vol. 106,
no. 2. Nature Publishing Group, pp. 205–206, 2011.
ista: Barton NH. 2011. Estimating linkage disequilibria. Heredity. 106(2), 205–206.
mla: Barton, Nicholas H. “Estimating Linkage Disequilibria.” Heredity, vol.
106, no. 2, Nature Publishing Group, 2011, pp. 205–06, doi:10.1038/hdy.2010.67.
short: N.H. Barton, Heredity 106 (2011) 205–206.
date_created: 2018-12-11T12:05:07Z
date_published: 2011-02-01T00:00:00Z
date_updated: 2021-01-12T07:52:08Z
day: '01'
department:
- _id: NiBa
doi: 10.1038/hdy.2010.67
external_id:
pmid:
- '20502479'
intvolume: ' 106'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183869/
month: '02'
oa: 1
oa_version: Submitted Version
page: 205 - 206
pmid: 1
publication: Heredity
publication_status: published
publisher: Nature Publishing Group
publist_id: '2449'
scopus_import: 1
status: public
title: Estimating linkage disequilibria
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 106
year: '2011'
...
---
_id: '3791'
abstract:
- lang: eng
text: During the development of multicellular organisms, cell fate specification
is followed by the sorting of different cell types into distinct domains from
where the different tissues and organs are formed. Cell sorting involves both
the segregation of a mixed population of cells with different fates and properties
into distinct domains, and the active maintenance of their segregated state. Because
of its biological importance and apparent resemblance to fluid segregation in
physics, cell sorting was extensively studied by both biologists and physicists
over the last decades. Different theories were developed that try to explain cell
sorting on the basis of the physical properties of the constituent cells. However,
only recently the molecular and cellular mechanisms that control the physical
properties driving cell sorting, have begun to be unraveled. In this review, we
will provide an overview of different cell-sorting processes in development and
discuss how these processes can be explained by the different sorting theories,
and how these theories in turn can be connected to the molecular and cellular
mechanisms driving these processes.
alternative_title:
- Current Topics in Developmental Biology
article_processing_charge: No
author:
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- 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: 'Krens G, Heisenberg C-PJ. Cell sorting in development. In: Labouesse M, ed.
Forces and Tension in Development. Vol 95. Elsevier; 2011:189-213. doi:10.1016/B978-0-12-385065-2.00006-2'
apa: Krens, G., & Heisenberg, C.-P. J. (2011). Cell sorting in development.
In M. Labouesse (Ed.), Forces and Tension in Development (Vol. 95, pp.
189–213). Elsevier. https://doi.org/10.1016/B978-0-12-385065-2.00006-2
chicago: Krens, Gabriel, and Carl-Philipp J Heisenberg. “Cell Sorting in Development.”
In Forces and Tension in Development, edited by Michel Labouesse, 95:189–213.
Elsevier, 2011. https://doi.org/10.1016/B978-0-12-385065-2.00006-2.
ieee: G. Krens and C.-P. J. Heisenberg, “Cell sorting in development,” in Forces
and Tension in Development, vol. 95, M. Labouesse, Ed. Elsevier, 2011, pp.
189–213.
ista: 'Krens G, Heisenberg C-PJ. 2011.Cell sorting in development. In: Forces and
Tension in Development. Current Topics in Developmental Biology, vol. 95, 189–213.'
mla: Krens, Gabriel, and Carl-Philipp J. Heisenberg. “Cell Sorting in Development.”
Forces and Tension in Development, edited by Michel Labouesse, vol. 95,
Elsevier, 2011, pp. 189–213, doi:10.1016/B978-0-12-385065-2.00006-2.
short: G. Krens, C.-P.J. Heisenberg, in:, M. Labouesse (Ed.), Forces and Tension
in Development, Elsevier, 2011, pp. 189–213.
date_created: 2018-12-11T12:05:11Z
date_published: 2011-01-01T00:00:00Z
date_updated: 2021-01-12T07:52:13Z
day: '01'
department:
- _id: CaHe
doi: 10.1016/B978-0-12-385065-2.00006-2
editor:
- first_name: Michel
full_name: Labouesse, Michel
last_name: Labouesse
intvolume: ' 95'
language:
- iso: eng
month: '01'
oa_version: None
page: 189 - 213
publication: Forces and Tension in Development
publication_status: published
publisher: Elsevier
publist_id: '2436'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cell sorting in development
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 95
year: '2011'
...
---
_id: '3364'
abstract:
- lang: eng
text: Molecular noise, which arises from the randomness of the discrete events in
the cell, significantly influences fundamental biological processes. Discrete-state
continuous-time stochastic models (CTMC) can be used to describe such effects,
but the calculation of the probabilities of certain events is computationally
expensive. We present a comparison of two analysis approaches for CTMC. On one
hand, we estimate the probabilities of interest using repeated Gillespie simulation
and determine the statistical accuracy that we obtain. On the other hand, we apply
a numerical reachability analysis that approximates the probability distributions
of the system at several time instances. We use examples of cellular processes
to demonstrate the superiority of the reachability analysis if accurate results
are required.
author:
- first_name: Frédéric
full_name: Didier, Frédéric
last_name: Didier
- first_name: Thomas A
full_name: Henzinger, Thomas A
id: 40876CD8-F248-11E8-B48F-1D18A9856A87
last_name: Henzinger
orcid: 0000−0002−2985−7724
- first_name: Maria
full_name: Mateescu, Maria
last_name: Mateescu
- first_name: Verena
full_name: Wolf, Verena
last_name: Wolf
citation:
ama: Didier F, Henzinger TA, Mateescu M, Wolf V. Approximation of event probabilities
in noisy cellular processes. Theoretical Computer Science. 2011;412(21):2128-2141.
doi:10.1016/j.tcs.2010.10.022
apa: Didier, F., Henzinger, T. A., Mateescu, M., & Wolf, V. (2011). Approximation
of event probabilities in noisy cellular processes. Theoretical Computer Science.
Elsevier. https://doi.org/10.1016/j.tcs.2010.10.022
chicago: Didier, Frédéric, Thomas A Henzinger, Maria Mateescu, and Verena Wolf.
“Approximation of Event Probabilities in Noisy Cellular Processes.” Theoretical
Computer Science. Elsevier, 2011. https://doi.org/10.1016/j.tcs.2010.10.022.
ieee: F. Didier, T. A. Henzinger, M. Mateescu, and V. Wolf, “Approximation of event
probabilities in noisy cellular processes,” Theoretical Computer Science,
vol. 412, no. 21. Elsevier, pp. 2128–2141, 2011.
ista: Didier F, Henzinger TA, Mateescu M, Wolf V. 2011. Approximation of event probabilities
in noisy cellular processes. Theoretical Computer Science. 412(21), 2128–2141.
mla: Didier, Frédéric, et al. “Approximation of Event Probabilities in Noisy Cellular
Processes.” Theoretical Computer Science, vol. 412, no. 21, Elsevier, 2011,
pp. 2128–41, doi:10.1016/j.tcs.2010.10.022.
short: F. Didier, T.A. Henzinger, M. Mateescu, V. Wolf, Theoretical Computer Science
412 (2011) 2128–2141.
date_created: 2018-12-11T12:02:55Z
date_published: 2011-05-06T00:00:00Z
date_updated: 2023-02-23T12:15:28Z
day: '06'
ddc:
- '000'
- '004'
department:
- _id: ToHe
doi: 10.1016/j.tcs.2010.10.022
file:
- access_level: open_access
checksum: e5503e25ce020d753e06b3431e16841e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:09Z
date_updated: 2020-07-14T12:46:10Z
file_id: '4862'
file_name: IST-2012-79-v1+1_Approximation_of_event_probabilities_in_noisy_cellular_processes.pdf
file_size: 230503
relation: main_file
file_date_updated: 2020-07-14T12:46:10Z
has_accepted_license: '1'
intvolume: ' 412'
issue: '21'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Submitted Version
page: 2128 - 2141
publication: Theoretical Computer Science
publication_status: published
publisher: Elsevier
publist_id: '3249'
pubrep_id: '79'
quality_controlled: '1'
related_material:
record:
- id: '4535'
relation: earlier_version
status: public
scopus_import: 1
status: public
title: Approximation of event probabilities in noisy cellular processes
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 412
year: '2011'
...
---
_id: '469'
abstract:
- lang: eng
text: 'Spontaneous release of glutamate is important for maintaining synaptic strength
and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis
remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates
Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently
is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular
Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report
that external Ca2+ triggers spontaneous glutamate release more weakly than evoked
release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous
release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases
in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement
of spontaneous release by extracellular calcium is insensitive to chelation of
intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR),
a G-protein-coupled receptor present in nerve terminals, by several specific agonists
increased spontaneous glutamate release. The frequency of spontaneous synaptic
transmission was decreased in CaSR mutant neurons. The concentration-effect relationship
for extracellular calcium regulation of spontaneous release was well described
by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these
results indicate that extracellular Ca2+ does not trigger spontaneous glutamate
release by simply increasing calcium influx but stimulates CaSR and thereby promotes
resting spontaneous glutamate release. '
author:
- first_name: Nicholas
full_name: Vyleta, Nicholas
id: 36C4978E-F248-11E8-B48F-1D18A9856A87
last_name: Vyleta
- first_name: Stephen
full_name: Smith, Stephen
last_name: Smith
citation:
ama: Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium
influx and tonically activated by the calcium-sensing receptor. European Journal
of Neuroscience. 2011;31(12):4593-4606. doi:10.1523/JNEUROSCI.6398-10.2011
apa: Vyleta, N., & Smith, S. (2011). Spontaneous glutamate release is independent
of calcium influx and tonically activated by the calcium-sensing receptor. European
Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1523/JNEUROSCI.6398-10.2011
chicago: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is
Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.”
European Journal of Neuroscience. Wiley-Blackwell, 2011. https://doi.org/10.1523/JNEUROSCI.6398-10.2011.
ieee: N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium
influx and tonically activated by the calcium-sensing receptor,” European Journal
of Neuroscience, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011.
ista: Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium
influx and tonically activated by the calcium-sensing receptor. European Journal
of Neuroscience. 31(12), 4593–4606.
mla: Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent
of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” European
Journal of Neuroscience, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606,
doi:10.1523/JNEUROSCI.6398-10.2011.
short: N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606.
date_created: 2018-12-11T11:46:39Z
date_published: 2011-03-23T00:00:00Z
date_updated: 2021-01-12T08:00:49Z
day: '23'
department:
- _id: PeJo
doi: 10.1523/JNEUROSCI.6398-10.2011
intvolume: ' 31'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/
month: '03'
oa: 1
oa_version: Submitted Version
page: 4593 - 4606
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7353'
quality_controlled: '1'
scopus_import: 1
status: public
title: Spontaneous glutamate release is independent of calcium influx and tonically
activated by the calcium-sensing receptor
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2011'
...
---
_id: '490'
abstract:
- lang: eng
text: 'BioSig is an open source software library for biomedical signal processing.
The aim of the BioSig project is to foster research in biomedical signal processing
by providing free and open source software tools for many different application
areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer
interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research.
Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram
(ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG),
or respiration signals is a very relevant element of the BioSig project. Specifically,
BioSig provides solutions for data acquisition, artifact processing, quality control,
feature extraction, classification, modeling, and data visualization, to name
a few. In this paper, we highlight several methods to help students and researchers
to work more efficiently with biomedical signals. '
article_number: '935364'
author:
- first_name: Alois
full_name: Schlögl, Alois
id: 45BF87EE-F248-11E8-B48F-1D18A9856A87
last_name: Schlögl
orcid: 0000-0002-5621-8100
- first_name: Carmen
full_name: Vidaurre, Carmen
last_name: Vidaurre
- first_name: Tilmann
full_name: Sander, Tilmann
last_name: Sander
citation:
ama: 'Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software
library for biomedical signal processing. Computational Intelligence and Neuroscience.
2011;2011. doi:10.1155/2011/935364'
apa: 'Schlögl, A., Vidaurre, C., & Sander, T. (2011). BioSig: The free and open
source software library for biomedical signal processing. Computational Intelligence
and Neuroscience. Hindawi Publishing Corporation. https://doi.org/10.1155/2011/935364'
chicago: 'Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free
and Open Source Software Library for Biomedical Signal Processing.” Computational
Intelligence and Neuroscience. Hindawi Publishing Corporation, 2011. https://doi.org/10.1155/2011/935364.'
ieee: 'A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source
software library for biomedical signal processing,” Computational Intelligence
and Neuroscience, vol. 2011. Hindawi Publishing Corporation, 2011.'
ista: 'Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software
library for biomedical signal processing. Computational Intelligence and Neuroscience.
2011, 935364.'
mla: 'Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library
for Biomedical Signal Processing.” Computational Intelligence and Neuroscience,
vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:10.1155/2011/935364.'
short: A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience
2011 (2011).
date_created: 2018-12-11T11:46:45Z
date_published: 2011-01-01T00:00:00Z
date_updated: 2021-01-12T08:01:02Z
day: '01'
ddc:
- '005'
department:
- _id: ScienComp
- _id: PeJo
doi: 10.1155/2011/935364
file:
- access_level: open_access
checksum: 8263bbf255171f2054f43f3db5f53b6e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:07:44Z
date_updated: 2020-07-14T12:46:35Z
file_id: '4642'
file_name: IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf
file_size: 2863551
relation: main_file
file_date_updated: 2020-07-14T12:46:35Z
has_accepted_license: '1'
intvolume: ' 2011'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Computational Intelligence and Neuroscience
publication_status: published
publisher: Hindawi Publishing Corporation
publist_id: '7330'
pubrep_id: '947'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'BioSig: The free and open source software library for biomedical signal processing'
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: 2011
year: '2011'
...
---
_id: '491'
abstract:
- lang: eng
text: In their search for antigens, lymphocytes continuously shuttle among blood
vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes
into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization
of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled
receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization,
a process that decreases their signaling output after previous exposure to high
ligand concentration. Such desensitization can explain why lymphocytes do not
take an intermediate position between two signals but rather oscillate between
them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase
2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high
vascular S1P concentrations, thereby reducing responsiveness to the chemokine
signal and trapping the cells in the vascular compartment. The desensitization
kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature
and lymphatic tissue, although the positional information in both compartments
is static.
article_number: pe43
author:
- 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
citation:
ama: Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science
Signaling. 2011;4(198). doi:10.1126/scisignal.2002617
apa: Eichner, A., & Sixt, M. K. (2011). Setting the clock for recirculating
lymphocytes. Science Signaling. American Association for the Advancement
of Science. https://doi.org/10.1126/scisignal.2002617
chicago: Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling. American Association for the Advancement
of Science, 2011. https://doi.org/10.1126/scisignal.2002617.
ieee: A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,”
Science Signaling, vol. 4, no. 198. American Association for the Advancement
of Science, 2011.
ista: Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes.
Science Signaling. 4(198), pe43.
mla: Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling, vol. 4, no. 198, pe43, American Association
for the Advancement of Science, 2011, doi:10.1126/scisignal.2002617.
short: A. Eichner, M.K. Sixt, Science Signaling 4 (2011).
date_created: 2018-12-11T11:46:46Z
date_published: 2011-11-08T00:00:00Z
date_updated: 2021-01-12T08:01:02Z
day: '08'
department:
- _id: MiSi
doi: 10.1126/scisignal.2002617
intvolume: ' 4'
issue: '198'
language:
- iso: eng
month: '11'
oa_version: None
publication: Science Signaling
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7329'
quality_controlled: '1'
scopus_import: 1
status: public
title: Setting the clock for recirculating lymphocytes
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2011'
...
---
_id: '518'
abstract:
- lang: eng
text: Cancer stem cells or cancer initiating cells are believed to contribute to
cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with
fundamental roles in gene regulation. The role of miRNAs in cancer stem cells
is only poorly understood. Here, we report miRNA expression profiles of glioblastoma
stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred
to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore,
inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates
cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is
a putative transcription factor, which induces the expression of the anti-proliferative
cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9
* and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation
and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour
suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival.
Our findings could provide a basis for novel strategies of glioblastoma therapy.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Schraivogel, Daniel
last_name: Schraivogel
- first_name: Lasse
full_name: Weinmann, Lasse
last_name: Weinmann
- first_name: Dagmar
full_name: Beier, Dagmar
last_name: Beier
- first_name: Ghazaleh
full_name: Tabatabai, Ghazaleh
last_name: Tabatabai
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jia
full_name: Zhu, Jia
last_name: Zhu
- first_name: Martina
full_name: Anton, Martina
last_name: Anton
- 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: Michael
full_name: Weller, Michael
last_name: Weller
- first_name: Christoph
full_name: Beier, Christoph
last_name: Beier
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 2011;30(20):4309-4322.
doi:10.1038/emboj.2011.301
apa: Schraivogel, D., Weinmann, L., Beier, D., Tabatabai, G., Eichner, A., Zhu,
J., … Meister, G. (2011). CAMTA1 is a novel tumour suppressor regulated by miR-9/9
* in glioblastoma stem cells. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2011.301
chicago: Schraivogel, Daniel, Lasse Weinmann, Dagmar Beier, Ghazaleh Tabatabai,
Alexander Eichner, Jia Zhu, Martina Anton, et al. “CAMTA1 Is a Novel Tumour Suppressor
Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal. Wiley-Blackwell,
2011. https://doi.org/10.1038/emboj.2011.301.
ieee: D. Schraivogel et al., “CAMTA1 is a novel tumour suppressor regulated
by miR-9/9 * in glioblastoma stem cells,” EMBO Journal, vol. 30, no. 20.
Wiley-Blackwell, pp. 4309–4322, 2011.
ista: Schraivogel D, Weinmann L, Beier D, Tabatabai G, Eichner A, Zhu J, Anton M,
Sixt MK, Weller M, Beier C, Meister G. 2011. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 30(20), 4309–4322.
mla: Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated
by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal, vol. 30, no. 20,
Wiley-Blackwell, 2011, pp. 4309–22, doi:10.1038/emboj.2011.301.
short: D. Schraivogel, L. Weinmann, D. Beier, G. Tabatabai, A. Eichner, J. Zhu,
M. Anton, M.K. Sixt, M. Weller, C. Beier, G. Meister, EMBO Journal 30 (2011) 4309–4322.
date_created: 2018-12-11T11:46:55Z
date_published: 2011-10-19T00:00:00Z
date_updated: 2021-01-12T08:01:19Z
day: '19'
department:
- _id: MiSi
doi: 10.1038/emboj.2011.301
external_id:
pmid:
- '21857646'
intvolume: ' 30'
issue: '20'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/
month: '10'
oa: 1
oa_version: Submitted Version
page: 4309 - 4322
pmid: 1
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7301'
quality_controlled: '1'
scopus_import: 1
status: public
title: CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma
stem cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2011'
...