[{"title":"The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection","oa":1,"publication_identifier":{"issn":["0021-9738"]},"pmid":1,"type":"journal_article","doi":"10.1172/JCI80631","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/"}],"scopus_import":"1","publication":"The Journal of Clinical Investigation","author":[{"first_name":"Florian","last_name":"Ebner","full_name":"Ebner, Florian"},{"first_name":"Vitaly","full_name":"Sedlyarov, Vitaly","last_name":"Sedlyarov"},{"full_name":"Tasciyan, Saren","last_name":"Tasciyan","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","first_name":"Saren","orcid":"0000-0003-1671-393X"},{"first_name":"Masa","last_name":"Ivin","full_name":"Ivin, Masa"},{"first_name":"Franz","full_name":"Kratochvill, Franz","last_name":"Kratochvill"},{"first_name":"Nina","full_name":"Gratz, Nina","last_name":"Gratz"},{"first_name":"Lukas","full_name":"Kenner, Lukas","last_name":"Kenner"},{"last_name":"Villunger","full_name":"Villunger, Andreas","first_name":"Andreas"},{"orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kovarik","full_name":"Kovarik, Pavel","first_name":"Pavel"}],"article_processing_charge":"No","date_created":"2018-12-11T11:47:53Z","project":[{"grant_number":"T00817-B21","_id":"25985A36-B435-11E9-9278-68D0E5697425","name":"The biochemical basis of PAR polarization","call_identifier":"FWF"},{"grant_number":"P27201-B22","name":"Revealing the mechanisms underlying drug interactions","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"quality_controlled":"1","related_material":{"record":[{"relation":"dissertation_contains","id":"12401","status":"public"}]},"page":"2051 - 2065","publication_status":"published","volume":127,"department":[{"_id":"MiSi"}],"language":[{"iso":"eng"}],"month":"06","date_published":"2017-06-01T00:00:00Z","fulldoi":"https://doi.org/10.1172/JCI80631","publist_id":"7038","date_updated":"2026-10-26T23:30:12Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","abstract":[{"text":"Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections.","lang":"eng"}],"issue":"6","external_id":{"isi":["000402620800008"],"pmid":["28504646"]},"intvolume":" 127","_id":"679","status":"public","oa_version":"Submitted Version","isi":1,"day":"01","publisher":"American Society for Clinical Investigation","year":"2017","citation":{"short":"F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065.","mla":"Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:10.1172/JCI80631.","chicago":"Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation. American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631.","apa":"Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631","ieee":"F. Ebner et al., “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” The Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017.","ama":"Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631","ista":"Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065."},"acknowledgement":"This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna."},{"corr_author":"1","scopus_import":"1","publication":"eLife","author":[{"id":"2C023F40-F248-11E8-B48F-1D18A9856A87","last_name":"Steinrück","full_name":"Steinrück, Magdalena","first_name":"Magdalena","orcid":"0000-0003-1229-9719"},{"orcid":"0000-0001-6220-2052","first_name":"Calin C","last_name":"Guet","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","full_name":"Guet, Calin C"}],"publication_identifier":{"issn":["2050-084X"]},"oa":1,"title":"Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection","doi":"10.7554/eLife.25100","type":"journal_article","article_number":"e25100","language":[{"iso":"eng"}],"department":[{"_id":"CaGu"}],"volume":6,"pubrep_id":"890","publication_status":"published","month":"07","date_created":"2018-12-11T11:48:01Z","article_processing_charge":"No","quality_controlled":"1","related_material":{"record":[{"id":"5564","relation":"popular_science","status":"public"},{"status":"public","id":"26","relation":"dissertation_contains"}]},"publist_id":"6990","date_updated":"2026-10-26T23:30:16Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","file_date_updated":"2020-07-14T12:47:48Z","abstract":[{"text":"How the organization of genes on a chromosome shapes adaptation is essential for understanding evolutionary paths. Here, we investigate how adaptation to rapidly increasing levels of antibiotic depends on the chromosomal neighborhood of a drug-resistance gene inserted at different positions of the Escherichia coli chromosome. Using a dual-fluorescence reporter that allows us to distinguish gene amplifications from other up-mutations, we track in real-time adaptive changes in expression of the drug-resistance gene. We find that the relative contribution of several mutation types differs systematically between loci due to properties of neighboring genes: essentiality, expression, orientation, termination, and presence of duplicates. These properties determine rate and fitness effects of gene amplification, deletions, and mutations compromising transcriptional termination. Thus, the adaptive potential of a gene under selection is a system-property with a complex genetic basis that is specific for each chromosomal locus, and it can be inferred from detailed functional and genomic data.","lang":"eng"}],"ddc":["576"],"date_published":"2017-07-25T00:00:00Z","has_accepted_license":"1","fulldoi":"https://doi.org/10.7554/eLife.25100","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"_id":"704","status":"public","oa_version":"Published Version","day":"25","isi":1,"citation":{"chicago":"Steinrück, Magdalena, and Calin C Guet. “Complex Chromosomal Neighborhood Effects Determine the Adaptive Potential of a Gene under Selection.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.25100.","short":"M. Steinrück, C.C. Guet, ELife 6 (2017).","mla":"Steinrück, Magdalena, and Calin C. Guet. “Complex Chromosomal Neighborhood Effects Determine the Adaptive Potential of a Gene under Selection.” ELife, vol. 6, e25100, eLife Sciences Publications, 2017, doi:10.7554/eLife.25100.","ama":"Steinrück M, Guet CC. Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection. eLife. 2017;6. doi:10.7554/eLife.25100","ista":"Steinrück M, Guet CC. 2017. Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection. eLife. 6, e25100.","apa":"Steinrück, M., & Guet, C. C. (2017). Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25100","ieee":"M. Steinrück and C. C. Guet, “Complex chromosomal neighborhood effects determine the adaptive potential of a gene under selection,” eLife, vol. 6. eLife Sciences Publications, 2017."},"year":"2017","publisher":"eLife Sciences Publications","external_id":{"isi":["000406183700001"]},"file":[{"checksum":"6b908b5db9f61f6820ebd7f8fa815571","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_updated":"2020-07-14T12:47:48Z","creator":"system","file_id":"4975","file_name":"IST-2017-890-v1+1_elife-25100-v1.pdf","file_size":2092088,"date_created":"2018-12-12T10:12:54Z"},{"creator":"system","content_type":"application/pdf","date_updated":"2020-07-14T12:47:48Z","checksum":"ca21530389b720243552678125fdba35","access_level":"open_access","relation":"main_file","file_size":3428681,"date_created":"2018-12-12T10:12:55Z","file_name":"IST-2017-890-v1+2_elife-25100-figures-v1.pdf","file_id":"4976"}],"intvolume":" 6"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ec_funded":1,"abstract":[{"lang":"eng","text":"Cell-cell contact formation constitutes an essential step in evolution, leading to the differentiation of specialized cell types. However, remarkably little is known about whether and how the interplay between contact formation and fate specification affects development. Here, we identify a positive feedback loop between cell-cell contact duration, morphogen signaling, and mesendoderm cell-fate specification during zebrafish gastrulation. We show that long-lasting cell-cell contacts enhance the competence of prechordal plate (ppl) progenitor cells to respond to Nodal signaling, required for ppl cell-fate specification. We further show that Nodal signaling promotes ppl cell-cell contact duration, generating a positive feedback loop between ppl cell-cell contact duration and cell-fate specification. Finally, by combining mathematical modeling and experimentation, we show that this feedback determines whether anterior axial mesendoderm cells become ppl or, instead, turn into endoderm. Thus, the interdependent activities of cell-cell signaling and contact formation control fate diversification within the developing embryo."}],"publist_id":"6934","date_updated":"2026-10-26T23:30:19Z","date_published":"2017-10-23T00:00:00Z","fulldoi":"https://doi.org/10.1016/j.devcel.2017.09.014","isi":1,"day":"23","publisher":"Cell Press","year":"2017","citation":{"apa":"Barone, V., Lang, M., Krens, G., Pradhan, S., Shamipour, S., Sako, K., … Heisenberg, C.-P. J. (2017). An effective feedback loop between cell-cell contact duration and morphogen signaling determines cell fate. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2017.09.014","ieee":"V. Barone et al., “An effective feedback loop between cell-cell contact duration and morphogen signaling determines cell fate,” Developmental Cell, vol. 43, no. 2. Cell Press, pp. 198–211, 2017.","ama":"Barone V, Lang M, Krens G, et al. An effective feedback loop between cell-cell contact duration and morphogen signaling determines cell fate. Developmental Cell. 2017;43(2):198-211. doi:10.1016/j.devcel.2017.09.014","ista":"Barone V, Lang M, Krens G, Pradhan S, Shamipour S, Sako K, Sikora MK, Guet CC, Heisenberg C-PJ. 2017. An effective feedback loop between cell-cell contact duration and morphogen signaling determines cell fate. Developmental Cell. 43(2), 198–211.","mla":"Barone, Vanessa, et al. “An Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling Determines Cell Fate.” Developmental Cell, vol. 43, no. 2, Cell Press, 2017, pp. 198–211, doi:10.1016/j.devcel.2017.09.014.","short":"V. Barone, M. Lang, G. Krens, S. Pradhan, S. Shamipour, K. Sako, M.K. Sikora, C.C. Guet, C.-P.J. Heisenberg, Developmental Cell 43 (2017) 198–211.","chicago":"Barone, Vanessa, Moritz Lang, Gabriel Krens, Saurabh Pradhan, Shayan Shamipour, Keisuke Sako, Mateusz K Sikora, Calin C Guet, and Carl-Philipp J Heisenberg. “An Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling Determines Cell Fate.” Developmental Cell. Cell Press, 2017. https://doi.org/10.1016/j.devcel.2017.09.014."},"status":"public","_id":"735","oa_version":"None","issue":"2","external_id":{"isi":["000413443700011"]},"intvolume":" 43","publication":"Developmental Cell","author":[{"id":"419EECCC-F248-11E8-B48F-1D18A9856A87","last_name":"Barone","full_name":"Barone, Vanessa","orcid":"0000-0003-2676-3367","first_name":"Vanessa"},{"id":"29E0800A-F248-11E8-B48F-1D18A9856A87","last_name":"Lang","full_name":"Lang, Moritz","first_name":"Moritz"},{"first_name":"Gabriel","orcid":"0000-0003-4761-5996","full_name":"Krens, Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87","last_name":"Krens"},{"full_name":"Pradhan, Saurabh","last_name":"Pradhan","first_name":"Saurabh"},{"first_name":"Shayan","full_name":"Shamipour, Shayan","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","last_name":"Shamipour"},{"full_name":"Sako, Keisuke","id":"3BED66BE-F248-11E8-B48F-1D18A9856A87","last_name":"Sako","orcid":"0000-0002-6453-8075","first_name":"Keisuke"},{"first_name":"Mateusz K","id":"2F74BCDE-F248-11E8-B48F-1D18A9856A87","last_name":"Sikora","full_name":"Sikora, Mateusz K"},{"first_name":"Calin C","orcid":"0000-0001-6220-2052","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","last_name":"Guet","full_name":"Guet, Calin C"},{"orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"corr_author":"1","scopus_import":"1","title":"An effective feedback loop between cell-cell contact duration and morphogen signaling determines cell fate","publication_identifier":{"issn":["1534-5807"]},"type":"journal_article","doi":"10.1016/j.devcel.2017.09.014","month":"10","page":"198 - 211","publication_status":"published","department":[{"_id":"CaHe"},{"_id":"CaGu"},{"_id":"GaTk"}],"language":[{"iso":"eng"}],"volume":43,"project":[{"grant_number":"291734","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme"},{"_id":"252DD2A6-B435-11E9-9278-68D0E5697425","name":"Cell segregation in gastrulation: the role of cell fate specification","call_identifier":"FWF","grant_number":"I2058"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"961"},{"status":"public","id":"8350","relation":"dissertation_contains"}]},"quality_controlled":"1","article_processing_charge":"No","date_created":"2018-12-11T11:48:13Z"},{"date_published":"2017-03-16T00:00:00Z","has_accepted_license":"1","ddc":["570"],"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"fulldoi":"https://doi.org/10.1371/journal.pone.0174066","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"lang":"eng","text":"RNA Polymerase II pauses and backtracks during transcription, with many consequences for gene expression and cellular physiology. Here, we show that the energy required to melt double-stranded nucleic acids in the transcription bubble predicts pausing in Saccharomyces cerevisiae far more accurately than nucleosome roadblocks do. In addition, the same energy difference also determines when the RNA polymerase backtracks instead of continuing to move forward. This data-driven model corroborates—in a genome wide and quantitative manner—previous evidence that sequence-dependent thermodynamic features of nucleic acids influence both transcriptional pausing and backtracking."}],"file_date_updated":"2018-12-12T10:09:47Z","date_updated":"2026-10-26T23:30:27Z","publist_id":"6361","issue":"3","external_id":{"isi":["000396318300121"]},"intvolume":" 12","file":[{"file_size":3429381,"date_created":"2018-12-12T10:09:47Z","file_name":"IST-2017-800-v1+1_journal.pone.0174066.pdf","file_id":"4772","creator":"system","date_updated":"2018-12-12T10:09:47Z","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"isi":1,"day":"16","publisher":"Public Library of Science","year":"2017","citation":{"ista":"Lukacisin M, Landon M, Jajoo R. 2017. Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast. PLoS One. 12(3), e0174066.","ama":"Lukacisin M, Landon M, Jajoo R. Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast. PLoS One. 2017;12(3). doi:10.1371/journal.pone.0174066","apa":"Lukacisin, M., Landon, M., & Jajoo, R. (2017). Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0174066","ieee":"M. Lukacisin, M. Landon, and R. Jajoo, “Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast,” PLoS One, vol. 12, no. 3. Public Library of Science, 2017.","chicago":"Lukacisin, Martin, Matthieu Landon, and Rishi Jajoo. “Sequence-Specific Thermodynamic Properties of Nucleic Acids Influence Both Transcriptional Pausing and Backtracking in Yeast.” PLoS One. Public Library of Science, 2017. https://doi.org/10.1371/journal.pone.0174066.","mla":"Lukacisin, Martin, et al. “Sequence-Specific Thermodynamic Properties of Nucleic Acids Influence Both Transcriptional Pausing and Backtracking in Yeast.” PLoS One, vol. 12, no. 3, e0174066, Public Library of Science, 2017, doi:10.1371/journal.pone.0174066.","short":"M. Lukacisin, M. Landon, R. Jajoo, PLoS One 12 (2017)."},"status":"public","_id":"1029","oa_version":"Published Version","article_number":"e0174066","title":"Sequence-specific thermodynamic properties of nucleic acids influence both transcriptional pausing and backtracking in yeast","oa":1,"publication_identifier":{"issn":["1932-6203"]},"type":"journal_article","doi":"10.1371/journal.pone.0174066","publication":"PLoS One","author":[{"orcid":"0000-0001-6549-4177","first_name":"Martin","id":"298FFE8C-F248-11E8-B48F-1D18A9856A87","last_name":"Lukacisin","full_name":"Lukacisin, Martin"},{"first_name":"Matthieu","last_name":"Landon","full_name":"Landon, Matthieu"},{"full_name":"Jajoo, Rishi","last_name":"Jajoo","first_name":"Rishi"}],"scopus_import":"1","related_material":{"record":[{"status":"public","relation":"popular_science","id":"5556"},{"status":"public","id":"6392","relation":"dissertation_contains"}]},"quality_controlled":"1","article_processing_charge":"Yes","date_created":"2018-12-11T11:49:46Z","month":"03","publication_status":"published","pubrep_id":"800","department":[{"_id":"ToBo"}],"volume":12,"language":[{"iso":"eng"}]},{"file":[{"file_name":"2017_Development_Krens.pdf","file_size":8194516,"date_created":"2019-09-24T06:56:22Z","file_id":"6905","date_updated":"2020-07-14T12:47:39Z","content_type":"application/pdf","creator":"dernst","relation":"main_file","checksum":"bc25125fb664706cdf180e061429f91d","access_level":"open_access"}],"intvolume":" 144","external_id":{"isi":["000402275900007"],"pmid":["28512197"]},"issue":"10","oa_version":"Published Version","_id":"676","status":"public","citation":{"ama":"Krens G, Veldhuis J, Barone V, et al. Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. Development. 2017;144(10):1798-1806. doi:10.1242/dev.144964","ista":"Krens G, Veldhuis J, Barone V, Capek D, Maître J-L, Brodland W, Heisenberg C-PJ. 2017. Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. Development. 144(10), 1798–1806.","apa":"Krens, G., Veldhuis, J., Barone, V., Capek, D., Maître, J.-L., Brodland, W., & Heisenberg, C.-P. J. (2017). Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. Development. Company of Biologists. https://doi.org/10.1242/dev.144964","ieee":"G. Krens et al., “Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation,” Development, vol. 144, no. 10. Company of Biologists, pp. 1798–1806, 2017.","chicago":"Krens, Gabriel, Jim Veldhuis, Vanessa Barone, Daniel Capek, Jean-Léon Maître, Wayne Brodland, and Carl-Philipp J Heisenberg. “Interstitial Fluid Osmolarity Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.” Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.144964.","short":"G. Krens, J. Veldhuis, V. Barone, D. Capek, J.-L. Maître, W. Brodland, C.-P.J. Heisenberg, Development 144 (2017) 1798–1806.","mla":"Krens, Gabriel, et al. “Interstitial Fluid Osmolarity Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.” Development, vol. 144, no. 10, Company of Biologists, 2017, pp. 1798–806, doi:10.1242/dev.144964."},"year":"2017","publisher":"Company of Biologists","day":"15","isi":1,"fulldoi":"https://doi.org/10.1242/dev.144964","article_type":"original","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"ddc":["570"],"has_accepted_license":"1","date_published":"2017-05-15T00:00:00Z","publist_id":"7047","date_updated":"2026-10-26T23:30:32Z","file_date_updated":"2020-07-14T12:47:39Z","abstract":[{"text":"The segregation of different cell types into distinct tissues is a fundamental process in metazoan development. Differences in cell adhesion and cortex tension are commonly thought to drive cell sorting by regulating tissue surface tension (TST). However, the role that differential TST plays in cell segregation within the developing embryo is as yet unclear. Here, we have analyzed the role of differential TST for germ layer progenitor cell segregation during zebrafish gastrulation. Contrary to previous observations that differential TST drives germ layer progenitor cell segregation in vitro, we show that germ layers display indistinguishable TST within the gastrulating embryo, arguing against differential TST driving germ layer progenitor cell segregation in vivo. We further show that the osmolarity of the interstitial fluid (IF) is an important factor that influences germ layer TST in vivo, and that lower osmolarity of the IF compared with standard cell culture medium can explain why germ layers display differential TST in culture but not in vivo. Finally, we show that directed migration of mesendoderm progenitors is required for germ layer progenitor cell segregation and germ layer formation.","lang":"eng"}],"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","date_created":"2018-12-11T11:47:52Z","article_processing_charge":"No","quality_controlled":"1","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"961"},{"status":"public","relation":"dissertation_contains","id":"50"}]},"language":[{"iso":"eng"}],"volume":144,"department":[{"_id":"Bio"},{"_id":"CaHe"}],"publication_status":"published","page":"1798 - 1806","month":"05","doi":"10.1242/dev.144964","type":"journal_article","publication_identifier":{"issn":["0950-1991"]},"pmid":1,"title":"Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation","oa":1,"scopus_import":"1","corr_author":"1","author":[{"first_name":"Gabriel","orcid":"0000-0003-4761-5996","full_name":"Krens, Gabriel","last_name":"Krens","id":"2B819732-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jim","full_name":"Veldhuis, Jim","last_name":"Veldhuis"},{"orcid":"0000-0003-2676-3367","first_name":"Vanessa","full_name":"Barone, Vanessa","id":"419EECCC-F248-11E8-B48F-1D18A9856A87","last_name":"Barone"},{"first_name":"Daniel","orcid":"0000-0001-5199-9940","id":"31C42484-F248-11E8-B48F-1D18A9856A87","last_name":"Capek","full_name":"Capek, Daniel"},{"first_name":"Jean-Léon","orcid":"0000-0002-3688-1474","last_name":"Maître","id":"48F1E0D8-F248-11E8-B48F-1D18A9856A87","full_name":"Maître, Jean-Léon"},{"first_name":"Wayne","full_name":"Brodland, Wayne","last_name":"Brodland"},{"last_name":"Heisenberg","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J","orcid":"0000-0002-0912-4566"}],"publication":"Development"},{"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","ec_funded":1,"abstract":[{"lang":"eng","text":"During embryonic development, mechanical forces are essential for cellular rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish embryo, friction forces are generated at the interface between anterior axial mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole and neurectoderm progenitors moving in the opposite direction towards the vegetal pole of the embryo. These friction forces lead to global rearrangement of cells within the neurectoderm and determine the position of the neural anlage. Using a combination of experiments and simulations, we show that this process depends on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated adhesion between those tissues. Our data thus establish the emergence of friction forces at the interface between moving tissues as a critical force-generating process shaping the embryo."}],"publist_id":"7074","date_updated":"2026-10-26T23:30:31Z","date_published":"2017-03-27T00:00:00Z","fulldoi":"https://doi.org/10.1038/ncb3492","isi":1,"day":"27","publisher":"Nature Publishing Group","citation":{"ieee":"M. Smutny et al., “Friction forces position the neural anlage,” Nature Cell Biology, vol. 19. Nature Publishing Group, pp. 306–317, 2017.","apa":"Smutny, M., Ákos, Z., Grigolon, S., Shamipour, S., Ruprecht, V., Capek, D., … Heisenberg, C.-P. J. (2017). Friction forces position the neural anlage. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3492","ista":"Smutny M, Ákos Z, Grigolon S, Shamipour S, Ruprecht V, Capek D, Behrndt M, Papusheva E, Tada M, Hof B, Vicsek T, Salbreux G, Heisenberg C-PJ. 2017. Friction forces position the neural anlage. Nature Cell Biology. 19, 306–317.","ama":"Smutny M, Ákos Z, Grigolon S, et al. Friction forces position the neural anlage. Nature Cell Biology. 2017;19:306-317. doi:10.1038/ncb3492","short":"M. Smutny, Z. Ákos, S. Grigolon, S. Shamipour, V. Ruprecht, D. Capek, M. Behrndt, E. Papusheva, M. Tada, B. Hof, T. Vicsek, G. Salbreux, C.-P.J. Heisenberg, Nature Cell Biology 19 (2017) 306–317.","mla":"Smutny, Michael, et al. “Friction Forces Position the Neural Anlage.” Nature Cell Biology, vol. 19, Nature Publishing Group, 2017, pp. 306–17, doi:10.1038/ncb3492.","chicago":"Smutny, Michael, Zsuzsa Ákos, Silvia Grigolon, Shayan Shamipour, Verena Ruprecht, Daniel Capek, Martin Behrndt, et al. “Friction Forces Position the Neural Anlage.” Nature Cell Biology. Nature Publishing Group, 2017. https://doi.org/10.1038/ncb3492."},"year":"2017","_id":"661","status":"public","oa_version":"Submitted Version","external_id":{"isi":["000397917000009"],"pmid":["28346437"]},"intvolume":" 19","acknowledged_ssus":[{"_id":"SSU"}],"publication":"Nature Cell Biology","author":[{"last_name":"Smutny","id":"3FE6E4E8-F248-11E8-B48F-1D18A9856A87","full_name":"Smutny, Michael","first_name":"Michael","orcid":"0000-0002-5920-9090"},{"first_name":"Zsuzsa","last_name":"Ákos","full_name":"Ákos, Zsuzsa"},{"last_name":"Grigolon","full_name":"Grigolon, Silvia","first_name":"Silvia"},{"full_name":"Shamipour, Shayan","last_name":"Shamipour","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","first_name":"Shayan"},{"first_name":"Verena","full_name":"Ruprecht, Verena","last_name":"Ruprecht"},{"full_name":"Capek, Daniel","last_name":"Capek","id":"31C42484-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5199-9940","first_name":"Daniel"},{"id":"3ECECA3A-F248-11E8-B48F-1D18A9856A87","last_name":"Behrndt","full_name":"Behrndt, Martin","first_name":"Martin"},{"first_name":"Ekaterina","full_name":"Papusheva, Ekaterina","last_name":"Papusheva","id":"41DB591E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Tada","full_name":"Tada, Masazumi","first_name":"Masazumi"},{"orcid":"0000-0003-2057-2754","first_name":"Björn","full_name":"Hof, Björn","last_name":"Hof","id":"3A374330-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Vicsek, Tamás","last_name":"Vicsek","first_name":"Tamás"},{"full_name":"Salbreux, Guillaume","last_name":"Salbreux","first_name":"Guillaume"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J"}],"corr_author":"1","scopus_import":"1","title":"Friction forces position the neural anlage","oa":1,"publication_identifier":{"issn":["1465-7392"]},"pmid":1,"type":"journal_article","doi":"10.1038/ncb3492","main_file_link":[{"open_access":"1","url":"https://europepmc.org/articles/pmc5635970"}],"month":"03","page":"306 - 317","publication_status":"published","language":[{"iso":"eng"}],"volume":19,"department":[{"_id":"CaHe"},{"_id":"BjHo"},{"_id":"Bio"}],"project":[{"grant_number":"306589","name":"Decoding the complexity of turbulence at its origin","_id":"25152F3A-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"call_identifier":"FWF","name":"Control of Epithelial Cell Layer Spreading in Zebrafish","_id":"252ABD0A-B435-11E9-9278-68D0E5697425","grant_number":"I930-B20"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"8350","status":"public"},{"relation":"dissertation_contains","id":"50","status":"public"}]},"quality_controlled":"1","article_processing_charge":"No","date_created":"2018-12-11T11:47:46Z"},{"day":"18","isi":1,"year":"2017","citation":{"apa":"Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.","ama":"Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520. doi:10.1016/j.immuni.2017.04.006","short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.","mla":"Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006.","chicago":"Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity. Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006."},"publisher":"Cell Press","_id":"664","status":"public","oa_version":"None","external_id":{"isi":["000399451100002"]},"issue":"4","intvolume":" 46","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","abstract":[{"text":"Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.","lang":"eng"}],"date_updated":"2026-10-26T23:30:42Z","publist_id":"7065","date_published":"2017-04-18T00:00:00Z","fulldoi":"https://doi.org/10.1016/j.immuni.2017.04.006","month":"04","page":"519 - 520","volume":46,"language":[{"iso":"eng"}],"department":[{"_id":"MiSi"}],"publication_status":"published","related_material":{"record":[{"id":"6947","relation":"dissertation_contains","status":"public"}]},"quality_controlled":"1","date_created":"2018-12-11T11:47:47Z","article_processing_charge":"No","publication":"Immunity","author":[{"full_name":"Assen, Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","last_name":"Assen","orcid":"0000-0003-3470-6119","first_name":"Frank P"},{"first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K"}],"corr_author":"1","scopus_import":"1","publication_identifier":{"issn":["1074-7613"]},"title":"The dynamic cytokine niche","doi":"10.1016/j.immuni.2017.04.006","type":"journal_article"},{"page":"59 - 66","language":[{"iso":"eng"}],"department":[{"_id":"KrCh"}],"volume":10482,"pubrep_id":"845","publication_status":"published","month":"01","date_created":"2018-12-11T11:49:22Z","article_processing_charge":"No","project":[{"name":"Game Theory","_id":"25863FF4-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"S11407"},{"grant_number":"279307","call_identifier":"FP7","_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"8934","status":"public"}]},"quality_controlled":"1","corr_author":"1","conference":{"name":"ATVA: Automated Technology for Verification and Analysis","end_date":"2017-10-06","location":"Pune, India","start_date":"2017-10-03"},"scopus_import":"1","author":[{"full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","first_name":"Krishnendu"},{"first_name":"Amir","orcid":"0000-0003-1702-6584","id":"391365CE-F248-11E8-B48F-1D18A9856A87","last_name":"Goharshady","full_name":"Goharshady, Amir"},{"full_name":"Pavlogiannis, Andreas","last_name":"Pavlogiannis","id":"49704004-F248-11E8-B48F-1D18A9856A87","first_name":"Andreas","orcid":"0000-0002-8943-0722"}],"publication_identifier":{"issn":["0302-9743"]},"title":"JTDec: A tool for tree decompositions in soot","oa":1,"doi":"10.1007/978-3-319-68167-2_4","type":"conference","status":"public","_id":"949","oa_version":"Submitted Version","editor":[{"full_name":"D'Souza, Deepak","last_name":"D'Souza","first_name":"Deepak"}],"day":"01","isi":1,"citation":{"ista":"Chatterjee K, Goharshady AK, Pavlogiannis A. 2017. JTDec: A tool for tree decompositions in soot. ATVA: Automated Technology for Verification and Analysis, LNCS, vol. 10482, 59–66.","ama":"Chatterjee K, Goharshady AK, Pavlogiannis A. JTDec: A tool for tree decompositions in soot. In: D’Souza D, ed. Vol 10482. Springer; 2017:59-66. doi:10.1007/978-3-319-68167-2_4","ieee":"K. Chatterjee, A. K. Goharshady, and A. Pavlogiannis, “JTDec: A tool for tree decompositions in soot,” presented at the ATVA: Automated Technology for Verification and Analysis, Pune, India, 2017, vol. 10482, pp. 59–66.","apa":"Chatterjee, K., Goharshady, A. K., & Pavlogiannis, A. (2017). JTDec: A tool for tree decompositions in soot. In D. D’Souza (Ed.) (Vol. 10482, pp. 59–66). Presented at the ATVA: Automated Technology for Verification and Analysis, Pune, India: Springer. https://doi.org/10.1007/978-3-319-68167-2_4","chicago":"Chatterjee, Krishnendu, Amir Kafshdar Goharshady, and Andreas Pavlogiannis. “JTDec: A Tool for Tree Decompositions in Soot.” edited by Deepak D’Souza, 10482:59–66. Springer, 2017. https://doi.org/10.1007/978-3-319-68167-2_4.","mla":"Chatterjee, Krishnendu, et al. JTDec: A Tool for Tree Decompositions in Soot. Edited by Deepak D’Souza, vol. 10482, Springer, 2017, pp. 59–66, doi:10.1007/978-3-319-68167-2_4.","short":"K. Chatterjee, A.K. Goharshady, A. Pavlogiannis, in:, D. D’Souza (Ed.), Springer, 2017, pp. 59–66."},"year":"2017","publisher":"Springer","external_id":{"isi":["000723567800004"]},"file":[{"access_level":"open_access","checksum":"a0d9f5f94dc594c4e71e78525c9942f1","relation":"main_file","content_type":"application/pdf","date_updated":"2020-07-14T12:48:16Z","creator":"system","file_id":"4835","file_name":"IST-2017-845-v1+1_2017_Chatterjee_JTDec.pdf","file_size":948514,"date_created":"2018-12-12T10:10:45Z"}],"intvolume":" 10482","publist_id":"6468","alternative_title":["LNCS"],"date_updated":"2026-10-26T23:30:46Z","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","abstract":[{"text":"The notion of treewidth of graphs has been exploited for faster algorithms for several problems arising in verification and program analysis. Moreover, various notions of balanced tree decompositions have been used for improved algorithms supporting dynamic updates and analysis of concurrent programs. In this work, we present a tool for constructing tree-decompositions of CFGs obtained from Java methods, which is implemented as an extension to the widely used Soot framework. The experimental results show that our implementation on real-world Java benchmarks is very efficient. Our tool also provides the first implementation for balancing tree-decompositions. In summary, we present the first tool support for exploiting treewidth in the static analysis problems on Java programs.","lang":"eng"}],"file_date_updated":"2020-07-14T12:48:16Z","ec_funded":1,"ddc":["005"],"has_accepted_license":"1","date_published":"2017-01-01T00:00:00Z","fulldoi":"https://doi.org/10.1007/978-3-319-68167-2_4"},{"oa":1,"title":"Non-polynomial worst case analysis of recursive programs","publication_identifier":{"isbn":["978-331963389-3"]},"type":"conference","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1705.00317"}],"doi":"10.1007/978-3-319-63390-9_3","author":[{"first_name":"Krishnendu","orcid":"0000-0002-4561-241X","full_name":"Chatterjee, Krishnendu","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","last_name":"Chatterjee"},{"full_name":"Fu, Hongfei","last_name":"Fu","first_name":"Hongfei"},{"first_name":"Amir","orcid":"0000-0003-1702-6584","full_name":"Goharshady, Amir","last_name":"Goharshady","id":"391365CE-F248-11E8-B48F-1D18A9856A87"}],"conference":{"location":"Heidelberg, Germany","end_date":"2017-07-28","name":"CAV: Computer Aided Verification","start_date":"2017-07-24"},"scopus_import":"1","project":[{"_id":"25863FF4-B435-11E9-9278-68D0E5697425","name":"Game Theory","call_identifier":"FWF","grant_number":"S11407"},{"grant_number":"279307","call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425"}],"related_material":{"record":[{"relation":"later_version","id":"7014","status":"public"},{"id":"8934","relation":"dissertation_contains","status":"public"}]},"quality_controlled":"1","article_processing_charge":"No","date_created":"2018-12-11T11:47:39Z","month":"01","page":"41 - 63","publication_status":"published","language":[{"iso":"eng"}],"department":[{"_id":"KrCh"}],"volume":10427,"date_published":"2017-01-01T00:00:00Z","fulldoi":"https://doi.org/10.1007/978-3-319-63390-9_3","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","abstract":[{"text":"We study the problem of developing efficient approaches for proving worst-case bounds of non-deterministic recursive programs. Ranking functions are sound and complete for proving termination and worst-case bounds of non-recursive programs. First, we apply ranking functions to recursion, resulting in measure functions, and show that they provide a sound and complete approach to prove worst-case bounds of non-deterministic recursive programs. Our second contribution is the synthesis of measure functions in non-polynomial forms. We show that non-polynomial measure functions with logarithm and exponentiation can be synthesized through abstraction of logarithmic or exponentiation terms, Farkas’ Lemma, and Handelman’s Theorem using linear programming. While previous methods obtain worst-case polynomial bounds, our approach can synthesize bounds of the form O(n log n) as well as O(nr) where r is not an integer. We present experimental results to demonstrate that our approach can efficiently obtain worst-case bounds of classical recursive algorithms such as Merge-Sort, Closest-Pair, Karatsuba’s algorithm and Strassen’s algorithm.","lang":"eng"}],"ec_funded":1,"alternative_title":["LNCS"],"publist_id":"7149","date_updated":"2026-10-26T23:30:46Z","external_id":{"isi":["000431900900003"],"arxiv":["1705.00317"]},"intvolume":" 10427","isi":1,"arxiv":1,"day":"01","publisher":"Springer","year":"2017","citation":{"short":"K. Chatterjee, H. Fu, A.K. Goharshady, in:, R. Majumdar, V. Kunčak (Eds.), Springer, 2017, pp. 41–63.","mla":"Chatterjee, Krishnendu, et al. Non-Polynomial Worst Case Analysis of Recursive Programs. Edited by Rupak Majumdar and Viktor Kunčak, vol. 10427, Springer, 2017, pp. 41–63, doi:10.1007/978-3-319-63390-9_3.","chicago":"Chatterjee, Krishnendu, Hongfei Fu, and Amir Kafshdar Goharshady. “Non-Polynomial Worst Case Analysis of Recursive Programs.” edited by Rupak Majumdar and Viktor Kunčak, 10427:41–63. Springer, 2017. https://doi.org/10.1007/978-3-319-63390-9_3.","ieee":"K. Chatterjee, H. Fu, and A. K. Goharshady, “Non-polynomial worst case analysis of recursive programs,” presented at the CAV: Computer Aided Verification, Heidelberg, Germany, 2017, vol. 10427, pp. 41–63.","apa":"Chatterjee, K., Fu, H., & Goharshady, A. K. (2017). Non-polynomial worst case analysis of recursive programs. In R. Majumdar & V. Kunčak (Eds.) (Vol. 10427, pp. 41–63). Presented at the CAV: Computer Aided Verification, Heidelberg, Germany: Springer. https://doi.org/10.1007/978-3-319-63390-9_3","ista":"Chatterjee K, Fu H, Goharshady AK. 2017. Non-polynomial worst case analysis of recursive programs. CAV: Computer Aided Verification, LNCS, vol. 10427, 41–63.","ama":"Chatterjee K, Fu H, Goharshady AK. Non-polynomial worst case analysis of recursive programs. In: Majumdar R, Kunčak V, eds. Vol 10427. 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Frontiers Research Foundation, 2017. https://doi.org/10.3389/fncel.2017.00176.","mla":"Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience, vol. 11, 176, Frontiers Research Foundation, 2017, doi:10.3389/fncel.2017.00176.","short":"A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers in Cellular Neuroscience 11 (2017).","ista":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 11, 176.","ama":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 2017;11. doi:10.3389/fncel.2017.00176","ieee":"A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks,” Frontiers in Cellular Neuroscience, vol. 11. Frontiers Research Foundation, 2017.","apa":"Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., & Hippenmeyer, S. (2017). Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. Frontiers Research Foundation. https://doi.org/10.3389/fncel.2017.00176"},"year":"2017","publisher":"Frontiers Research Foundation","day":"28","isi":1,"oa_version":"Published Version","_id":"960","status":"public","fulldoi":"https://doi.org/10.3389/fncel.2017.00176","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"ddc":["570"],"date_published":"2017-06-28T00:00:00Z","has_accepted_license":"1","ec_funded":1,"file_date_updated":"2020-07-14T12:48:16Z","abstract":[{"text":"The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context.","lang":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"6445","date_updated":"2026-10-26T23:30:47Z"},{"status":"public","_id":"696","oa_version":"Published Version","day":"18","isi":1,"year":"2017","citation":{"mla":"Lukacisinova, Marta, et al. “Stress Induced Mutagenesis: Stress Diversity Facilitates the Persistence of Mutator Genes.” PLoS Computational Biology, vol. 13, no. 7, e1005609, Public Library of Science, 2017, doi:10.1371/journal.pcbi.1005609.","short":"M. Lukacisinova, S. Novak, T. Paixao, PLoS Computational Biology 13 (2017).","chicago":"Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Stress Induced Mutagenesis: Stress Diversity Facilitates the Persistence of Mutator Genes.” PLoS Computational Biology. Public Library of Science, 2017. https://doi.org/10.1371/journal.pcbi.1005609.","apa":"Lukacisinova, M., Novak, S., & Paixao, T. (2017). Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes. PLoS Computational Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1005609","ieee":"M. Lukacisinova, S. Novak, and T. Paixao, “Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes,” PLoS Computational Biology, vol. 13, no. 7. Public Library of Science, 2017.","ama":"Lukacisinova M, Novak S, Paixao T. Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes. PLoS Computational Biology. 2017;13(7). doi:10.1371/journal.pcbi.1005609","ista":"Lukacisinova M, Novak S, Paixao T. 2017. Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes. PLoS Computational Biology. 13(7), e1005609."},"publisher":"Public Library of Science","external_id":{"isi":["000406619800014"]},"issue":"7","file":[{"date_updated":"2020-07-14T12:47:46Z","content_type":"application/pdf","creator":"system","relation":"main_file","access_level":"open_access","checksum":"9143c290fa6458ed2563bff4b295554a","file_name":"IST-2017-894-v1+1_journal.pcbi.1005609.pdf","date_created":"2018-12-12T10:15:01Z","file_size":3775716,"file_id":"5117"}],"intvolume":" 13","publist_id":"7004","date_updated":"2026-10-26T23:30:48Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","file_date_updated":"2020-07-14T12:47:46Z","ec_funded":1,"abstract":[{"lang":"eng","text":"Mutator strains are expected to evolve when the availability and effect of beneficial mutations are high enough to counteract the disadvantage from deleterious mutations that will inevitably accumulate. As the population becomes more adapted to its environment, both availability and effect of beneficial mutations necessarily decrease and mutation rates are predicted to decrease. It has been shown that certain molecular mechanisms can lead to increased mutation rates when the organism finds itself in a stressful environment. While this may be a correlated response to other functions, it could also be an adaptive mechanism, raising mutation rates only when it is most advantageous. Here, we use a mathematical model to investigate the plausibility of the adaptive hypothesis. We show that such a mechanism can be mantained if the population is subjected to diverse stresses. By simulating various antibiotic treatment schemes, we find that combination treatments can reduce the effectiveness of second-order selection on stress-induced mutagenesis. We discuss the implications of our results to strategies of antibiotic therapy."}],"ddc":["576"],"date_published":"2017-07-18T00:00:00Z","has_accepted_license":"1","fulldoi":"https://doi.org/10.1371/journal.pcbi.1005609","article_type":"original","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"volume":13,"department":[{"_id":"ToBo"},{"_id":"NiBa"},{"_id":"CaGu"}],"language":[{"iso":"eng"}],"pubrep_id":"894","publication_status":"published","month":"07","date_created":"2018-12-11T11:47:58Z","article_processing_charge":"No","project":[{"grant_number":"618091","name":"Speed of Adaptation in Population Genetics and Evolutionary Computation","_id":"25B1EC9E-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"quality_controlled":"1","related_material":{"record":[{"id":"9849","relation":"research_data","status":"public"},{"status":"public","relation":"research_data","id":"9850"},{"relation":"research_data","id":"9851","status":"public"},{"status":"public","id":"9852","relation":"research_data"},{"id":"6263","relation":"dissertation_contains","status":"public"}]},"corr_author":"1","scopus_import":"1","publication":"PLoS Computational Biology","author":[{"orcid":"0000-0002-2519-8004","first_name":"Marta","full_name":"Lukacisinova, Marta","id":"4342E402-F248-11E8-B48F-1D18A9856A87","last_name":"Lukacisinova"},{"first_name":"Sebastian","orcid":"0000-0002-2519-824X","full_name":"Novak, Sebastian","last_name":"Novak","id":"461468AE-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0003-2361-3953","first_name":"Tiago","last_name":"Paixao","id":"2C5658E6-F248-11E8-B48F-1D18A9856A87","full_name":"Paixao, Tiago"}],"publication_identifier":{"issn":["1553-734X"]},"title":"Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes","oa":1,"doi":"10.1371/journal.pcbi.1005609","type":"journal_article","article_number":"e1005609"},{"date_created":"2018-12-11T11:49:45Z","article_processing_charge":"Yes (in subscription journal)","quality_controlled":"1","related_material":{"record":[{"status":"public","id":"6263","relation":"dissertation_contains"}]},"project":[{"call_identifier":"FWF","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22"},{"call_identifier":"FP7","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","name":"Optimality principles in responses to antibiotics","grant_number":"303507"},{"_id":"25EB3A80-B435-11E9-9278-68D0E5697425","name":"Revealing the fundamental limits of cell growth","grant_number":"RGP0042/2013"}],"department":[{"_id":"ToBo"}],"volume":46,"language":[{"iso":"eng"}],"pubrep_id":"801","publication_status":"published","page":"90 - 97","month":"08","doi":"10.1016/j.copbio.2017.02.013","type":"journal_article","oa":1,"title":"Toward a quantitative understanding of antibiotic resistance evolution","scopus_import":"1","corr_author":"1","author":[{"first_name":"Marta","orcid":"0000-0002-2519-8004","full_name":"Lukacisinova, Marta","id":"4342E402-F248-11E8-B48F-1D18A9856A87","last_name":"Lukacisinova"},{"full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4398-476X","first_name":"Mark Tobias"}],"publication":"Current Opinion in Biotechnology","file":[{"relation":"main_file","access_level":"open_access","creator":"dernst","date_updated":"2019-01-18T09:57:57Z","content_type":"application/pdf","file_id":"5846","success":1,"date_created":"2019-01-18T09:57:57Z","file_size":858338,"file_name":"2017_CurrentOpinion_Lukaciinova.pdf"}],"intvolume":" 46","external_id":{"isi":["000408077400015"]},"oa_version":"Published Version","_id":"1027","status":"public","citation":{"mla":"Lukacisinova, Marta, and Mark Tobias Bollenbach. “Toward a Quantitative Understanding of Antibiotic Resistance Evolution.” Current Opinion in Biotechnology, vol. 46, Elsevier, 2017, pp. 90–97, doi:10.1016/j.copbio.2017.02.013.","short":"M. Lukacisinova, M.T. Bollenbach, Current Opinion in Biotechnology 46 (2017) 90–97.","chicago":"Lukacisinova, Marta, and Mark Tobias Bollenbach. “Toward a Quantitative Understanding of Antibiotic Resistance Evolution.” Current Opinion in Biotechnology. Elsevier, 2017. https://doi.org/10.1016/j.copbio.2017.02.013.","ieee":"M. Lukacisinova and M. T. Bollenbach, “Toward a quantitative understanding of antibiotic resistance evolution,” Current Opinion in Biotechnology, vol. 46. Elsevier, pp. 90–97, 2017.","apa":"Lukacisinova, M., & Bollenbach, M. T. (2017). Toward a quantitative understanding of antibiotic resistance evolution. Current Opinion in Biotechnology. Elsevier. https://doi.org/10.1016/j.copbio.2017.02.013","ama":"Lukacisinova M, Bollenbach MT. Toward a quantitative understanding of antibiotic resistance evolution. Current Opinion in Biotechnology. 2017;46:90-97. doi:10.1016/j.copbio.2017.02.013","ista":"Lukacisinova M, Bollenbach MT. 2017. Toward a quantitative understanding of antibiotic resistance evolution. Current Opinion in Biotechnology. 46, 90–97."},"year":"2017","publisher":"Elsevier","day":"01","isi":1,"article_type":"original","fulldoi":"https://doi.org/10.1016/j.copbio.2017.02.013","tmp":{"image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"},"ddc":["570"],"has_accepted_license":"1","date_published":"2017-08-01T00:00:00Z","date_updated":"2026-10-26T23:30:48Z","publist_id":"6364","ec_funded":1,"abstract":[{"text":"The rising prevalence of antibiotic resistant bacteria is an increasingly serious public health challenge. To address this problem, recent work ranging from clinical studies to theoretical modeling has provided valuable insights into the mechanisms of resistance, its emergence and spread, and ways to counteract it. A deeper understanding of the underlying dynamics of resistance evolution will require a combination of experimental and theoretical expertise from different disciplines and new technology for studying evolution in the laboratory. Here, we review recent advances in the quantitative understanding of the mechanisms and evolution of antibiotic resistance. We focus on key theoretical concepts and new technology that enables well-controlled experiments. We further highlight key challenges that can be met in the near future to ultimately develop effective strategies for combating resistance.","lang":"eng"}],"file_date_updated":"2019-01-18T09:57:57Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1"},{"date_updated":"2026-10-26T23:30:50Z","publist_id":"7034","file_date_updated":"2020-07-14T12:47:40Z","abstract":[{"text":"Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry.","lang":"eng"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_type":"original","fulldoi":"https://doi.org/10.1371/journal.pone.0179377","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"ddc":["571"],"date_published":"2017-06-01T00:00:00Z","has_accepted_license":"1","oa_version":"Published Version","_id":"682","status":"public","citation":{"short":"H. Ukai, A. Kawahara, K. Hirayama, M.J. Case, S. Aino, M. Miyabe, K. Wakita, R. Oogi, M. Kasayuki, S. Kawashima, S. Sugimoto, K. Chikamatsu, N. Nitta, T. Koga, R. Shigemoto, T. Takai, I. Ito, PLoS One 12 (2017).","mla":"Ukai, Hikari, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.” PLoS One, vol. 12, no. 6, e0179377, Public Library of Science, 2017, doi:10.1371/journal.pone.0179377.","chicago":"Ukai, Hikari, Aiko Kawahara, Keiko Hirayama, Matthew J Case, Shotaro Aino, Masahiro Miyabe, Ken Wakita, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.” PLoS One. Public Library of Science, 2017. https://doi.org/10.1371/journal.pone.0179377.","ieee":"H. Ukai et al., “PirB regulates asymmetries in hippocampal circuitry,” PLoS One, vol. 12, no. 6. Public Library of Science, 2017.","apa":"Ukai, H., Kawahara, A., Hirayama, K., Case, M. J., Aino, S., Miyabe, M., … Ito, I. (2017). PirB regulates asymmetries in hippocampal circuitry. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0179377","ama":"Ukai H, Kawahara A, Hirayama K, et al. PirB regulates asymmetries in hippocampal circuitry. PLoS One. 2017;12(6). doi:10.1371/journal.pone.0179377","ista":"Ukai H, Kawahara A, Hirayama K, Case MJ, Aino S, Miyabe M, Wakita K, Oogi R, Kasayuki M, Kawashima S, Sugimoto S, Chikamatsu K, Nitta N, Koga T, Shigemoto R, Takai T, Ito I. 2017. PirB regulates asymmetries in hippocampal circuitry. PLoS One. 12(6), e0179377."},"year":"2017","publisher":"Public Library of Science","day":"01","isi":1,"file":[{"date_updated":"2020-07-14T12:47:40Z","content_type":"application/pdf","creator":"system","relation":"main_file","checksum":"24dd19c46fb1c761b0bcbbcd1025a3a8","access_level":"open_access","file_name":"IST-2017-897-v1+1_journal.pone.0179377.pdf","date_created":"2018-12-12T10:12:16Z","file_size":5798454,"file_id":"4934"}],"intvolume":" 12","external_id":{"isi":["000402923200125"]},"issue":"6","scopus_import":"1","author":[{"last_name":"Ukai","full_name":"Ukai, Hikari","first_name":"Hikari"},{"full_name":"Kawahara, Aiko","last_name":"Kawahara","first_name":"Aiko"},{"first_name":"Keiko","full_name":"Hirayama, Keiko","last_name":"Hirayama"},{"last_name":"Case","id":"44B7CA5A-F248-11E8-B48F-1D18A9856A87","full_name":"Case, Matthew J","first_name":"Matthew J"},{"last_name":"Aino","full_name":"Aino, Shotaro","first_name":"Shotaro"},{"first_name":"Masahiro","full_name":"Miyabe, Masahiro","last_name":"Miyabe"},{"first_name":"Ken","full_name":"Wakita, Ken","last_name":"Wakita"},{"first_name":"Ryohei","last_name":"Oogi","full_name":"Oogi, Ryohei"},{"first_name":"Michiyo","full_name":"Kasayuki, Michiyo","last_name":"Kasayuki"},{"first_name":"Shihomi","last_name":"Kawashima","full_name":"Kawashima, Shihomi"},{"last_name":"Sugimoto","full_name":"Sugimoto, Shunichi","first_name":"Shunichi"},{"full_name":"Chikamatsu, Kanako","last_name":"Chikamatsu","first_name":"Kanako"},{"full_name":"Nitta, Noritaka","last_name":"Nitta","first_name":"Noritaka"},{"first_name":"Tsuneyuki","last_name":"Koga","full_name":"Koga, Tsuneyuki"},{"full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","orcid":"0000-0001-8761-9444"},{"first_name":"Toshiyuki","last_name":"Takai","full_name":"Takai, Toshiyuki"},{"last_name":"Ito","full_name":"Ito, Isao","first_name":"Isao"}],"publication":"PLoS One","doi":"10.1371/journal.pone.0179377","type":"journal_article","publication_identifier":{"issn":["1932-6203"]},"title":"PirB regulates asymmetries in hippocampal circuitry","oa":1,"article_number":"e0179377","language":[{"iso":"eng"}],"department":[{"_id":"RySh"}],"volume":12,"pubrep_id":"897","publication_status":"published","month":"06","date_created":"2018-12-11T11:47:54Z","article_processing_charge":"No","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"51"}]},"quality_controlled":"1"},{"page":"1 - 29","publication_status":"published","pubrep_id":"1019","volume":1569,"department":[{"_id":"EvBe"}],"language":[{"iso":"eng"}],"month":"03","article_processing_charge":"No","date_created":"2018-12-11T11:49:45Z","project":[{"grant_number":"I 1774-B16","call_identifier":"FWF","_id":"2542D156-B435-11E9-9278-68D0E5697425","name":"Hormone cross-talk drives nutrient dependent plant development"}],"quality_controlled":"1","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"539"}]},"corr_author":"1","scopus_import":"1","publication":"Auxins and Cytokinins in Plant Biology","author":[{"first_name":"Andrej","orcid":"0000-0003-3638-1426","full_name":"Hurny, Andrej","id":"4DC4AF46-F248-11E8-B48F-1D18A9856A87","last_name":"Hurny"},{"full_name":"Benková, Eva","id":"38F4F166-F248-11E8-B48F-1D18A9856A87","last_name":"Benková","first_name":"Eva","orcid":"0000-0002-8510-9739"}],"title":"Methodological advances in auxin and cytokinin biology","oa":1,"publication_identifier":{"issn":["1064-3745"]},"type":"journal_article","doi":"10.1007/978-1-4939-6831-2_1","_id":"1024","status":"public","oa_version":"Submitted Version","day":"17","publisher":"Springer","citation":{"chicago":"Hurny, Andrej, and Eva Benková. “Methodological Advances in Auxin and Cytokinin Biology.” Auxins and Cytokinins in Plant Biology. Springer, 2017. https://doi.org/10.1007/978-1-4939-6831-2_1.","short":"A. Hurny, E. Benková, Auxins and Cytokinins in Plant Biology 1569 (2017) 1–29.","mla":"Hurny, Andrej, and Eva Benková. “Methodological Advances in Auxin and Cytokinin Biology.” Auxins and Cytokinins in Plant Biology, vol. 1569, Springer, 2017, pp. 1–29, doi:10.1007/978-1-4939-6831-2_1.","ista":"Hurny A, Benková E. 2017. Methodological advances in auxin and cytokinin biology. Auxins and Cytokinins in Plant Biology. 1569, 1–29.","ama":"Hurny A, Benková E. Methodological advances in auxin and cytokinin biology. Auxins and Cytokinins in Plant Biology. 2017;1569:1-29. doi:10.1007/978-1-4939-6831-2_1","apa":"Hurny, A., & Benková, E. (2017). Methodological advances in auxin and cytokinin biology. Auxins and Cytokinins in Plant Biology. Springer. https://doi.org/10.1007/978-1-4939-6831-2_1","ieee":"A. Hurny and E. Benková, “Methodological advances in auxin and cytokinin biology,” Auxins and Cytokinins in Plant Biology, vol. 1569. Springer, pp. 1–29, 2017."},"year":"2017","intvolume":" 1569","file":[{"file_id":"5068","file_name":"IST-2018-1019-v1+1_Hurny_MethodsMolBiol_2017.pdf","date_created":"2018-12-12T10:14:18Z","file_size":840646,"relation":"main_file","access_level":"open_access","content_type":"application/pdf","date_updated":"2019-10-15T07:47:05Z","creator":"system"}],"alternative_title":["Methods in Molecular Biology"],"publist_id":"6369","date_updated":"2026-10-26T23:30:50Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"text":"The history of auxin and cytokinin biology including the initial discoveries by father–son duo Charles Darwin and Francis Darwin (1880), and Gottlieb Haberlandt (1919) is a beautiful demonstration of unceasing continuity of research. Novel findings are integrated into existing hypotheses and models and deepen our understanding of biological principles. At the same time new questions are triggered and hand to hand with this new methodologies are developed to address these new challenges.","lang":"eng"}],"file_date_updated":"2019-10-15T07:47:05Z","date_published":"2017-03-17T00:00:00Z","has_accepted_license":"1","ddc":["575"],"fulldoi":"https://doi.org/10.1007/978-1-4939-6831-2_1"},{"page":"4608-4611","language":[{"iso":"eng"}],"department":[{"_id":"CaGu"},{"_id":"HaJa"}],"volume":56,"publication_status":"published","month":"03","date_created":"2018-12-11T11:49:46Z","article_processing_charge":"No","project":[{"call_identifier":"FP7","name":"Microbial Ion Channels for Synthetic Neurobiology","_id":"25548C20-B435-11E9-9278-68D0E5697425","grant_number":"303564"},{"call_identifier":"FWF","name":"Molecular Drug Targets","_id":"26AA4EF2-B435-11E9-9278-68D0E5697425","grant_number":"W1232-B24"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"418"},{"relation":"part_of_dissertation","id":"7680","status":"public"}]},"quality_controlled":"1","corr_author":"1","scopus_import":"1","publication":"Angewandte Chemie International Edition","author":[{"first_name":"Stephanie","orcid":"0000-0002-6709-2195","full_name":"Kainrath, Stephanie","id":"32CFBA64-F248-11E8-B48F-1D18A9856A87","last_name":"Kainrath"},{"full_name":"Stadler, Manuela","last_name":"Stadler","first_name":"Manuela"},{"last_name":"Gschaider-Reichhart","id":"3FEE232A-F248-11E8-B48F-1D18A9856A87","full_name":"Gschaider-Reichhart, Eva","first_name":"Eva","orcid":"0000-0002-7218-7738"},{"first_name":"Martin","last_name":"Distel","full_name":"Distel, Martin"},{"last_name":"Janovjak","id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","full_name":"Janovjak, Harald L","first_name":"Harald L","orcid":"0000-0002-8023-9315"}],"publication_identifier":{"issn":["1433-7851"]},"oa":1,"title":"Green-light-induced inactivation of receptor signaling using cobalamin-binding domains","doi":"10.1002/anie.201611998","type":"journal_article","_id":"1028","status":"public","oa_version":"Published Version","day":"20","das_tickbox":"1","isi":1,"citation":{"ieee":"S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, and H. L. Janovjak, “Green-light-induced inactivation of receptor signaling using cobalamin-binding domains,” Angewandte Chemie International Edition, vol. 56, no. 16. Wiley, pp. 4608–4611, 2017.","apa":"Kainrath, S., Stadler, M., Gschaider-Reichhart, E., Distel, M., & Janovjak, H. L. (2017). Green-light-induced inactivation of receptor signaling using cobalamin-binding domains. Angewandte Chemie International Edition. Wiley. https://doi.org/10.1002/anie.201611998","ama":"Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. Green-light-induced inactivation of receptor signaling using cobalamin-binding domains. Angewandte Chemie International Edition. 2017;56(16):4608-4611. doi:10.1002/anie.201611998","ista":"Kainrath S, Stadler M, Gschaider-Reichhart E, Distel M, Janovjak HL. 2017. Green-light-induced inactivation of receptor signaling using cobalamin-binding domains. Angewandte Chemie International Edition. 56(16), 4608–4611.","short":"S. Kainrath, M. Stadler, E. Gschaider-Reichhart, M. Distel, H.L. Janovjak, Angewandte Chemie International Edition 56 (2017) 4608–4611.","mla":"Kainrath, Stephanie, et al. “Green-Light-Induced Inactivation of Receptor Signaling Using Cobalamin-Binding Domains.” Angewandte Chemie International Edition, vol. 56, no. 16, Wiley, 2017, pp. 4608–11, doi:10.1002/anie.201611998.","chicago":"Kainrath, Stephanie, Manuela Stadler, Eva Gschaider-Reichhart, Martin Distel, and Harald L Janovjak. “Green-Light-Induced Inactivation of Receptor Signaling Using Cobalamin-Binding Domains.” Angewandte Chemie International Edition. Wiley, 2017. https://doi.org/10.1002/anie.201611998."},"acknowledgement":"This work was supported by a grant from the European Union􏰝s Seventh Framework Programme (CIG-303564). E.R. was supported by the graduate program MolecularDrugTargets (Austrian Science Fund (FWF), W1232) and a FemTech fellowship (Austrian Research Promotion Agency, 3580812)","year":"2017","publisher":"Wiley","external_id":{"isi":["000398154000038"]},"issue":"16","file":[{"creator":"dernst","content_type":"application/pdf","date_updated":"2019-01-18T09:39:55Z","relation":"main_file","access_level":"open_access","date_created":"2019-01-18T09:39:55Z","file_size":2614942,"file_name":"2017_communications_Kainrath.pdf","file_id":"5845","success":1}],"intvolume":" 56","date_updated":"2026-10-26T23:30:51Z","publist_id":"6362","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"text":"Optogenetics and photopharmacology provide spatiotemporally precise control over protein interactions and protein function in cells and animals. Optogenetic methods that are sensitive to green light and can be used to break protein complexes are not broadly available but would enable multichromatic experiments with previously inaccessible biological targets. Herein, we repurposed cobalamin (vitamin B12) binding domains of bacterial CarH transcription factors for green-light-induced receptor dissociation. In cultured cells, we observed oligomerization-induced cell signaling for the fibroblast growth factor receptor 1 fused to cobalamin-binding domains in the dark that was rapidly eliminated upon illumination. In zebrafish embryos expressing fusion receptors, green light endowed control over aberrant fibroblast growth factor signaling during development. Green-light-induced domain dissociation and light-inactivated receptors will critically expand the optogenetic toolbox for control of biological processes.","lang":"eng"}],"file_date_updated":"2019-01-18T09:39:55Z","ec_funded":1,"ddc":["540"],"has_accepted_license":"1","date_published":"2017-03-20T00:00:00Z","fulldoi":"https://doi.org/10.1002/anie.201611998","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"}},{"main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1605.07332"}],"type":"conference","oa":1,"title":"Relevant sparse codes with variational information bottleneck","author":[{"first_name":"Matthew J","orcid":"0000-0001-7782-4436","full_name":"Chalk, Matthew J","id":"2BAAC544-F248-11E8-B48F-1D18A9856A87","last_name":"Chalk"},{"first_name":"Olivier","full_name":"Marre, Olivier","last_name":"Marre"},{"full_name":"Tkacik, Gasper","last_name":"Tkacik","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","first_name":"Gasper"}],"scopus_import":"1","conference":{"location":"Barcelona, Spain","end_date":"2016-12-10","name":"NIPS: Neural Information Processing Systems","start_date":"2016-12-05"},"related_material":{"link":[{"url":"https://papers.nips.cc/paper/6101-relevant-sparse-codes-with-variational-information-bottleneck","relation":"other"}]},"quality_controlled":"1","date_created":"2018-12-11T11:50:03Z","article_processing_charge":"No","month":"12","volume":29,"language":[{"iso":"eng"}],"department":[{"_id":"GaTk"}],"publication_status":"published","page":"1965-1973","date_published":"2016-12-01T00:00:00Z","abstract":[{"text":"In many applications, it is desirable to extract only the relevant aspects of data. A principled way to do this is the information bottleneck (IB) method, where one seeks a code that maximises information about a relevance variable, Y, while constraining the information encoded about the original data, X. Unfortunately however, the IB method is computationally demanding when data are high-dimensional and/or non-gaussian. Here we propose an approximate variational scheme for maximising a lower bound on the IB objective, analogous to variational EM. Using this method, we derive an IB algorithm to recover features that are both relevant and sparse. Finally, we demonstrate how kernelised versions of the algorithm can be used to address a broad range of problems with non-linear relation between X and Y.","lang":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"6298","date_updated":"2025-06-03T11:33:51Z","alternative_title":["Advances in Neural Information Processing Systems"],"intvolume":" 29","external_id":{"arxiv":["1605.07332"]},"citation":{"ista":"Chalk MJ, Marre O, Tkačik G. 2016. Relevant sparse codes with variational information bottleneck. NIPS: Neural Information Processing Systems, Advances in Neural Information Processing Systems, vol. 29, 1965–1973.","ama":"Chalk MJ, Marre O, Tkačik G. Relevant sparse codes with variational information bottleneck. In: Vol 29. Neural Information Processing Systems Foundation; 2016:1965-1973.","apa":"Chalk, M. J., Marre, O., & Tkačik, G. (2016). Relevant sparse codes with variational information bottleneck (Vol. 29, pp. 1965–1973). Presented at the NIPS: Neural Information Processing Systems, Barcelona, Spain: Neural Information Processing Systems Foundation.","ieee":"M. J. Chalk, O. Marre, and G. Tkačik, “Relevant sparse codes with variational information bottleneck,” presented at the NIPS: Neural Information Processing Systems, Barcelona, Spain, 2016, vol. 29, pp. 1965–1973.","chicago":"Chalk, Matthew J, Olivier Marre, and Gašper Tkačik. “Relevant Sparse Codes with Variational Information Bottleneck,” 29:1965–73. Neural Information Processing Systems Foundation, 2016.","mla":"Chalk, Matthew J., et al. Relevant Sparse Codes with Variational Information Bottleneck. Vol. 29, Neural Information Processing Systems Foundation, 2016, pp. 1965–73.","short":"M.J. Chalk, O. Marre, G. Tkačik, in:, Neural Information Processing Systems Foundation, 2016, pp. 1965–1973."},"year":"2016","publisher":"Neural Information Processing Systems Foundation","arxiv":1,"day":"01","oa_version":"Preprint","_id":"1082","status":"public"},{"day":"12","isi":1,"acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (DFG SFB 780 A2, A.K.; SFB TR3 I.V. and EXC 257, I.V.; FOR 2143, A.K. and I.V.), Spemann Graduate School (D.A.), BIOSS-2 (A6, A.K.), the Swiss National Science Foundation (3100A0-117816, B.B.), The McNaught Bequest (S.A.B. and I.V.), and Tenovus Scotland (I.V.).\r\n\r\n\r\nWe thank Cheryl Hutton and Chinmaya Sadangi for their contributions to neuronal reconstruction as well as Natalie Wernet, Sigrun Nestel, Anikó Schneider, Ina Wolter, and Ulrich Noeller for their excellent technical support. VGAT-Venus transgenic rats were generated by Drs Y. Yanagawa, M. Hirabayashi, and Y. Kawaguchi in National Institute for Physiological Sciences, Okazaki, Japan, using pCS2-Venus provided by Dr A. Miyawaki. The monoclonal mouse CCK antibody was generously provided by Dr G.V. Ohning, CURE Center, UCLA, CA. ","year":"2016","citation":{"chicago":"Booker, Sam, Daniel Althof, Anna Gross, Desiree Loreth, Johanna Müller, Andreas Unger, Bernd Fakler, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.” Cerebral Cortex. Oxford University Press, 2016. https://doi.org/10.1093/cercor/bhw090.","mla":"Booker, Sam, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.” Cerebral Cortex, vol. 27, no. 3, Oxford University Press, 2016, pp. 2318–34, doi:10.1093/cercor/bhw090.","short":"S. Booker, D. Althof, A. Gross, D. Loreth, J. Müller, A. Unger, B. Fakler, A. Varro, M. Watanabe, M. Gassmann, B. Bettler, R. Shigemoto, I. Vida, Á. Kulik, Cerebral Cortex 27 (2016) 2318–2334.","ista":"Booker S, Althof D, Gross A, Loreth D, Müller J, Unger A, Fakler B, Varro A, Watanabe M, Gassmann M, Bettler B, Shigemoto R, Vida I, Kulik Á. 2016. KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. 27(3), 2318–2334.","ama":"Booker S, Althof D, Gross A, et al. KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. 2016;27(3):2318-2334. doi:10.1093/cercor/bhw090","apa":"Booker, S., Althof, D., Gross, A., Loreth, D., Müller, J., Unger, A., … Kulik, Á. (2016). KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bhw090","ieee":"S. Booker et al., “KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons,” Cerebral Cortex, vol. 27, no. 3. Oxford University Press, pp. 2318–2334, 2016."},"publisher":"Oxford University Press","_id":"1083","status":"public","oa_version":"None","external_id":{"isi":["000397636600048"]},"issue":"3","intvolume":" 27","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","abstract":[{"lang":"eng","text":" Cholecystokinin-expressing interneurons (CCK-INs) mediate behavior state-dependent inhibition in cortical circuits and themselves receive strong GABAergic input. However, it remains unclear to what extent GABABreceptors (GABABRs) contribute to their inhibitory control. Using immunoelectron microscopy, we found that CCK-INs in the rat hippocampus possessed high levels of dendritic GABABRs and KCTD12 auxiliary proteins, whereas postsynaptic effector Kir3 channels were present at lower levels. Consistently, whole-cell recordings revealed slow GABABR-mediated inhibitory postsynaptic currents (IPSCs) in most CCK-INs. In spite of the higher surface density of GABABRs in CCK-INs than in CA1 principal cells, the amplitudes of IPSCs were comparable, suggesting that the expression of Kir3 channels is the limiting factor for the GABABR currents in these INs. Morphological analysis showed that CCK-INs were diverse, comprising perisomatic-targeting basket cells (BCs), as well as dendrite-targeting (DT) interneurons, including a previously undescribed DT type. GABABR-mediated IPSCs in CCK-INs were large in BCs, but small in DT subtypes. In response to prolonged activation, GABABR-mediated currents displayed strong desensitization, which was absent in KCTD12-deficient mice. This study highlights that GABABRs differentially control CCK-IN subtypes, and the kinetics and desensitization of GABABR-mediated currents are modulated by KCTD12 proteins. "}],"publist_id":"6297","date_updated":"2025-09-22T14:19:11Z","date_published":"2016-04-12T00:00:00Z","fulldoi":"https://doi.org/10.1093/cercor/bhw090","month":"04","page":"2318 - 2334","department":[{"_id":"RySh"}],"language":[{"iso":"eng"}],"volume":27,"publication_status":"published","quality_controlled":"1","date_created":"2018-12-11T11:50:03Z","article_processing_charge":"No","publication":"Cerebral Cortex","author":[{"first_name":"Sam","last_name":"Booker","full_name":"Booker, Sam"},{"last_name":"Althof","full_name":"Althof, Daniel","first_name":"Daniel"},{"first_name":"Anna","full_name":"Gross, Anna","last_name":"Gross"},{"first_name":"Desiree","full_name":"Loreth, Desiree","last_name":"Loreth"},{"first_name":"Johanna","last_name":"Müller","full_name":"Müller, Johanna"},{"first_name":"Andreas","last_name":"Unger","full_name":"Unger, Andreas"},{"first_name":"Bernd","full_name":"Fakler, Bernd","last_name":"Fakler"},{"first_name":"Andrea","last_name":"Varro","full_name":"Varro, Andrea"},{"first_name":"Masahiko","full_name":"Watanabe, Masahiko","last_name":"Watanabe"},{"first_name":"Martin","last_name":"Gassmann","full_name":"Gassmann, Martin"},{"first_name":"Bernhard","last_name":"Bettler","full_name":"Bettler, Bernhard"},{"first_name":"Ryuichi","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi"},{"first_name":"Imre","full_name":"Vida, Imre","last_name":"Vida"},{"full_name":"Kulik, Ákos","last_name":"Kulik","first_name":"Ákos"}],"scopus_import":"1","title":"KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons","doi":"10.1093/cercor/bhw090","type":"journal_article"},{"oa_version":"Published Version","_id":"1090","status":"public","publisher":"Schloss Dagstuhl - Leibniz-Zentrum für Informatik","citation":{"ieee":"K. Chatterjee, T. A. Henzinger, and J. Otop, “Nested weighted limit-average automata of bounded width,” presented at the MFCS: Mathematical Foundations of Computer Science, Krakow; Poland, 2016, vol. 58.","apa":"Chatterjee, K., Henzinger, T. A., & Otop, J. (2016). Nested weighted limit-average automata of bounded width (Vol. 58). Presented at the MFCS: Mathematical Foundations of Computer Science, Krakow; Poland: Schloss Dagstuhl - Leibniz-Zentrum für Informatik. https://doi.org/10.4230/LIPIcs.MFCS.2016.24","ista":"Chatterjee K, Henzinger TA, Otop J. 2016. Nested weighted limit-average automata of bounded width. MFCS: Mathematical Foundations of Computer Science, LIPIcs, vol. 58, 24.","ama":"Chatterjee K, Henzinger TA, Otop J. Nested weighted limit-average automata of bounded width. In: Vol 58. Schloss Dagstuhl - Leibniz-Zentrum für Informatik; 2016. doi:10.4230/LIPIcs.MFCS.2016.24","short":"K. Chatterjee, T.A. Henzinger, J. Otop, in:, Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016.","mla":"Chatterjee, Krishnendu, et al. Nested Weighted Limit-Average Automata of Bounded Width. Vol. 58, 24, Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016, doi:10.4230/LIPIcs.MFCS.2016.24.","chicago":"Chatterjee, Krishnendu, Thomas A Henzinger, and Jan Otop. “Nested Weighted Limit-Average Automata of Bounded Width,” Vol. 58. Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016. https://doi.org/10.4230/LIPIcs.MFCS.2016.24."},"acknowledgement":"This research was supported in part by the Austrian Science Fund (FWF) under grants S11402-N23\r\n(RiSE/SHiNE) and Z211-N23 (Wittgenstein Award), ERC Start grant (279307: Graph Games), Vienna\r\nScience and Technology Fund (WWTF) through project ICT15-003 and by the National Science Centre\r\n(NCN), Poland under grant 2014/15/D/ST6/04543.","year":"2016","day":"01","intvolume":" 58","file":[{"creator":"system","content_type":"application/pdf","date_updated":"2018-12-12T10:17:31Z","relation":"main_file","access_level":"open_access","date_created":"2018-12-12T10:17:31Z","file_size":564560,"file_name":"IST-2017-795-v1+1_LIPIcs-MFCS-2016-24.pdf","file_id":"5286"}],"alternative_title":["LIPIcs"],"date_updated":"2025-07-10T11:50:02Z","publist_id":"6286","ec_funded":1,"abstract":[{"lang":"eng","text":" While weighted automata provide a natural framework to express quantitative properties, many basic properties like average response time cannot be expressed with weighted automata. Nested weighted automata extend weighted automata and consist of a master automaton and a set of slave automata that are invoked by the master automaton. Nested weighted automata are strictly more expressive than weighted automata (e.g., average response time can be expressed with nested weighted automata), but the basic decision questions have higher complexity (e.g., for deterministic automata, the emptiness question for nested weighted automata is PSPACE-hard, whereas the corresponding complexity for weighted automata is PTIME). We consider a natural subclass of nested weighted automata where at any point at most a bounded number k of slave automata can be active. We focus on automata whose master value function is the limit average. We show that these nested weighted automata with bounded width are strictly more expressive than weighted automata (e.g., average response time with no overlapping requests can be expressed with bound k=1, but not with non-nested weighted automata). We show that the complexity of the basic decision problems (i.e., emptiness and universality) for the subclass with k constant matches the complexity for weighted automata. Moreover, when k is part of the input given in unary we establish PSPACE-completeness."}],"file_date_updated":"2018-12-12T10:17:31Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"fulldoi":"https://doi.org/10.4230/LIPIcs.MFCS.2016.24","has_accepted_license":"1","date_published":"2016-08-01T00:00:00Z","ddc":["004"],"pubrep_id":"795","publication_status":"published","volume":58,"department":[{"_id":"KrCh"},{"_id":"ToHe"}],"language":[{"iso":"eng"}],"month":"08","article_processing_charge":"No","date_created":"2018-12-11T11:50:05Z","quality_controlled":"1","project":[{"call_identifier":"FWF","name":"Rigorous Systems Engineering","_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23"},{"call_identifier":"FWF","_id":"25F42A32-B435-11E9-9278-68D0E5697425","name":"Formal methods for the design and analysis of complex systems","grant_number":"Z211"},{"call_identifier":"FP7","name":"Quantitative Graph Games: Theory and Applications","_id":"2581B60A-B435-11E9-9278-68D0E5697425","grant_number":"279307"},{"grant_number":"ICT15-003","name":"Efficient Algorithms for Computer Aided Verification","_id":"25892FC0-B435-11E9-9278-68D0E5697425"}],"scopus_import":"1","conference":{"location":"Krakow; Poland","end_date":"2016-08-26","name":"MFCS: Mathematical Foundations of Computer Science","start_date":"2016-08-22"},"author":[{"orcid":"0000-0002-4561-241X","first_name":"Krishnendu","full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000−0002−2985−7724","first_name":"Thomas A","full_name":"Henzinger, Thomas A","last_name":"Henzinger","id":"40876CD8-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jan","id":"2FC5DA74-F248-11E8-B48F-1D18A9856A87","last_name":"Otop","full_name":"Otop, Jan"}],"type":"conference","doi":"10.4230/LIPIcs.MFCS.2016.24","title":"Nested weighted limit-average automata of bounded width","oa":1,"article_number":"24"},{"date_updated":"2026-04-15T10:02:12Z","publist_id":"6283","alternative_title":["LIPIcs"],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","abstract":[{"lang":"eng","text":"We introduce a general class of distances (metrics) between Markov chains, which are based on linear behaviour. This class encompasses distances given topologically (such as the total variation distance or trace distance) as well as by temporal logics or automata. We investigate which of the distances can be approximated by observing the systems, i.e. by black-box testing or simulation, and we provide both negative and positive results. "}],"ec_funded":1,"file_date_updated":"2018-12-12T10:11:39Z","ddc":["004"],"date_published":"2016-08-01T00:00:00Z","has_accepted_license":"1","fulldoi":"https://doi.org/10.4230/LIPIcs.CONCUR.2016.20","tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"status":"public","_id":"1093","oa_version":"Published Version","day":"01","acknowledgement":"This research was funded in part by the European Research Council (ERC) under grant agreement 267989\r\n(QUAREM), the Austrian Science Fund (FWF) under grants project S11402-N23 (RiSE and SHiNE)\r\nand Z211-N23 (Wittgenstein Award), by the Czech Science Foundation Grant No. P202/12/G061, and\r\nby the SNSF Advanced Postdoc. Mobility Fellowship – grant number P300P2_161067.","citation":{"apa":"Daca, P., Henzinger, T. A., Kretinsky, J., & Petrov, T. (2016). Linear distances between Markov chains (Vol. 59). Presented at the CONCUR: Concurrency Theory, Quebec City; Canada: Schloss Dagstuhl - Leibniz-Zentrum für Informatik. https://doi.org/10.4230/LIPIcs.CONCUR.2016.20","ieee":"P. Daca, T. A. Henzinger, J. Kretinsky, and T. Petrov, “Linear distances between Markov chains,” presented at the CONCUR: Concurrency Theory, Quebec City; Canada, 2016, vol. 59.","ista":"Daca P, Henzinger TA, Kretinsky J, Petrov T. 2016. Linear distances between Markov chains. CONCUR: Concurrency Theory, LIPIcs, vol. 59, 20.","ama":"Daca P, Henzinger TA, Kretinsky J, Petrov T. Linear distances between Markov chains. In: Vol 59. Schloss Dagstuhl - Leibniz-Zentrum für Informatik; 2016. doi:10.4230/LIPIcs.CONCUR.2016.20","mla":"Daca, Przemyslaw, et al. Linear Distances between Markov Chains. Vol. 59, 20, Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016, doi:10.4230/LIPIcs.CONCUR.2016.20.","short":"P. Daca, T.A. Henzinger, J. Kretinsky, T. Petrov, in:, Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016.","chicago":"Daca, Przemyslaw, Thomas A Henzinger, Jan Kretinsky, and Tatjana Petrov. “Linear Distances between Markov Chains,” Vol. 59. Schloss Dagstuhl - Leibniz-Zentrum für Informatik, 2016. https://doi.org/10.4230/LIPIcs.CONCUR.2016.20."},"year":"2016","publisher":"Schloss Dagstuhl - Leibniz-Zentrum für Informatik","file":[{"file_id":"4895","file_size":501827,"date_created":"2018-12-12T10:11:39Z","file_name":"IST-2017-794-v1+1_LIPIcs-CONCUR-2016-20.pdf","access_level":"open_access","relation":"main_file","creator":"system","date_updated":"2018-12-12T10:11:39Z","content_type":"application/pdf"}],"intvolume":" 59","conference":{"name":"CONCUR: Concurrency Theory","end_date":"2016-08-26","location":"Quebec City; Canada","start_date":"2016-08-23"},"scopus_import":1,"author":[{"full_name":"Daca, Przemyslaw","id":"49351290-F248-11E8-B48F-1D18A9856A87","last_name":"Daca","first_name":"Przemyslaw"},{"orcid":"0000−0002−2985−7724","first_name":"Thomas A","full_name":"Henzinger, Thomas A","last_name":"Henzinger","id":"40876CD8-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jan","orcid":"0000-0002-8122-2881","id":"44CEF464-F248-11E8-B48F-1D18A9856A87","last_name":"Kretinsky","full_name":"Kretinsky, Jan"},{"first_name":"Tatjana","orcid":"0000-0002-9041-0905","full_name":"Petrov, Tatjana","last_name":"Petrov","id":"3D5811FC-F248-11E8-B48F-1D18A9856A87"}],"oa":1,"title":"Linear distances between Markov chains","doi":"10.4230/LIPIcs.CONCUR.2016.20","type":"conference","article_number":"20","department":[{"_id":"ToHe"},{"_id":"KrCh"},{"_id":"CaGu"}],"language":[{"iso":"eng"}],"volume":59,"publication_status":"published","pubrep_id":"794","month":"08","date_created":"2018-12-11T11:50:06Z","project":[{"grant_number":"267989","call_identifier":"FP7","_id":"25EE3708-B435-11E9-9278-68D0E5697425","name":"Quantitative Reactive Modeling"},{"grant_number":"S 11407_N23","name":"Rigorous Systems Engineering","_id":"25832EC2-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"Z211","call_identifier":"FWF","_id":"25F42A32-B435-11E9-9278-68D0E5697425","name":"Formal methods for the design and analysis of complex systems"}],"related_material":{"record":[{"status":"public","id":"1155","relation":"dissertation_contains"}]},"quality_controlled":"1"},{"quality_controlled":"1","project":[{"call_identifier":"FP7","_id":"25CD3DD2-B435-11E9-9278-68D0E5697425","name":"Localization of ion channels and receptors by two and three-dimensional immunoelectron microscopic approaches","grant_number":"604102"}],"date_created":"2018-12-11T11:50:06Z","article_processing_charge":"No","month":"08","department":[{"_id":"RySh"}],"volume":1474,"language":[{"iso":"eng"}],"publication_status":"published","page":"203 - 216","doi":"10.1007/978-1-4939-6352-2_12","type":"book_chapter","publication_identifier":{"eissn":["1611-3349"],"issn":["0302-9743"]},"title":"Immunogold protein localization on grid-glued freeze-fracture replicas","author":[{"first_name":"Harumi","orcid":"0000-0001-7429-7896","full_name":"Harada, Harumi","id":"2E55CDF2-F248-11E8-B48F-1D18A9856A87","last_name":"Harada"},{"first_name":"Ryuichi","orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto"}],"publication":"High-Resolution Imaging of Cellular Proteins","intvolume":" 1474","acknowledged_ssus":[{"_id":"EM-Fac"}],"citation":{"ista":"Harada H, Shigemoto R. 2016.Immunogold protein localization on grid-glued freeze-fracture replicas. In: High-Resolution Imaging of Cellular Proteins. Methods in Molecular Biology, vol. 1474, 203–216.","ama":"Harada H, Shigemoto R. Immunogold protein localization on grid-glued freeze-fracture replicas. In: High-Resolution Imaging of Cellular Proteins. Vol 1474. Springer; 2016:203-216. doi:10.1007/978-1-4939-6352-2_12","apa":"Harada, H., & Shigemoto, R. (2016). Immunogold protein localization on grid-glued freeze-fracture replicas. In High-Resolution Imaging of Cellular Proteins (Vol. 1474, pp. 203–216). Springer. https://doi.org/10.1007/978-1-4939-6352-2_12","ieee":"H. Harada and R. Shigemoto, “Immunogold protein localization on grid-glued freeze-fracture replicas,” in High-Resolution Imaging of Cellular Proteins, vol. 1474, Springer, 2016, pp. 203–216.","chicago":"Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization on Grid-Glued Freeze-Fracture Replicas.” In High-Resolution Imaging of Cellular Proteins, 1474:203–16. Springer, 2016. https://doi.org/10.1007/978-1-4939-6352-2_12.","short":"H. Harada, R. Shigemoto, in:, High-Resolution Imaging of Cellular Proteins, Springer, 2016, pp. 203–216.","mla":"Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization on Grid-Glued Freeze-Fracture Replicas.” High-Resolution Imaging of Cellular Proteins, vol. 1474, Springer, 2016, pp. 203–16, doi:10.1007/978-1-4939-6352-2_12."},"acknowledgement":"We thank Prof. Elek Molnár for providing us a pan-AMPAR anti-body used in Fig.2 and Dr. Ludek Lovicar for technical assistance in scanning electron microscope imaging. This work was supported by the European Union (HBP—Project Ref. 604102). ","year":"2016","publisher":"Springer","day":"12","oa_version":"None","status":"public","_id":"1094","fulldoi":"https://doi.org/10.1007/978-1-4939-6352-2_12","date_published":"2016-08-12T00:00:00Z","ec_funded":1,"abstract":[{"lang":"eng","text":"Immunogold labeling of freeze-fracture replicas has recently been used for high-resolution visualization of protein localization in electron microscopy. This method has higher labeling efficiency than conventional immunogold methods for membrane molecules allowing precise quantitative measurements. However, one of the limitations of freeze-fracture replica immunolabeling is difficulty in keeping structural orientation and identifying labeled profiles in complex tissues like brain. The difficulty is partly due to fragmentation of freeze-fracture replica preparations during labeling procedures and limited morphological clues on the replica surface. To overcome these issues, we introduce here a grid-glued replica method combined with SEM observation. This method allows histological staining before dissolving the tissue and easy handling of replicas during immunogold labeling, and keeps the whole replica surface intact without fragmentation. The procedure described here is also useful for matched double-replica analysis allowing further identification of labeled profiles in corresponding P-face and E-face."}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","alternative_title":["Methods in Molecular Biology"],"publist_id":"6281","date_updated":"2025-04-15T07:12:21Z"}]