[{"date_updated":"2024-03-25T11:52:26Z","extern":"1","_id":"15160","type":"journal_article","article_type":"original","status":"public","keyword":["Cell Biology","Molecular Biology"],"publication_identifier":{"issn":["1097-2765"]},"publication_status":"published","language":[{"iso":"eng"}],"issue":"5","volume":58,"abstract":[{"text":"The circadian clock orchestrates global changes in transcriptional regulation on a daily basis via the bHLH-PAS transcription factor CLOCK:BMAL1. Pathways driven by other bHLH-PAS transcription factors have a homologous repressor that modulates activity on a tissue-specific basis, but none have been identified for CLOCK:BMAL1. We show here that the cancer/testis antigen PASD1 fulfills this role to suppress circadian rhythms. PASD1 is evolutionarily related to CLOCK and interacts with the CLOCK:BMAL1 complex to repress transcriptional activation. Expression of PASD1 is restricted to germline tissues in healthy individuals but can be induced in cells of somatic origin upon oncogenic transformation. Reducing PASD1 in human cancer cells significantly increases the amplitude of transcriptional oscillations to generate more robust circadian rhythms. Our results describe a function for a germline-specific protein in regulation of the circadian clock and provide a molecular link from oncogenic transformation to suppression of circadian rhythms.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.molcel.2015.03.031"}],"month":"06","intvolume":" 58","citation":{"ieee":"A. K. Michael et al., “Cancer/Testis antigen PASD1 silences the circadian clock,” Molecular Cell, vol. 58, no. 5. Elsevier, pp. 743–754, 2015.","short":"A.K. Michael, S.L. Harvey, P.J. Sammons, A.P. Anderson, H.M. Kopalle, A.H. Banham, C.L. Partch, Molecular Cell 58 (2015) 743–754.","ama":"Michael AK, Harvey SL, Sammons PJ, et al. Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. 2015;58(5):743-754. doi:10.1016/j.molcel.2015.03.031","apa":"Michael, A. K., Harvey, S. L., Sammons, P. J., Anderson, A. P., Kopalle, H. M., Banham, A. H., & Partch, C. L. (2015). Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. Elsevier. https://doi.org/10.1016/j.molcel.2015.03.031","mla":"Michael, Alicia K., et al. “Cancer/Testis Antigen PASD1 Silences the Circadian Clock.” Molecular Cell, vol. 58, no. 5, Elsevier, 2015, pp. 743–54, doi:10.1016/j.molcel.2015.03.031.","ista":"Michael AK, Harvey SL, Sammons PJ, Anderson AP, Kopalle HM, Banham AH, Partch CL. 2015. Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. 58(5), 743–754.","chicago":"Michael, Alicia K., Stacy L. Harvey, Patrick J. Sammons, Amanda P. Anderson, Hema M. Kopalle, Alison H. Banham, and Carrie L. Partch. “Cancer/Testis Antigen PASD1 Silences the Circadian Clock.” Molecular Cell. Elsevier, 2015. https://doi.org/10.1016/j.molcel.2015.03.031."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Michael","full_name":"Michael, Alicia Kathleen","first_name":"Alicia Kathleen","id":"6437c950-2a03-11ee-914d-d6476dd7b75c"},{"first_name":"Stacy L.","full_name":"Harvey, Stacy L.","last_name":"Harvey"},{"first_name":"Patrick J.","full_name":"Sammons, Patrick J.","last_name":"Sammons"},{"last_name":"Anderson","full_name":"Anderson, Amanda P.","first_name":"Amanda P."},{"first_name":"Hema M.","full_name":"Kopalle, Hema M.","last_name":"Kopalle"},{"first_name":"Alison H.","full_name":"Banham, Alison H.","last_name":"Banham"},{"full_name":"Partch, Carrie L.","last_name":"Partch","first_name":"Carrie L."}],"article_processing_charge":"No","title":"Cancer/Testis antigen PASD1 silences the circadian clock","year":"2015","day":"04","publication":"Molecular Cell","page":"743-754","doi":"10.1016/j.molcel.2015.03.031","date_published":"2015-06-04T00:00:00Z","date_created":"2024-03-21T07:58:08Z","publisher":"Elsevier","quality_controlled":"1","oa":1},{"_id":"15159","type":"journal_article","article_type":"original","status":"public","keyword":["Molecular Biology","Biochemistry"],"date_updated":"2024-03-25T11:53:58Z","extern":"1","abstract":[{"lang":"eng","text":"It is widely recognized that BMAL1 is an essential subunit of the primary transcription factor that drives rhythmic circadian transcription in the nucleus. In a surprising turn, Lipton et al. now show that BMAL1 rhythmically interacts with translational machinery in the cytosol to stimulate protein synthesis in response to mTOR signaling."}],"oa_version":"None","scopus_import":"1","month":"09","intvolume":" 40","publication_identifier":{"issn":["0968-0004"]},"publication_status":"published","language":[{"iso":"eng"}],"issue":"9","volume":40,"citation":{"chicago":"Michael, Alicia K., Hande Asimgil, and Carrie L. Partch. “Cytosolic BMAL1 Moonlights as a Translation Factor.” Trends in Biochemical Sciences. Elsevier, 2015. https://doi.org/10.1016/j.tibs.2015.07.006.","ista":"Michael AK, Asimgil H, Partch CL. 2015. Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. 40(9), 489–490.","mla":"Michael, Alicia K., et al. “Cytosolic BMAL1 Moonlights as a Translation Factor.” Trends in Biochemical Sciences, vol. 40, no. 9, Elsevier, 2015, pp. 489–90, doi:10.1016/j.tibs.2015.07.006.","ieee":"A. K. Michael, H. Asimgil, and C. L. Partch, “Cytosolic BMAL1 moonlights as a translation factor,” Trends in Biochemical Sciences, vol. 40, no. 9. Elsevier, pp. 489–490, 2015.","short":"A.K. Michael, H. Asimgil, C.L. Partch, Trends in Biochemical Sciences 40 (2015) 489–490.","ama":"Michael AK, Asimgil H, Partch CL. Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. 2015;40(9):489-490. doi:10.1016/j.tibs.2015.07.006","apa":"Michael, A. K., Asimgil, H., & Partch, C. L. (2015). Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. Elsevier. https://doi.org/10.1016/j.tibs.2015.07.006"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Alicia Kathleen","id":"6437c950-2a03-11ee-914d-d6476dd7b75c","last_name":"Michael","full_name":"Michael, Alicia Kathleen"},{"full_name":"Asimgil, Hande","last_name":"Asimgil","first_name":"Hande"},{"first_name":"Carrie L.","full_name":"Partch, Carrie L.","last_name":"Partch"}],"article_processing_charge":"No","title":"Cytosolic BMAL1 moonlights as a translation factor","quality_controlled":"1","publisher":"Elsevier","year":"2015","day":"01","publication":"Trends in Biochemical Sciences","page":"489-490","date_published":"2015-09-01T00:00:00Z","doi":"10.1016/j.tibs.2015.07.006","date_created":"2024-03-21T07:57:44Z"},{"abstract":[{"text":"The emergence of drug resistant pathogens is a serious public health problem. It is a long-standing goal to predict rates of resistance evolution and design optimal treatment strategies accordingly. To this end, it is crucial to reveal the underlying causes of drug-specific differences in the evolutionary dynamics leading to resistance. However, it remains largely unknown why the rates of resistance evolution via spontaneous mutations and the diversity of mutational paths vary substantially between drugs. Here we comprehensively quantify the distribution of fitness effects (DFE) of mutations, a key determinant of evolutionary dynamics, in the presence of eight antibiotics representing the main modes of action. Using precise high-throughput fitness measurements for genome-wide Escherichia coli gene deletion strains, we find that the width of the DFE varies dramatically between antibiotics and, contrary to conventional wisdom, for some drugs the DFE width is lower than in the absence of stress. We show that this previously underappreciated divergence in DFE width among antibiotics is largely caused by their distinct drug-specific dose-response characteristics. Unlike the DFE, the magnitude of the changes in tolerated drug concentration resulting from genome-wide mutations is similar for most drugs but exceptionally small for the antibiotic nitrofurantoin, i.e., mutations generally have considerably smaller resistance effects for nitrofurantoin than for other drugs. A population genetics model predicts that resistance evolution for drugs with this property is severely limited and confined to reproducible mutational paths. We tested this prediction in laboratory evolution experiments using the “morbidostat”, a device for evolving bacteria in well-controlled drug environments. Nitrofurantoin resistance indeed evolved extremely slowly via reproducible mutations—an almost paradoxical behavior since this drug causes DNA damage and increases the mutation rate. Overall, we identified novel quantitative characteristics of the evolutionary landscape that provide the conceptual foundation for predicting the dynamics of drug resistance evolution.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 13","month":"11","publication_status":"published","language":[{"iso":"eng"}],"file":[{"creator":"system","file_size":1387760,"date_updated":"2020-07-14T12:45:07Z","file_name":"IST-2016-468-v1+1_journal.pbio.1002299.pdf","date_created":"2018-12-12T10:09:00Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"4723","checksum":"0e82e3279f50b15c6c170c042627802b"}],"ec_funded":1,"license":"https://creativecommons.org/licenses/by/4.0/","issue":"11","volume":13,"related_material":{"record":[{"id":"9711","status":"public","relation":"research_data"},{"relation":"research_data","id":"9765","status":"public"},{"status":"public","id":"6263","relation":"dissertation_contains"}]},"_id":"1619","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"468","status":"public","date_updated":"2024-03-27T23:30:28Z","ddc":["570"],"department":[{"_id":"ToBo"}],"file_date_updated":"2020-07-14T12:45:07Z","oa":1,"publisher":"Public Library of Science","quality_controlled":"1","year":"2015","has_accepted_license":"1","publication":"PLoS Biology","day":"18","date_created":"2018-12-11T11:53:04Z","doi":"10.1371/journal.pbio.1002299","date_published":"2015-11-18T00:00:00Z","article_number":"e1002299","project":[{"grant_number":"RGP0042/2013","name":"Revealing the fundamental limits of cell growth","_id":"25EB3A80-B435-11E9-9278-68D0E5697425"},{"name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FP7","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","grant_number":"303507","name":"Optimality principles in responses to antibiotics"}],"citation":{"ista":"Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan D, Toprak E, Bollenbach MT. 2015. Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. 13(11), e1002299.","chicago":"Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek, Dilay Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Quantifying the Determinants of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology. Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.","apa":"Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D., Toprak, E., & Bollenbach, M. T. (2015). Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299","ama":"Chevereau G, Lukacisinova M, Batur T, et al. Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. 2015;13(11). doi:10.1371/journal.pbio.1002299","ieee":"G. Chevereau et al., “Quantifying the determinants of evolutionary dynamics leading to drug resistance,” PLoS Biology, vol. 13, no. 11. Public Library of Science, 2015.","short":"G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D. Ayhan, E. Toprak, M.T. Bollenbach, PLoS Biology 13 (2015).","mla":"Chevereau, Guillaume, et al. “Quantifying the Determinants of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology, vol. 13, no. 11, e1002299, Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"5547","author":[{"full_name":"Chevereau, Guillaume","last_name":"Chevereau","first_name":"Guillaume","id":"424D78A0-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Dravecka","full_name":"Dravecka, Marta","orcid":"0000-0002-2519-8004","first_name":"Marta","id":"4342E402-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Tugce","last_name":"Batur","full_name":"Batur, Tugce"},{"first_name":"Aysegul","last_name":"Guvenek","full_name":"Guvenek, Aysegul"},{"first_name":"Dilay","full_name":"Ayhan, Dilay","last_name":"Ayhan"},{"last_name":"Toprak","full_name":"Toprak, Erdal","first_name":"Erdal"},{"orcid":"0000-0003-4398-476X","full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach","first_name":"Mark Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"}],"title":"Quantifying the determinants of evolutionary dynamics leading to drug resistance"},{"oa":1,"publisher":"National Academy of Sciences","quality_controlled":"1","acknowledgement":"We thank Michele Vendruscolo, Iskra Staneva, and William M. Jacobs, for helpful discussions. A.Š. acknowledges support from the Human Frontier Science Program and Emmanuel College. Y.C.C. and D.F. are supported by Engineering and Physical Sciences Research Council Programme Grant EP/I001352/1. T.P.J.K. acknowledges the Frances and Augustus Newman Foundation, the European Research Council, and the Biotechnology and Biological Sciences Research Council. D.F. acknowledges European Research Council Advanced Grant 227758.","date_created":"2021-11-29T13:09:53Z","doi":"10.1073/pnas.1410159111","date_published":"2014-12-01T00:00:00Z","page":"17869-17874","publication":"Proceedings of the National Academy of Sciences","day":"01","year":"2014","title":"Crucial role of nonspecific interactions in amyloid nucleation","article_processing_charge":"No","external_id":{"pmid":["25453085"],"arxiv":["1412.0897"]},"author":[{"orcid":"0000-0002-7854-2139","full_name":"Šarić, Anđela","last_name":"Šarić","first_name":"Anđela","id":"bf63d406-f056-11eb-b41d-f263a6566d8b"},{"full_name":"Chebaro, Yassmine C.","last_name":"Chebaro","first_name":"Yassmine C."},{"first_name":"Tuomas P. J.","full_name":"Knowles, Tuomas P. J.","last_name":"Knowles"},{"first_name":"Daan","full_name":"Frenkel, Daan","last_name":"Frenkel"}],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","citation":{"ista":"Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. 2014. Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. 111(50), 17869–17874.","chicago":"Šarić, Anđela, Yassmine C. Chebaro, Tuomas P. J. Knowles, and Daan Frenkel. “Crucial Role of Nonspecific Interactions in Amyloid Nucleation.” Proceedings of the National Academy of Sciences. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1410159111.","ieee":"A. Šarić, Y. C. Chebaro, T. P. J. Knowles, and D. Frenkel, “Crucial role of nonspecific interactions in amyloid nucleation,” Proceedings of the National Academy of Sciences, vol. 111, no. 50. National Academy of Sciences, pp. 17869–17874, 2014.","short":"A. Šarić, Y.C. Chebaro, T.P.J. Knowles, D. Frenkel, Proceedings of the National Academy of Sciences 111 (2014) 17869–17874.","ama":"Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. 2014;111(50):17869-17874. doi:10.1073/pnas.1410159111","apa":"Šarić, A., Chebaro, Y. C., Knowles, T. P. J., & Frenkel, D. (2014). Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1410159111","mla":"Šarić, Anđela, et al. “Crucial Role of Nonspecific Interactions in Amyloid Nucleation.” Proceedings of the National Academy of Sciences, vol. 111, no. 50, National Academy of Sciences, 2014, pp. 17869–74, doi:10.1073/pnas.1410159111."},"intvolume":" 111","month":"12","main_file_link":[{"open_access":"1","url":"https://www.pnas.org/content/111/50/17869"}],"scopus_import":"1","oa_version":"Published Version","pmid":1,"abstract":[{"text":"Protein oligomers have been implicated as toxic agents in a wide range of amyloid-related diseases. However, it has remained unsolved whether the oligomers are a necessary step in the formation of amyloid fibrils or just a dangerous byproduct. Analogously, it has not been resolved if the amyloid nucleation process is a classical one-step nucleation process or a two-step process involving prenucleation clusters. We use coarse-grained computer simulations to study the effect of nonspecific attractions between peptides on the primary nucleation process underlying amyloid fibrillization. We find that, for peptides that do not attract, the classical one-step nucleation mechanism is possible but only at nonphysiologically high peptide concentrations. At low peptide concentrations, which mimic the physiologically relevant regime, attractive interpeptide interactions are essential for fibril formation. Nucleation then inevitably takes place through a two-step mechanism involving prefibrillar oligomers. We show that oligomers not only help peptides meet each other but also, create an environment that facilitates the conversion of monomers into the β-sheet–rich form characteristic of fibrils. Nucleation typically does not proceed through the most prevalent oligomers but through an oligomer size that is only observed in rare fluctuations, which is why such aggregates might be hard to capture experimentally. Finally, we find that the nucleation of amyloid fibrils cannot be described by classical nucleation theory: in the two-step mechanism, the critical nucleus size increases with increases in both concentration and interpeptide interactions, which is in direct contrast with predictions from classical nucleation theory.","lang":"eng"}],"issue":"50","volume":111,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["0027-8424"],"eissn":["1091-6490"]},"keyword":["multidisciplinary"],"status":"public","type":"journal_article","article_type":"original","_id":"10382","extern":"1","date_updated":"2021-11-29T13:29:05Z"},{"intvolume":" 89","month":"05","main_file_link":[{"url":"https://arxiv.org/abs/1310.0826","open_access":"1"}],"scopus_import":"1","pmid":1,"oa_version":"Preprint","abstract":[{"text":"We use numerical simulations to compute the equation of state of a suspension of spherical self-propelled nanoparticles in two and three dimensions. We study in detail the effect of excluded volume interactions and confinement as a function of the system's temperature, concentration, and strength of the propulsion. We find a striking nonmonotonic dependence of the pressure on the temperature and provide simple scaling arguments to predict and explain the occurrence of such anomalous behavior. We explicitly show how our results have important implications for the effective forces on passive components suspended in a bath of active particles.","lang":"eng"}],"volume":89,"issue":"5","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["1539-3755"],"eissn":["1550-2376"]},"status":"public","article_type":"original","type":"journal_article","_id":"10383","extern":"1","date_updated":"2021-11-29T13:29:01Z","oa":1,"publisher":"American Physical Society","quality_controlled":"1","date_created":"2021-11-29T13:10:33Z","doi":"10.1103/physreve.89.052303","date_published":"2014-05-06T00:00:00Z","publication":"Physical Review E","day":"06","year":"2014","article_number":"052303","title":"Anomalous thermomechanical properties of a self-propelled colloidal fluid","article_processing_charge":"No","external_id":{"pmid":["25353796"],"arxiv":["1310.0826"]},"author":[{"full_name":"Mallory, S. A.","last_name":"Mallory","first_name":"S. A."},{"id":"bf63d406-f056-11eb-b41d-f263a6566d8b","first_name":"Anđela","full_name":"Šarić, Anđela","orcid":"0000-0002-7854-2139","last_name":"Šarić"},{"last_name":"Valeriani","full_name":"Valeriani, C.","first_name":"C."},{"full_name":"Cacciuto, A.","last_name":"Cacciuto","first_name":"A."}],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","citation":{"mla":"Mallory, S. A., et al. “Anomalous Thermomechanical Properties of a Self-Propelled Colloidal Fluid.” Physical Review E, vol. 89, no. 5, 052303, American Physical Society, 2014, doi:10.1103/physreve.89.052303.","ama":"Mallory SA, Šarić A, Valeriani C, Cacciuto A. Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. 2014;89(5). doi:10.1103/physreve.89.052303","apa":"Mallory, S. A., Šarić, A., Valeriani, C., & Cacciuto, A. (2014). Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. American Physical Society. https://doi.org/10.1103/physreve.89.052303","short":"S.A. Mallory, A. Šarić, C. Valeriani, A. Cacciuto, Physical Review E 89 (2014).","ieee":"S. A. Mallory, A. Šarić, C. Valeriani, and A. Cacciuto, “Anomalous thermomechanical properties of a self-propelled colloidal fluid,” Physical Review E, vol. 89, no. 5. American Physical Society, 2014.","chicago":"Mallory, S. A., Anđela Šarić, C. Valeriani, and A. Cacciuto. “Anomalous Thermomechanical Properties of a Self-Propelled Colloidal Fluid.” Physical Review E. American Physical Society, 2014. https://doi.org/10.1103/physreve.89.052303.","ista":"Mallory SA, Šarić A, Valeriani C, Cacciuto A. 2014. Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. 89(5), 052303."}},{"extern":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Jensen, Nickels, et al. “Coordinate-Targeted and Coordinate-Stochastic Super-Resolution Microscopy with the Reversibly Switchable Fluorescent Protein Dreiklang.” ChemPhysChem, vol. 15, no. 4, Wiley-Blackwell, 2014, pp. 756–62, doi:10.1002/cphc.201301034.","short":"N. Jensen, J.G. Danzl, K. Willig, F. Lavoie Cardinal, T. Brakemann, S. Hell, S. Jakobs, ChemPhysChem 15 (2014) 756–762.","ieee":"N. Jensen et al., “Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang,” ChemPhysChem, vol. 15, no. 4. Wiley-Blackwell, pp. 756–762, 2014.","ama":"Jensen N, Danzl JG, Willig K, et al. Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. 2014;15(4):756-762. doi:10.1002/cphc.201301034","apa":"Jensen, N., Danzl, J. G., Willig, K., Lavoie Cardinal, F., Brakemann, T., Hell, S., & Jakobs, S. (2014). Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. Wiley-Blackwell. https://doi.org/10.1002/cphc.201301034","chicago":"Jensen, Nickels, Johann G Danzl, Katrin Willig, Flavie Lavoie Cardinal, Tanja Brakemann, Stefan Hell, and Stefan Jakobs. “Coordinate-Targeted and Coordinate-Stochastic Super-Resolution Microscopy with the Reversibly Switchable Fluorescent Protein Dreiklang.” ChemPhysChem. Wiley-Blackwell, 2014. https://doi.org/10.1002/cphc.201301034.","ista":"Jensen N, Danzl JG, Willig K, Lavoie Cardinal F, Brakemann T, Hell S, Jakobs S. 2014. Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. 15(4), 756–762."},"date_updated":"2021-01-12T06:47:58Z","title":"Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang","publist_id":"6332","author":[{"first_name":"Nickels","last_name":"Jensen","full_name":"Jensen, Nickels"},{"orcid":"0000-0001-8559-3973","full_name":"Danzl, Johann G","last_name":"Danzl","first_name":"Johann G","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Willig","full_name":"Willig, Katrin","first_name":"Katrin"},{"first_name":"Flavie","full_name":"Lavoie Cardinal, Flavie","last_name":"Lavoie Cardinal"},{"first_name":"Tanja","full_name":"Brakemann, Tanja","last_name":"Brakemann"},{"full_name":"Hell, Stefan","last_name":"Hell","first_name":"Stefan"},{"first_name":"Stefan","full_name":"Jakobs, Stefan","last_name":"Jakobs"}],"article_processing_charge":"No","_id":"1058","status":"public","type":"journal_article","day":"17","publication":"ChemPhysChem","language":[{"iso":"eng"}],"publication_status":"published","year":"2014","date_published":"2014-03-17T00:00:00Z","doi":"10.1002/cphc.201301034","issue":"4","volume":15,"date_created":"2018-12-11T11:49:55Z","page":"756 - 762","oa_version":"None","abstract":[{"text":"Diffraction-unlimited far-field super-resolution fluorescence (nanoscopy) methods typically rely on transiently transferring fluorophores between two states, whereby this transfer is usually laid out as a switch. However, depending on whether this is induced in a spatially controlled manner using a pattern of light (coordinate-targeted) or stochastically on a single-molecule basis, specific requirements on the fluorophores are imposed. Therefore, the fluorophores are usually utilized just for one class of methods only. In this study we demonstrate that the reversibly switchable fluorescent protein Dreiklang enables live-cell recordings in both spatially controlled and stochastic modes. We show that the Dreiklang chromophore entails three different light-induced switching mechanisms, namely a reversible photochemical one, off-switching by stimulated emission, and a reversible transfer to a long-lived dark state from the S1 state, all of which can be utilized to overcome the diffraction barrier. We also find that for the single-molecule- based stochastic GSDIM approach (ground-state depletion followed by individual molecule return), Dreiklang provides a larger number of on-off localization events as compared to its progenitor Citrine. Altogether, Dreiklang is a versatile probe for essentially all popular forms of live-cell fluorescence nanoscopy.","lang":"eng"}],"month":"03","intvolume":" 15","publisher":"Wiley-Blackwell"},{"_id":"10815","keyword":["Developmental Biology","Embryology","General Medicine","Pediatrics","Perinatology","and Child Health"],"status":"public","type":"journal_article","article_type":"original","date_updated":"2022-03-04T08:26:05Z","department":[{"_id":"CaHe"}],"pmid":1,"oa_version":"None","abstract":[{"lang":"eng","text":"In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest."}],"intvolume":" 54","month":"02","main_file_link":[{"url":"https://doi.org/10.1111/cga.12039","open_access":"1"}],"scopus_import":"1","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["0914-3505"]},"volume":54,"issue":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1, Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039.","short":"M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.","ieee":"M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of development underlying congenital diseases,” Congenital Anomalies, vol. 54, no. 1. Wiley, pp. 1–7, 2014.","ama":"Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039","apa":"Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. Wiley. https://doi.org/10.1111/cga.12039","chicago":"Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies. Wiley, 2014. https://doi.org/10.1111/cga.12039.","ista":"Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7."},"title":"Molecular and cellular mechanisms of development underlying congenital diseases","article_processing_charge":"No","external_id":{"pmid":["24666178"]},"author":[{"first_name":"Masakazu","full_name":"Hashimoto, Masakazu","last_name":"Hashimoto"},{"id":"4C6E54C6-F248-11E8-B48F-1D18A9856A87","first_name":"Hitoshi","full_name":"Morita, Hitoshi","last_name":"Morita"},{"first_name":"Naoto","full_name":"Ueno, Naoto","last_name":"Ueno"}],"acknowledgement":"The authors thank all the members of the Division of Morphogenesis, National Institute for Basic Biology, for their contributions to the research, their encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical reading of the manuscript. We also thank the Model Animal Research and Spectrography and Bioimaging Facilities, NIBB Core Research Facilities, for technical support. M.H. was supported by a research fellowship from the Japan Society for the Promotion of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan, to N.U.","oa":1,"quality_controlled":"1","publisher":"Wiley","publication":"Congenital Anomalies","day":"01","year":"2014","date_created":"2022-03-04T08:17:25Z","doi":"10.1111/cga.12039","date_published":"2014-02-01T00:00:00Z","page":"1-7"},{"_id":"10811","type":"book_editor","status":"public","citation":{"mla":"Zažímalová, Eva, et al., editors. Auxin and Its Role in Plant Development. 1st ed., Springer Nature, 2014, doi:10.1007/978-3-7091-1526-8.","ama":"Zažímalová E, Petrášek J, Benková E, eds. Auxin and Its Role in Plant Development. 1st ed. Vienna: Springer Nature; 2014. doi:10.1007/978-3-7091-1526-8","apa":"Zažímalová, E., Petrášek, J., & Benková, E. (Eds.). (2014). Auxin and Its Role in Plant Development (1st ed.). Vienna: Springer Nature. https://doi.org/10.1007/978-3-7091-1526-8","short":"E. Zažímalová, J. Petrášek, E. Benková, eds., Auxin and Its Role in Plant Development, 1st ed., Springer Nature, Vienna, 2014.","ieee":"E. Zažímalová, J. Petrášek, and E. Benková, Eds., Auxin and Its Role in Plant Development, 1st ed. Vienna: Springer Nature, 2014.","chicago":"Zažímalová, Eva, Jan Petrášek, and Eva Benková, eds. Auxin and Its Role in Plant Development. 1st ed. Vienna: Springer Nature, 2014. https://doi.org/10.1007/978-3-7091-1526-8.","ista":"Zažímalová E, Petrášek J, Benková E eds. 2014. Auxin and Its Role in Plant Development 1st ed., Vienna: Springer Nature, 444p."},"date_updated":"2022-03-04T07:38:15Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","title":"Auxin and Its Role in Plant Development","department":[{"_id":"EvBe"}],"editor":[{"full_name":"Zažímalová, Eva","last_name":"Zažímalová","first_name":"Eva"},{"last_name":"Petrášek","full_name":"Petrášek, Jan","first_name":"Jan"},{"last_name":"Benková","full_name":"Benková, Eva","orcid":"0000-0002-8510-9739","id":"38F4F166-F248-11E8-B48F-1D18A9856A87","first_name":"Eva"}],"abstract":[{"lang":"eng","text":"Auxin is an important signaling compound in plants and vital for plant development and growth. The present book, Auxin and its Role in Plant Development, provides the reader with detailed and comprehensive insight into the functioning of the molecule on the whole and specifically in plant development. In the first part, the functioning, metabolism and signaling pathways of auxin in plants are explained, the second part depicts the specific role of auxin in plant development and the third part describes the interaction and functioning of the signaling compound upon stimuli of the environment. Each chapter is written by international experts in the respective field and designed for scientists and researchers in plant biology, plant development and cell biology to summarize the recent progress in understanding the role of auxin and suggest future perspectives for auxin research."}],"oa_version":"None","quality_controlled":"1","publisher":"Springer Nature","scopus_import":"1","edition":"1","place":"Vienna","month":"04","publication_identifier":{"eisbn":["9783709115268"],"isbn":["9783709115251"]},"publication_status":"published","year":"2014","day":"01","language":[{"iso":"eng"}],"page":"444","date_published":"2014-04-01T00:00:00Z","doi":"10.1007/978-3-7091-1526-8","date_created":"2022-03-03T11:52:44Z"},{"abstract":[{"lang":"eng","text":"We revisit the parameterized model checking problem for token-passing systems and specifications in indexed CTL ∗ \\X. Emerson and Namjoshi (1995, 2003) have shown that parameterized model checking of indexed CTL ∗ \\X in uni-directional token rings can be reduced to checking rings up to some cutoff size. Clarke et al. (2004) have shown a similar result for general topologies and indexed LTL \\X, provided processes cannot choose the directions for sending or receiving the token.\r\nWe unify and substantially extend these results by systematically exploring fragments of indexed CTL ∗ \\X with respect to general topologies. For each fragment we establish whether a cutoff exists, and for some concrete topologies, such as rings, cliques and stars, we infer small cutoffs. Finally, we show that the problem becomes undecidable, and thus no cutoffs exist, if processes are allowed to choose the directions in which they send or from which they receive the token."}],"oa_version":"Preprint","main_file_link":[{"url":" https://doi.org/10.48550/arXiv.1311.4425","open_access":"1"}],"alternative_title":["LNCS"],"scopus_import":"1","intvolume":" 8318","month":"01","publication_status":"published","publication_identifier":{"eisbn":["9783642540134"],"eissn":["1611-3349"],"isbn":["9783642540127"],"issn":["0302-9743"]},"language":[{"iso":"eng"}],"ec_funded":1,"volume":8318,"_id":"10884","conference":{"start_date":"2014-01-19","end_date":"2014-01-21","location":"San Diego, CA, United States","name":"VMCAI: Verifcation, Model Checking, and Abstract Interpretation"},"type":"conference","status":"public","date_updated":"2022-05-17T08:36:01Z","department":[{"_id":"KrCh"}],"acknowledgement":"This work was supported by the Austrian Science Fund through grant P23499-N23\r\nand through the RiSE network (S11403, S11405, S11406, S11407-N23); ERC Starting Grant (279307: Graph Games); Vienna Science and Technology Fund (WWTF)\r\ngrants PROSEED, ICT12-059, and VRG11-005.","oa":1,"quality_controlled":"1","publisher":"Springer Nature","year":"2014","publication":"Verification, Model Checking, and Abstract Interpretation","day":"30","page":"262-281","date_created":"2022-03-18T13:01:22Z","doi":"10.1007/978-3-642-54013-4_15","date_published":"2014-01-30T00:00:00Z","project":[{"_id":"2584A770-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Modern Graph Algorithmic Techniques in Formal Verification","grant_number":"P 23499-N23"},{"call_identifier":"FWF","_id":"25863FF4-B435-11E9-9278-68D0E5697425","name":"Game Theory","grant_number":"S11407"},{"name":"Quantitative Graph Games: Theory and Applications","grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"citation":{"mla":"Aminof, Benjamin, et al. “Parameterized Model Checking of Token-Passing Systems.” Verification, Model Checking, and Abstract Interpretation, vol. 8318, Springer Nature, 2014, pp. 262–81, doi:10.1007/978-3-642-54013-4_15.","short":"B. Aminof, S. Jacobs, A. Khalimov, S. Rubin, in:, Verification, Model Checking, and Abstract Interpretation, Springer Nature, 2014, pp. 262–281.","ieee":"B. Aminof, S. Jacobs, A. Khalimov, and S. Rubin, “Parameterized model checking of token-passing systems,” in Verification, Model Checking, and Abstract Interpretation, San Diego, CA, United States, 2014, vol. 8318, pp. 262–281.","apa":"Aminof, B., Jacobs, S., Khalimov, A., & Rubin, S. (2014). Parameterized model checking of token-passing systems. In Verification, Model Checking, and Abstract Interpretation (Vol. 8318, pp. 262–281). San Diego, CA, United States: Springer Nature. https://doi.org/10.1007/978-3-642-54013-4_15","ama":"Aminof B, Jacobs S, Khalimov A, Rubin S. Parameterized model checking of token-passing systems. In: Verification, Model Checking, and Abstract Interpretation. Vol 8318. Springer Nature; 2014:262-281. doi:10.1007/978-3-642-54013-4_15","chicago":"Aminof, Benjamin, Swen Jacobs, Ayrat Khalimov, and Sasha Rubin. “Parameterized Model Checking of Token-Passing Systems.” In Verification, Model Checking, and Abstract Interpretation, 8318:262–81. Springer Nature, 2014. https://doi.org/10.1007/978-3-642-54013-4_15.","ista":"Aminof B, Jacobs S, Khalimov A, Rubin S. 2014. Parameterized model checking of token-passing systems. Verification, Model Checking, and Abstract Interpretation. VMCAI: Verifcation, Model Checking, and Abstract Interpretation, LNCS, vol. 8318, 262–281."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","external_id":{"arxiv":["1311.4425"]},"article_processing_charge":"No","author":[{"id":"4A55BD00-F248-11E8-B48F-1D18A9856A87","first_name":"Benjamin","full_name":"Aminof, Benjamin","last_name":"Aminof"},{"last_name":"Jacobs","full_name":"Jacobs, Swen","first_name":"Swen"},{"first_name":"Ayrat","full_name":"Khalimov, Ayrat","last_name":"Khalimov"},{"first_name":"Sasha","id":"2EC51194-F248-11E8-B48F-1D18A9856A87","last_name":"Rubin","full_name":"Rubin, Sasha"}],"title":"Parameterized model checking of token-passing systems"},{"language":[{"iso":"eng"}],"publication_identifier":{"eisbn":["9783319040998"],"issn":["1612-3786"],"eissn":["2197-666X"],"isbn":["9783319040981"]},"publication_status":"published","volume":1,"ec_funded":1,"oa_version":"None","abstract":[{"text":"Saddle periodic orbits are an essential and stable part of the topological skeleton of a 3D vector field. Nevertheless, there is currently no efficient algorithm to robustly extract these features. In this chapter, we present a novel technique to extract saddle periodic orbits. Exploiting the analytic properties of such an orbit, we propose a scalar measure based on the finite-time Lyapunov exponent (FTLE) that indicates its presence. Using persistent homology, we can then extract the robust cycles of this field. These cycles thereby represent the saddle periodic orbits of the given vector field. We discuss the different existing FTLE approximation schemes regarding their applicability to this specific problem and propose an adapted version of FTLE called Normalized Velocity Separation. Finally, we evaluate our method using simple analytic vector field data.","lang":"eng"}],"month":"03","place":"Cham","intvolume":" 1","scopus_import":"1","date_updated":"2022-06-21T12:01:47Z","department":[{"_id":"HeEd"}],"_id":"10893","series_title":"Mathematics and Visualization","status":"public","type":"book_chapter","day":"19","publication":"Topological Methods in Data Analysis and Visualization III ","year":"2014","doi":"10.1007/978-3-319-04099-8_4","date_published":"2014-03-19T00:00:00Z","date_created":"2022-03-21T07:11:23Z","page":"55-69","acknowledgement":"First, we thank the reviewers of this paper for their ideas and critical comments. In addition, we thank Ronny Peikert and Filip Sadlo for a fruitful discussions. This research is supported by the European Commission under the TOPOSYS project FP7-ICT-318493-STREP, the European Social Fund (ESF App. No. 100098251), and the European Science Foundation under the ACAT Research Network Program.","publisher":"Springer","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Kasten, Jens, Jan Reininghaus, Wieland Reich, and Gerik Scheuermann. “Toward the Extraction of Saddle Periodic Orbits.” In Topological Methods in Data Analysis and Visualization III , edited by Peer-Timo Bremer, Ingrid Hotz, Valerio Pascucci, and Ronald Peikert, 1:55–69. Mathematics and Visualization. Cham: Springer, 2014. https://doi.org/10.1007/978-3-319-04099-8_4.","ista":"Kasten J, Reininghaus J, Reich W, Scheuermann G. 2014.Toward the extraction of saddle periodic orbits. In: Topological Methods in Data Analysis and Visualization III . vol. 1, 55–69.","mla":"Kasten, Jens, et al. “Toward the Extraction of Saddle Periodic Orbits.” Topological Methods in Data Analysis and Visualization III , edited by Peer-Timo Bremer et al., vol. 1, Springer, 2014, pp. 55–69, doi:10.1007/978-3-319-04099-8_4.","short":"J. Kasten, J. Reininghaus, W. Reich, G. Scheuermann, in:, P.-T. Bremer, I. Hotz, V. Pascucci, R. Peikert (Eds.), Topological Methods in Data Analysis and Visualization III , Springer, Cham, 2014, pp. 55–69.","ieee":"J. Kasten, J. Reininghaus, W. Reich, and G. Scheuermann, “Toward the extraction of saddle periodic orbits,” in Topological Methods in Data Analysis and Visualization III , vol. 1, P.-T. Bremer, I. Hotz, V. Pascucci, and R. Peikert, Eds. Cham: Springer, 2014, pp. 55–69.","apa":"Kasten, J., Reininghaus, J., Reich, W., & Scheuermann, G. (2014). Toward the extraction of saddle periodic orbits. In P.-T. Bremer, I. Hotz, V. Pascucci, & R. Peikert (Eds.), Topological Methods in Data Analysis and Visualization III (Vol. 1, pp. 55–69). Cham: Springer. https://doi.org/10.1007/978-3-319-04099-8_4","ama":"Kasten J, Reininghaus J, Reich W, Scheuermann G. Toward the extraction of saddle periodic orbits. In: Bremer P-T, Hotz I, Pascucci V, Peikert R, eds. Topological Methods in Data Analysis and Visualization III . Vol 1. Mathematics and Visualization. Cham: Springer; 2014:55-69. doi:10.1007/978-3-319-04099-8_4"},"title":"Toward the extraction of saddle periodic orbits","editor":[{"full_name":"Bremer, Peer-Timo","last_name":"Bremer","first_name":"Peer-Timo"},{"last_name":"Hotz","full_name":"Hotz, Ingrid","first_name":"Ingrid"},{"first_name":"Valerio","full_name":"Pascucci, Valerio","last_name":"Pascucci"},{"first_name":"Ronald","last_name":"Peikert","full_name":"Peikert, Ronald"}],"author":[{"full_name":"Kasten, Jens","last_name":"Kasten","first_name":"Jens"},{"id":"4505473A-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","full_name":"Reininghaus, Jan","last_name":"Reininghaus"},{"first_name":"Wieland","last_name":"Reich","full_name":"Reich, Wieland"},{"first_name":"Gerik","full_name":"Scheuermann, Gerik","last_name":"Scheuermann"}],"article_processing_charge":"No","project":[{"call_identifier":"FP7","_id":"255D761E-B435-11E9-9278-68D0E5697425","grant_number":"318493","name":"Topological Complex Systems"}]}]