--- _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' ...