[{"article_type":"original","oa":1,"keyword":["Genetics","Molecular Biology","Biochemistry","General Medicine"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-2649"],"eissn":["2041-2657"]},"doi":"10.1093/bfgp/ely007","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication":"Briefings in Functional Genomics","day":"01","main_file_link":[{"url":"https://doi.org/10.1093/bfgp/ely007","open_access":"1"}],"title":"Significance of whole-genome duplications on the emergence of evolutionary novelties","acknowledgement":"This work was supported by JSPS overseas research fellowships (Y.M.) and SENSHIN Medical Research Foundation (K.K.T.).","year":"2018","department":[{"_id":"CaHe"}],"pmid":1,"type":"journal_article","article_processing_charge":"No","citation":{"apa":"Yuuta, M., &#38; Koshiba-Takeuchi, K. (2018). Significance of whole-genome duplications on the emergence of evolutionary novelties. <i>Briefings in Functional Genomics</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/bfgp/ely007\">https://doi.org/10.1093/bfgp/ely007</a>","ieee":"M. Yuuta and K. Koshiba-Takeuchi, “Significance of whole-genome duplications on the emergence of evolutionary novelties,” <i>Briefings in Functional Genomics</i>, vol. 17, no. 5. Oxford University Press, pp. 329–338, 2018.","chicago":"Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome Duplications on the Emergence of Evolutionary Novelties.” <i>Briefings in Functional Genomics</i>. Oxford University Press, 2018. <a href=\"https://doi.org/10.1093/bfgp/ely007\">https://doi.org/10.1093/bfgp/ely007</a>.","mla":"Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome Duplications on the Emergence of Evolutionary Novelties.” <i>Briefings in Functional Genomics</i>, vol. 17, no. 5, Oxford University Press, 2018, pp. 329–38, doi:<a href=\"https://doi.org/10.1093/bfgp/ely007\">10.1093/bfgp/ely007</a>.","short":"M. Yuuta, K. Koshiba-Takeuchi, Briefings in Functional Genomics 17 (2018) 329–338.","ama":"Yuuta M, Koshiba-Takeuchi K. Significance of whole-genome duplications on the emergence of evolutionary novelties. <i>Briefings in Functional Genomics</i>. 2018;17(5):329-338. doi:<a href=\"https://doi.org/10.1093/bfgp/ely007\">10.1093/bfgp/ely007</a>","ista":"Yuuta M, Koshiba-Takeuchi K. 2018. Significance of whole-genome duplications on the emergence of evolutionary novelties. Briefings in Functional Genomics. 17(5), 329–338."},"publisher":"Oxford University Press","date_updated":"2023-09-19T15:11:22Z","oa_version":"Published Version","isi":1,"month":"09","status":"public","scopus_import":"1","publication_status":"published","external_id":{"isi":["000456054400004"],"pmid":["29579140"]},"date_created":"2022-03-18T12:40:35Z","abstract":[{"lang":"eng","text":"Acquisition of evolutionary novelties is a fundamental process for adapting to the external environment and invading new niches and results in the diversification of life, which we can see in the world today. How such novel phenotypic traits are acquired in the course of evolution and are built up in developing embryos has been a central question in biology. Whole-genome duplication (WGD) is a process of genome doubling that supplies raw genetic materials and increases genome complexity. Recently, it has been gradually revealed that WGD and subsequent fate changes of duplicated genes can facilitate phenotypic evolution. Here, we review the current understanding of the relationship between WGD and the acquisition of evolutionary novelties. We show some examples of this link and discuss how WGD and subsequent duplicated genes can facilitate phenotypic evolution as well as when such genomic doubling can be advantageous for adaptation."}],"issue":"5","quality_controlled":"1","_id":"10880","date_published":"2018-09-01T00:00:00Z","intvolume":"        17","page":"329-338","volume":17,"author":[{"orcid":"0000-0002-2853-8051","id":"4968E7C8-F248-11E8-B48F-1D18A9856A87","first_name":"Moriyama","full_name":"Yuuta, Moriyama","last_name":"Yuuta"},{"first_name":"Kazuko","full_name":"Koshiba-Takeuchi, Kazuko","last_name":"Koshiba-Takeuchi"}]},{"extern":"1","pmid":1,"year":"2018","title":"Tpr regulates the total number of nuclear pore complexes per cell nucleus","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.315523.118"}],"publication":"Genes & Development","day":"18","doi":"10.1101/gad.315523.118","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","oa":1,"keyword":["Developmental Biology","Genetics"],"publication_identifier":{"issn":["0890-9369","1549-5477"]},"language":[{"iso":"eng"}],"article_type":"original","intvolume":"        32","date_published":"2018-09-18T00:00:00Z","author":[{"first_name":"Asako","full_name":"McCloskey, Asako","last_name":"McCloskey"},{"last_name":"Ibarra","full_name":"Ibarra, Arkaitz","first_name":"Arkaitz"},{"last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"volume":32,"page":"1321-1331","issue":"19-20","quality_controlled":"1","_id":"11063","external_id":{"pmid":["30228202"]},"date_created":"2022-04-07T07:45:30Z","publication_status":"published","abstract":[{"text":"The total number of nuclear pore complexes (NPCs) per nucleus varies greatly between different cell types and is known to change during cell differentiation and cell transformation. However, the underlying mechanisms that control how many nuclear transport channels are assembled into a given nuclear envelope remain unclear. Here, we report that depletion of the NPC basket protein Tpr, but not Nup153, dramatically increases the total NPC number in various cell types. This negative regulation of Tpr occurs via a phosphorylation cascade of extracellular signal-regulated kinase (ERK), the central kinase of the mitogen-activated protein kinase (MAPK) pathway. Tpr serves as a scaffold for ERK to phosphorylate the nucleoporin (Nup) Nup153, which is critical for early stages of NPC biogenesis. Our results reveal a critical role of the Nup Tpr in coordinating signal transduction pathways during cell proliferation and the dynamic organization of the nucleus.","lang":"eng"}],"scopus_import":"1","date_updated":"2022-07-18T08:32:32Z","oa_version":"Published Version","status":"public","month":"09","article_processing_charge":"No","citation":{"apa":"McCloskey, A., Ibarra, A., &#38; Hetzer, M. (2018). Tpr regulates the total number of nuclear pore complexes per cell nucleus. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.315523.118\">https://doi.org/10.1101/gad.315523.118</a>","ieee":"A. McCloskey, A. Ibarra, and M. Hetzer, “Tpr regulates the total number of nuclear pore complexes per cell nucleus,” <i>Genes &#38; Development</i>, vol. 32, no. 19–20. Cold Spring Harbor Laboratory, pp. 1321–1331, 2018.","chicago":"McCloskey, Asako, Arkaitz Ibarra, and Martin Hetzer. “Tpr Regulates the Total Number of Nuclear Pore Complexes per Cell Nucleus.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2018. <a href=\"https://doi.org/10.1101/gad.315523.118\">https://doi.org/10.1101/gad.315523.118</a>.","mla":"McCloskey, Asako, et al. “Tpr Regulates the Total Number of Nuclear Pore Complexes per Cell Nucleus.” <i>Genes &#38; Development</i>, vol. 32, no. 19–20, Cold Spring Harbor Laboratory, 2018, pp. 1321–31, doi:<a href=\"https://doi.org/10.1101/gad.315523.118\">10.1101/gad.315523.118</a>.","short":"A. McCloskey, A. Ibarra, M. Hetzer, Genes &#38; Development 32 (2018) 1321–1331.","ama":"McCloskey A, Ibarra A, Hetzer M. Tpr regulates the total number of nuclear pore complexes per cell nucleus. <i>Genes &#38; Development</i>. 2018;32(19-20):1321-1331. doi:<a href=\"https://doi.org/10.1101/gad.315523.118\">10.1101/gad.315523.118</a>","ista":"McCloskey A, Ibarra A, Hetzer M. 2018. Tpr regulates the total number of nuclear pore complexes per cell nucleus. Genes &#38; Development. 32(19–20), 1321–1331."},"publisher":"Cold Spring Harbor Laboratory","type":"journal_article"},{"year":"2017","extern":"1","pmid":1,"main_file_link":[{"url":"https://doi.org/10.1038/ncomms15651","open_access":"1"}],"title":"Dynamics of valence-shell electrons and nuclei probed by strong-field holography and rescattering","doi":"10.1038/ncomms15651","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"15","publication":"Nature Communications","article_number":"15651","article_type":"original","keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry","Multidisciplinary"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["2041-1723"]},"quality_controlled":"1","_id":"14005","author":[{"full_name":"Walt, Samuel G.","first_name":"Samuel G.","last_name":"Walt"},{"first_name":"Niraghatam","full_name":"Bhargava Ram, Niraghatam","last_name":"Bhargava Ram"},{"last_name":"Atala","first_name":"Marcos","full_name":"Atala, Marcos"},{"last_name":"Shvetsov-Shilovski","first_name":"Nikolay I","full_name":"Shvetsov-Shilovski, Nikolay I"},{"last_name":"von Conta","full_name":"von Conta, Aaron","first_name":"Aaron"},{"last_name":"Baykusheva","first_name":"Denitsa Rangelova","id":"71b4d059-2a03-11ee-914d-dfa3beed6530","full_name":"Baykusheva, Denitsa Rangelova"},{"first_name":"Manfred","full_name":"Lein, Manfred","last_name":"Lein"},{"last_name":"Wörner","first_name":"Hans Jakob","full_name":"Wörner, Hans Jakob"}],"volume":8,"intvolume":"         8","date_published":"2017-06-15T00:00:00Z","scopus_import":"1","date_created":"2023-08-10T06:36:09Z","publication_status":"published","external_id":{"pmid":["28643771"]},"abstract":[{"lang":"eng","text":"Strong-field photoelectron holography and laser-induced electron diffraction (LIED) are two powerful emerging methods for probing the ultrafast dynamics of molecules. However, both of them have remained restricted to static systems and to nuclear dynamics induced by strong-field ionization. Here we extend these promising methods to image purely electronic valence-shell dynamics in molecules using photoelectron holography. In the same experiment, we use LIED and photoelectron holography simultaneously, to observe coupled electronic-rotational dynamics taking place on similar timescales. These results offer perspectives for imaging ultrafast dynamics of molecules on femtosecond to attosecond timescales."}],"oa_version":"Published Version","date_updated":"2023-08-22T08:26:06Z","month":"06","status":"public","type":"journal_article","article_processing_charge":"No","publisher":"Springer Nature","citation":{"chicago":"Walt, Samuel G., Niraghatam Bhargava Ram, Marcos Atala, Nikolay I Shvetsov-Shilovski, Aaron von Conta, Denitsa Rangelova Baykusheva, Manfred Lein, and Hans Jakob Wörner. “Dynamics of Valence-Shell Electrons and Nuclei Probed by Strong-Field Holography and Rescattering.” <i>Nature Communications</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/ncomms15651\">https://doi.org/10.1038/ncomms15651</a>.","apa":"Walt, S. G., Bhargava Ram, N., Atala, M., Shvetsov-Shilovski, N. I., von Conta, A., Baykusheva, D. R., … Wörner, H. J. (2017). Dynamics of valence-shell electrons and nuclei probed by strong-field holography and rescattering. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/ncomms15651\">https://doi.org/10.1038/ncomms15651</a>","ieee":"S. G. Walt <i>et al.</i>, “Dynamics of valence-shell electrons and nuclei probed by strong-field holography and rescattering,” <i>Nature Communications</i>, vol. 8. Springer Nature, 2017.","ista":"Walt SG, Bhargava Ram N, Atala M, Shvetsov-Shilovski NI, von Conta A, Baykusheva DR, Lein M, Wörner HJ. 2017. Dynamics of valence-shell electrons and nuclei probed by strong-field holography and rescattering. Nature Communications. 8, 15651.","ama":"Walt SG, Bhargava Ram N, Atala M, et al. Dynamics of valence-shell electrons and nuclei probed by strong-field holography and rescattering. <i>Nature Communications</i>. 2017;8. doi:<a href=\"https://doi.org/10.1038/ncomms15651\">10.1038/ncomms15651</a>","short":"S.G. Walt, N. Bhargava Ram, M. Atala, N.I. Shvetsov-Shilovski, A. von Conta, D.R. Baykusheva, M. Lein, H.J. Wörner, Nature Communications 8 (2017).","mla":"Walt, Samuel G., et al. “Dynamics of Valence-Shell Electrons and Nuclei Probed by Strong-Field Holography and Rescattering.” <i>Nature Communications</i>, vol. 8, 15651, Springer Nature, 2017, doi:<a href=\"https://doi.org/10.1038/ncomms15651\">10.1038/ncomms15651</a>."}},{"intvolume":"         6","date_published":"2017-11-09T00:00:00Z","volume":6,"author":[{"last_name":"Helle","full_name":"Helle, Sebastian Carsten Johannes","first_name":"Sebastian Carsten Johannes"},{"last_name":"Feng","first_name":"Qian","full_name":"Feng, Qian"},{"last_name":"Aebersold","first_name":"Mathias J","full_name":"Aebersold, Mathias J"},{"last_name":"Hirt","first_name":"Luca","full_name":"Hirt, Luca"},{"full_name":"Grüter, Raphael R","first_name":"Raphael R","last_name":"Grüter"},{"first_name":"Afshin","full_name":"Vahid, Afshin","last_name":"Vahid"},{"full_name":"Sirianni, Andrea","first_name":"Andrea","last_name":"Sirianni"},{"last_name":"Mostowy","full_name":"Mostowy, Serge","first_name":"Serge"},{"full_name":"Snedeker, Jess G","first_name":"Jess G","last_name":"Snedeker"},{"last_name":"Šarić","first_name":"Anđela","orcid":"0000-0002-7854-2139","id":"bf63d406-f056-11eb-b41d-f263a6566d8b","full_name":"Šarić, Anđela"},{"full_name":"Idema, Timon","first_name":"Timon","last_name":"Idema"},{"full_name":"Zambelli, Tomaso","first_name":"Tomaso","last_name":"Zambelli"},{"first_name":"Benoît","full_name":"Kornmann, Benoît","last_name":"Kornmann"}],"_id":"10370","quality_controlled":"1","abstract":[{"lang":"eng","text":"Eukaryotic cells are densely packed with macromolecular complexes and intertwining organelles, continually transported and reshaped. Intriguingly, organelles avoid clashing and entangling with each other in such limited space. Mitochondria form extensive networks constantly remodeled by fission and fusion. Here, we show that mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of mitochondria – via encounter with motile intracellular pathogens, via external pressure applied by an atomic force microscope, or via cell migration across uneven microsurfaces – results in the recruitment of the mitochondrial fission machinery, and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria, acts as a membrane-bound force sensor to recruit the fission machinery to mechanically strained sites. Thus, mitochondria adapt to the environment by sensing and responding to biomechanical cues. Our findings that mechanical triggers can be coupled to biochemical responses in membrane dynamics may explain how organelles orderly cohabit in the crowded cytoplasm."}],"file_date_updated":"2021-11-29T09:07:41Z","publication_status":"published","date_created":"2021-11-29T08:51:38Z","external_id":{"pmid":["29119945"]},"scopus_import":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"file":[{"relation":"main_file","content_type":"application/pdf","date_updated":"2021-11-29T09:07:41Z","file_size":6120157,"success":1,"file_name":"2017_eLife_Helle.pdf","access_level":"open_access","date_created":"2021-11-29T09:07:41Z","checksum":"c35f42dcfb007f6d6c761a27e24c26d3","creator":"cchlebak","file_id":"10372"}],"ddc":["572"],"status":"public","month":"11","date_updated":"2021-11-29T09:28:14Z","oa_version":"Published Version","citation":{"ieee":"S. C. J. Helle <i>et al.</i>, “Mechanical force induces mitochondrial fission,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","apa":"Helle, S. C. J., Feng, Q., Aebersold, M. J., Hirt, L., Grüter, R. R., Vahid, A., … Kornmann, B. (2017). Mechanical force induces mitochondrial fission. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>","chicago":"Helle, Sebastian Carsten Johannes, Qian Feng, Mathias J Aebersold, Luca Hirt, Raphael R Grüter, Afshin Vahid, Andrea Sirianni, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>.","short":"S.C.J. Helle, Q. Feng, M.J. Aebersold, L. Hirt, R.R. Grüter, A. Vahid, A. Sirianni, S. Mostowy, J.G. Snedeker, A. Šarić, T. Idema, T. Zambelli, B. Kornmann, ELife 6 (2017).","mla":"Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>, vol. 6, e30292, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>.","ama":"Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial fission. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>","ista":"Helle SCJ, Feng Q, Aebersold MJ, Hirt L, Grüter RR, Vahid A, Sirianni A, Mostowy S, Snedeker JG, Šarić A, Idema T, Zambelli T, Kornmann B. 2017. Mechanical force induces mitochondrial fission. eLife. 6, e30292."},"publisher":"eLife Sciences Publications","has_accepted_license":"1","article_processing_charge":"No","type":"journal_article","pmid":1,"extern":"1","year":"2017","title":"Mechanical force induces mitochondrial fission","main_file_link":[{"open_access":"1","url":"https://elifesciences.org/articles/30292"}],"publication":"eLife","day":"09","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.7554/elife.30292","language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050-084X"]},"oa":1,"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"article_type":"original","article_number":"e30292"},{"quality_controlled":"1","_id":"11065","author":[{"last_name":"Buchwalter","first_name":"Abigail","full_name":"Buchwalter, Abigail"},{"last_name":"HETZER","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W"}],"volume":8,"intvolume":"         8","date_published":"2017-08-30T00:00:00Z","scopus_import":"1","publication_status":"published","external_id":{"pmid":["28855503"]},"date_created":"2022-04-07T07:45:50Z","abstract":[{"lang":"eng","text":"Premature aging disorders provide an opportunity to study the mechanisms that drive aging. In Hutchinson-Gilford progeria syndrome (HGPS), a mutant form of the nuclear scaffold protein lamin A distorts nuclei and sequesters nuclear proteins. We sought to investigate protein homeostasis in this disease. Here, we report a widespread increase in protein turnover in HGPS-derived cells compared to normal cells. We determine that global protein synthesis is elevated as a consequence of activated nucleoli and enhanced ribosome biogenesis in HGPS-derived fibroblasts. Depleting normal lamin A or inducing mutant lamin A expression are each sufficient to drive nucleolar expansion. We further show that nucleolar size correlates with donor age in primary fibroblasts derived from healthy individuals and that ribosomal RNA production increases with age, indicating that nucleolar size and activity can serve as aging biomarkers. While limiting ribosome biogenesis extends lifespan in several systems, we show that increased ribosome biogenesis and activity are a hallmark of premature aging."}],"oa_version":"Published Version","date_updated":"2022-07-18T08:33:03Z","month":"08","status":"public","type":"journal_article","article_processing_charge":"No","publisher":"Springer Nature","citation":{"ista":"Buchwalter A, Hetzer M. 2017. Nucleolar expansion and elevated protein translation in premature aging. Nature Communications. 8, 328.","ama":"Buchwalter A, Hetzer M. Nucleolar expansion and elevated protein translation in premature aging. <i>Nature Communications</i>. 2017;8. doi:<a href=\"https://doi.org/10.1038/s41467-017-00322-z\">10.1038/s41467-017-00322-z</a>","short":"A. Buchwalter, M. Hetzer, Nature Communications 8 (2017).","mla":"Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated Protein Translation in Premature Aging.” <i>Nature Communications</i>, vol. 8, 328, Springer Nature, 2017, doi:<a href=\"https://doi.org/10.1038/s41467-017-00322-z\">10.1038/s41467-017-00322-z</a>.","chicago":"Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated Protein Translation in Premature Aging.” <i>Nature Communications</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/s41467-017-00322-z\">https://doi.org/10.1038/s41467-017-00322-z</a>.","ieee":"A. Buchwalter and M. Hetzer, “Nucleolar expansion and elevated protein translation in premature aging,” <i>Nature Communications</i>, vol. 8. Springer Nature, 2017.","apa":"Buchwalter, A., &#38; Hetzer, M. (2017). Nucleolar expansion and elevated protein translation in premature aging. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-017-00322-z\">https://doi.org/10.1038/s41467-017-00322-z</a>"},"year":"2017","extern":"1","pmid":1,"main_file_link":[{"url":"https://doi.org/10.1038/s41467-017-00322-z","open_access":"1"}],"title":"Nucleolar expansion and elevated protein translation in premature aging","doi":"10.1038/s41467-017-00322-z","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","day":"30","publication":"Nature Communications","article_number":"328","article_type":"original","oa":1,"keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-1723"]}},{"article_type":"original","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0890-9369","1549-5477"]},"oa":1,"keyword":["Developmental Biology","Genetics"],"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1101/gad.306753.117","day":"21","publication":"Genes & Development","main_file_link":[{"url":"https://doi.org/10.1101/gad.306753.117","open_access":"1"}],"title":"Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells","year":"2017","pmid":1,"extern":"1","type":"journal_article","publisher":"Cold Spring Harbor Laboratory","citation":{"ieee":"T. M. Franks, A. McCloskey, M. N. Shokhirev, C. Benner, A. Rathore, and M. Hetzer, “Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells,” <i>Genes &#38; Development</i>, vol. 31, no. 22. Cold Spring Harbor Laboratory, pp. 2222–2234, 2017.","apa":"Franks, T. M., McCloskey, A., Shokhirev, M. N., Benner, C., Rathore, A., &#38; Hetzer, M. (2017). Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>","chicago":"Franks, Tobias M., Asako McCloskey, Maxim Nikolaievich Shokhirev, Chris Benner, Annie Rathore, and Martin Hetzer. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2017. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>.","mla":"Franks, Tobias M., et al. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>, vol. 31, no. 22, Cold Spring Harbor Laboratory, 2017, pp. 2222–34, doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>.","short":"T.M. Franks, A. McCloskey, M.N. Shokhirev, C. Benner, A. Rathore, M. Hetzer, Genes &#38; Development 31 (2017) 2222–2234.","ista":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. 2017. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. Genes &#38; Development. 31(22), 2222–2234.","ama":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. 2017;31(22):2222-2234. doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>"},"article_processing_charge":"No","month":"12","status":"public","oa_version":"Published Version","date_updated":"2022-07-18T08:33:05Z","scopus_import":"1","abstract":[{"lang":"eng","text":"Recent studies have shown that a subset of nucleoporins (Nups) can detach from the nuclear pore complex and move into the nuclear interior to regulate transcription. One such dynamic Nup, called Nup98, has been implicated in gene activation in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98 binds predominantly to transcription start sites to recruit the Wdr82–Set1A/COMPASS (complex of proteins associated with Set1) complex, which is required for deposition of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98 or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3 at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation of associated genes. Our findings establish a function of Nup98 in hematopoietic gene activation and provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML."}],"date_created":"2022-04-07T07:45:59Z","publication_status":"published","external_id":{"pmid":["29269482"]},"_id":"11066","quality_controlled":"1","issue":"22","volume":31,"author":[{"last_name":"Franks","first_name":"Tobias M.","full_name":"Franks, Tobias M."},{"full_name":"McCloskey, Asako","first_name":"Asako","last_name":"McCloskey"},{"full_name":"Shokhirev, Maxim Nikolaievich","first_name":"Maxim Nikolaievich","last_name":"Shokhirev"},{"last_name":"Benner","full_name":"Benner, Chris","first_name":"Chris"},{"last_name":"Rathore","first_name":"Annie","full_name":"Rathore, Annie"},{"orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER"}],"page":"2222-2234","date_published":"2017-12-21T00:00:00Z","intvolume":"        31"},{"title":"Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells","main_file_link":[{"url":"https://doi.org/10.1016/j.stem.2017.08.012","open_access":"1"}],"extern":"1","pmid":1,"year":"2017","keyword":["Cell Biology","Genetics","Molecular Medicine"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["1934-5909"]},"article_type":"original","publication":"Cell Stem Cell","day":"02","doi":"10.1016/j.stem.2017.08.012","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","date_created":"2022-04-07T07:46:12Z","external_id":{"pmid":["28919367"]},"publication_status":"published","abstract":[{"text":"Neural progenitor cells (NeuPCs) possess a unique nuclear architecture that changes during differentiation. Nucleoporins are linked with cell-type-specific gene regulation, coupling physical changes in nuclear structure to transcriptional output; but, whether and how they coordinate with key fate-determining transcription factors is unclear. Here we show that the nucleoporin Nup153 interacts with Sox2 in adult NeuPCs, where it is indispensable for their maintenance and controls neuronal differentiation. Genome-wide analyses show that Nup153 and Sox2 bind and co-regulate hundreds of genes. Binding of Nup153 to gene promoters or transcriptional end sites correlates with increased or decreased gene expression, respectively, and inhibiting Nup153 expression alters open chromatin configurations at its target genes, disrupts genomic localization of Sox2, and promotes differentiation in vitro and a gliogenic fate switch in vivo. Together, these findings reveal that nuclear structural proteins may exert bimodal transcriptional effects to control cell fate.","lang":"eng"}],"scopus_import":"1","date_published":"2017-11-02T00:00:00Z","intvolume":"        21","author":[{"last_name":"Toda","first_name":"Tomohisa","full_name":"Toda, Tomohisa"},{"first_name":"Jonathan Y.","full_name":"Hsu, Jonathan Y.","last_name":"Hsu"},{"last_name":"Linker","full_name":"Linker, Sara B.","first_name":"Sara B."},{"last_name":"Hu","full_name":"Hu, Lauren","first_name":"Lauren"},{"last_name":"Schafer","full_name":"Schafer, Simon T.","first_name":"Simon T."},{"first_name":"Jerome","full_name":"Mertens, Jerome","last_name":"Mertens"},{"full_name":"Jacinto, Filipe V.","first_name":"Filipe V.","last_name":"Jacinto"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","first_name":"Martin W","full_name":"HETZER, Martin W","last_name":"HETZER"},{"last_name":"Gage","full_name":"Gage, Fred H.","first_name":"Fred H."}],"volume":21,"page":"618-634.e7","issue":"5","quality_controlled":"1","_id":"11067","article_processing_charge":"No","citation":{"short":"T. Toda, J.Y. Hsu, S.B. Linker, L. Hu, S.T. Schafer, J. Mertens, F.V. Jacinto, M. Hetzer, F.H. Gage, Cell Stem Cell 21 (2017) 618–634.e7.","mla":"Toda, Tomohisa, et al. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor Cells.” <i>Cell Stem Cell</i>, vol. 21, no. 5, Elsevier, 2017, p. 618–634.e7, doi:<a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">10.1016/j.stem.2017.08.012</a>.","ama":"Toda T, Hsu JY, Linker SB, et al. Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>. 2017;21(5):618-634.e7. doi:<a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">10.1016/j.stem.2017.08.012</a>","ista":"Toda T, Hsu JY, Linker SB, Hu L, Schafer ST, Mertens J, Jacinto FV, Hetzer M, Gage FH. 2017. Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. Cell Stem Cell. 21(5), 618–634.e7.","apa":"Toda, T., Hsu, J. Y., Linker, S. B., Hu, L., Schafer, S. T., Mertens, J., … Gage, F. H. (2017). Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">https://doi.org/10.1016/j.stem.2017.08.012</a>","ieee":"T. Toda <i>et al.</i>, “Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells,” <i>Cell Stem Cell</i>, vol. 21, no. 5. Elsevier, p. 618–634.e7, 2017.","chicago":"Toda, Tomohisa, Jonathan Y. Hsu, Sara B. Linker, Lauren Hu, Simon T. Schafer, Jerome Mertens, Filipe V. Jacinto, Martin Hetzer, and Fred H. Gage. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor Cells.” <i>Cell Stem Cell</i>. Elsevier, 2017. <a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">https://doi.org/10.1016/j.stem.2017.08.012</a>."},"publisher":"Elsevier","type":"journal_article","date_updated":"2022-07-18T08:33:07Z","oa_version":"Published Version","month":"11","status":"public"},{"day":"03","publication":"Journal of Cell Biology","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1083/jcb.201603053","publication_identifier":{"issn":["0021-9525","1540-8140"]},"language":[{"iso":"eng"}],"oa":1,"keyword":["Cell Biology"],"article_type":"original","pmid":1,"extern":"1","year":"2016","title":"Nuclear envelope rupture is induced by actin-based nucleus confinement","main_file_link":[{"url":"https://doi.org/10.1083/jcb.201603053","open_access":"1"}],"month":"10","status":"public","oa_version":"Published Version","date_updated":"2022-07-18T08:33:47Z","publisher":"Rockefeller University Press","citation":{"chicago":"Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced by Actin-Based Nucleus Confinement.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2016. <a href=\"https://doi.org/10.1083/jcb.201603053\">https://doi.org/10.1083/jcb.201603053</a>.","ieee":"E. M. Hatch and M. Hetzer, “Nuclear envelope rupture is induced by actin-based nucleus confinement,” <i>Journal of Cell Biology</i>, vol. 215, no. 1. Rockefeller University Press, pp. 27–36, 2016.","apa":"Hatch, E. M., &#38; Hetzer, M. (2016). Nuclear envelope rupture is induced by actin-based nucleus confinement. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.201603053\">https://doi.org/10.1083/jcb.201603053</a>","ama":"Hatch EM, Hetzer M. Nuclear envelope rupture is induced by actin-based nucleus confinement. <i>Journal of Cell Biology</i>. 2016;215(1):27-36. doi:<a href=\"https://doi.org/10.1083/jcb.201603053\">10.1083/jcb.201603053</a>","ista":"Hatch EM, Hetzer M. 2016. Nuclear envelope rupture is induced by actin-based nucleus confinement. Journal of Cell Biology. 215(1), 27–36.","mla":"Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced by Actin-Based Nucleus Confinement.” <i>Journal of Cell Biology</i>, vol. 215, no. 1, Rockefeller University Press, 2016, pp. 27–36, doi:<a href=\"https://doi.org/10.1083/jcb.201603053\">10.1083/jcb.201603053</a>.","short":"E.M. Hatch, M. Hetzer, Journal of Cell Biology 215 (2016) 27–36."},"article_processing_charge":"No","type":"journal_article","volume":215,"page":"27-36","author":[{"last_name":"Hatch","full_name":"Hatch, Emily M.","first_name":"Emily M."},{"last_name":"HETZER","full_name":"HETZER, Martin W","first_name":"Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"date_published":"2016-10-03T00:00:00Z","intvolume":"       215","_id":"11069","quality_controlled":"1","issue":"1","abstract":[{"lang":"eng","text":"Repeated rounds of nuclear envelope (NE) rupture and repair have been observed in laminopathy and cancer cells and result in intermittent loss of nucleus compartmentalization. Currently, the causes of NE rupture are unclear. Here, we show that NE rupture in cancer cells relies on the assembly of contractile actin bundles that interact with the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex. We found that the loss of actin bundles or the LINC complex did not rescue nuclear lamina defects, a previously identified determinant of nuclear membrane stability, but did decrease the number and size of chromatin hernias. Finally, NE rupture inhibition could be rescued in cells treated with actin-depolymerizing drugs by mechanically constraining nucleus height. These data suggest a model of NE rupture where weak membrane areas, caused by defects in lamina organization, rupture because of an increase in intranuclear pressure from actin-based nucleus confinement."}],"publication_status":"published","date_created":"2022-04-07T07:47:42Z","external_id":{"pmid":["27697922"]},"scopus_import":"1"},{"type":"journal_article","publisher":"Cold Spring Harbor Laboratory","citation":{"ama":"Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. Nucleoporin-mediated regulation of cell identity genes. <i>Genes &#38; Development</i>. 2016;30(20):2253-2258. doi:<a href=\"https://doi.org/10.1101/gad.287417.116\">10.1101/gad.287417.116</a>","ista":"Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. 2016. Nucleoporin-mediated regulation of cell identity genes. Genes &#38; Development. 30(20), 2253–2258.","short":"A. Ibarra, C. Benner, S. Tyagi, J. Cool, M. Hetzer, Genes &#38; Development 30 (2016) 2253–2258.","mla":"Ibarra, Arkaitz, et al. “Nucleoporin-Mediated Regulation of Cell Identity Genes.” <i>Genes &#38; Development</i>, vol. 30, no. 20, Cold Spring Harbor Laboratory, 2016, pp. 2253–58, doi:<a href=\"https://doi.org/10.1101/gad.287417.116\">10.1101/gad.287417.116</a>.","chicago":"Ibarra, Arkaitz, Chris Benner, Swati Tyagi, Jonah Cool, and Martin Hetzer. “Nucleoporin-Mediated Regulation of Cell Identity Genes.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2016. <a href=\"https://doi.org/10.1101/gad.287417.116\">https://doi.org/10.1101/gad.287417.116</a>.","apa":"Ibarra, A., Benner, C., Tyagi, S., Cool, J., &#38; Hetzer, M. (2016). Nucleoporin-mediated regulation of cell identity genes. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.287417.116\">https://doi.org/10.1101/gad.287417.116</a>","ieee":"A. Ibarra, C. Benner, S. Tyagi, J. Cool, and M. Hetzer, “Nucleoporin-mediated regulation of cell identity genes,” <i>Genes &#38; Development</i>, vol. 30, no. 20. Cold Spring Harbor Laboratory, pp. 2253–2258, 2016."},"article_processing_charge":"No","month":"11","status":"public","oa_version":"Published Version","date_updated":"2022-07-18T08:33:49Z","scopus_import":"1","abstract":[{"text":"The organization of the genome in the three-dimensional space of the nucleus is coupled with cell type-specific gene expression. However, how nuclear architecture influences transcription that governs cell identity remains unknown. Here, we show that nuclear pore complex (NPC) components Nup93 and Nup153 bind superenhancers (SE), regulatory structures that drive the expression of key genes that specify cell identity. We found that nucleoporin-associated SEs localize preferentially to the nuclear periphery, and absence of Nup153 and Nup93 results in dramatic transcriptional changes of SE-associated genes. Our results reveal a crucial role of NPC components in the regulation of cell type-specifying genes and highlight nuclear architecture as a regulatory layer of genome functions in cell fate.","lang":"eng"}],"publication_status":"published","date_created":"2022-04-07T07:48:08Z","external_id":{"pmid":["27807035"]},"_id":"11070","issue":"20","quality_controlled":"1","volume":30,"page":"2253-2258","author":[{"first_name":"Arkaitz","full_name":"Ibarra, Arkaitz","last_name":"Ibarra"},{"full_name":"Benner, Chris","first_name":"Chris","last_name":"Benner"},{"full_name":"Tyagi, Swati","first_name":"Swati","last_name":"Tyagi"},{"last_name":"Cool","full_name":"Cool, Jonah","first_name":"Jonah"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","first_name":"Martin W","orcid":"0000-0002-2111-992X","last_name":"HETZER"}],"date_published":"2016-11-02T00:00:00Z","intvolume":"        30","article_type":"original","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"oa":1,"keyword":["Developmental Biology","Genetics"],"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1101/gad.287417.116","day":"02","publication":"Genes & Development","main_file_link":[{"url":"https://doi.org/10.1101/gad.287417.116","open_access":"1"}],"title":"Nucleoporin-mediated regulation of cell identity genes","year":"2016","pmid":1,"extern":"1"},{"date_updated":"2022-07-18T08:33:50Z","oa_version":"Published Version","month":"05","status":"public","article_processing_charge":"No","citation":{"ama":"Franks TM, Benner C, Narvaiza I, et al. Evolution of a transcriptional regulator from a transmembrane nucleoporin. <i>Genes &#38; Development</i>. 2016;30(10):1155-1171. doi:<a href=\"https://doi.org/10.1101/gad.280941.116\">10.1101/gad.280941.116</a>","ista":"Franks TM, Benner C, Narvaiza I, Marchetto MCN, Young JM, Malik HS, Gage FH, Hetzer M. 2016. Evolution of a transcriptional regulator from a transmembrane nucleoporin. Genes &#38; Development. 30(10), 1155–1171.","short":"T.M. Franks, C. Benner, I. Narvaiza, M.C.N. Marchetto, J.M. Young, H.S. Malik, F.H. Gage, M. Hetzer, Genes &#38; Development 30 (2016) 1155–1171.","mla":"Franks, Tobias M., et al. “Evolution of a Transcriptional Regulator from a Transmembrane Nucleoporin.” <i>Genes &#38; Development</i>, vol. 30, no. 10, Cold Spring Harbor Laboratory, 2016, pp. 1155–71, doi:<a href=\"https://doi.org/10.1101/gad.280941.116\">10.1101/gad.280941.116</a>.","chicago":"Franks, Tobias M., Chris Benner, Iñigo Narvaiza, Maria C.N. Marchetto, Janet M. Young, Harmit S. Malik, Fred H. Gage, and Martin Hetzer. “Evolution of a Transcriptional Regulator from a Transmembrane Nucleoporin.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2016. <a href=\"https://doi.org/10.1101/gad.280941.116\">https://doi.org/10.1101/gad.280941.116</a>.","ieee":"T. M. Franks <i>et al.</i>, “Evolution of a transcriptional regulator from a transmembrane nucleoporin,” <i>Genes &#38; Development</i>, vol. 30, no. 10. Cold Spring Harbor Laboratory, pp. 1155–1171, 2016.","apa":"Franks, T. M., Benner, C., Narvaiza, I., Marchetto, M. C. N., Young, J. M., Malik, H. S., … Hetzer, M. (2016). Evolution of a transcriptional regulator from a transmembrane nucleoporin. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.280941.116\">https://doi.org/10.1101/gad.280941.116</a>"},"publisher":"Cold Spring Harbor Laboratory","type":"journal_article","date_published":"2016-05-19T00:00:00Z","intvolume":"        30","volume":30,"author":[{"first_name":"Tobias M.","full_name":"Franks, Tobias M.","last_name":"Franks"},{"full_name":"Benner, Chris","first_name":"Chris","last_name":"Benner"},{"last_name":"Narvaiza","first_name":"Iñigo","full_name":"Narvaiza, Iñigo"},{"first_name":"Maria C.N.","full_name":"Marchetto, Maria C.N.","last_name":"Marchetto"},{"full_name":"Young, Janet M.","first_name":"Janet M.","last_name":"Young"},{"first_name":"Harmit S.","full_name":"Malik, Harmit S.","last_name":"Malik"},{"full_name":"Gage, Fred H.","first_name":"Fred H.","last_name":"Gage"},{"full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W","last_name":"HETZER"}],"page":"1155-1171","quality_controlled":"1","issue":"10","_id":"11071","date_created":"2022-04-07T07:48:20Z","publication_status":"published","external_id":{"pmid":["27198230"]},"abstract":[{"lang":"eng","text":"Nuclear pore complexes (NPCs) emerged as nuclear transport channels in eukaryotic cells ∼1.5 billion years ago. While the primary role of NPCs is to regulate nucleo–cytoplasmic transport, recent research suggests that certain NPC proteins have additionally acquired the role of affecting gene expression at the nuclear periphery and in the nucleoplasm in metazoans. Here we identify a widely expressed variant of the transmembrane nucleoporin (Nup) Pom121 (named sPom121, for “soluble Pom121”) that arose by genomic rearrangement before the divergence of hominoids. sPom121 lacks the nuclear membrane-anchoring domain and thus does not localize to the NPC. Instead, sPom121 colocalizes and interacts with nucleoplasmic Nup98, a previously identified transcriptional regulator, at gene promoters to control transcription of its target genes in human cells. Interestingly, sPom121 transcripts appear independently in several mammalian species, suggesting convergent innovation of Nup-mediated transcription regulation during mammalian evolution. Our findings implicate alternate transcription initiation as a mechanism to increase the functional diversity of NPC components."}],"scopus_import":"1","publication":"Genes & Development","day":"19","doi":"10.1101/gad.280941.116","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","oa":1,"keyword":["Developmental Biology","Genetics"],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1549-5477"],"issn":["0890-9369"]},"article_type":"original","extern":"1","pmid":1,"year":"2016","title":"Evolution of a transcriptional regulator from a transmembrane nucleoporin","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.280941.116"}]},{"related_material":{"link":[{"relation":"erratum","url":"https://doi.org/10.1038/ncomms16030"}]},"month":"12","status":"public","oa_version":"Published Version","date_updated":"2022-07-18T08:34:32Z","publisher":"Springer Nature","citation":{"mla":"van de Ven, Robert A. H., et al. “P120-Catenin Prevents Multinucleation through Control of MKLP1-Dependent RhoA Activity during Cytokinesis.” <i>Nature Communications</i>, vol. 7, 13874, Springer Nature, 2016, doi:<a href=\"https://doi.org/10.1038/ncomms13874\">10.1038/ncomms13874</a>.","short":"R.A.H. van de Ven, J.S. de Groot, D. Park, R. van Domselaar, D. de Jong, K. Szuhai, E. van der Wall, O.M. Rueda, H.R. Ali, C. Caldas, P.J. van Diest, M. Hetzer, E. Sahai, P.W.B. Derksen, Nature Communications 7 (2016).","ama":"van de Ven RAH, de Groot JS, Park D, et al. p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis. <i>Nature Communications</i>. 2016;7. doi:<a href=\"https://doi.org/10.1038/ncomms13874\">10.1038/ncomms13874</a>","ista":"van de Ven RAH, de Groot JS, Park D, van Domselaar R, de Jong D, Szuhai K, van der Wall E, Rueda OM, Ali HR, Caldas C, van Diest PJ, Hetzer M, Sahai E, Derksen PWB. 2016. p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis. Nature Communications. 7, 13874.","apa":"van de Ven, R. A. H., de Groot, J. S., Park, D., van Domselaar, R., de Jong, D., Szuhai, K., … Derksen, P. W. B. (2016). p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/ncomms13874\">https://doi.org/10.1038/ncomms13874</a>","ieee":"R. A. H. van de Ven <i>et al.</i>, “p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis,” <i>Nature Communications</i>, vol. 7. Springer Nature, 2016.","chicago":"Ven, Robert A.H. van de, Jolien S. de Groot, Danielle Park, Robert van Domselaar, Danielle de Jong, Karoly Szuhai, Elsken van der Wall, et al. “P120-Catenin Prevents Multinucleation through Control of MKLP1-Dependent RhoA Activity during Cytokinesis.” <i>Nature Communications</i>. Springer Nature, 2016. <a href=\"https://doi.org/10.1038/ncomms13874\">https://doi.org/10.1038/ncomms13874</a>."},"article_processing_charge":"No","type":"journal_article","author":[{"full_name":"van de Ven, Robert A.H.","first_name":"Robert A.H.","last_name":"van de Ven"},{"last_name":"de Groot","first_name":"Jolien S.","full_name":"de Groot, Jolien S."},{"last_name":"Park","full_name":"Park, Danielle","first_name":"Danielle"},{"last_name":"van Domselaar","full_name":"van Domselaar, Robert","first_name":"Robert"},{"full_name":"de Jong, Danielle","first_name":"Danielle","last_name":"de Jong"},{"full_name":"Szuhai, Karoly","first_name":"Karoly","last_name":"Szuhai"},{"last_name":"van der Wall","full_name":"van der Wall, Elsken","first_name":"Elsken"},{"full_name":"Rueda, Oscar M.","first_name":"Oscar M.","last_name":"Rueda"},{"first_name":"H. Raza","full_name":"Ali, H. Raza","last_name":"Ali"},{"full_name":"Caldas, Carlos","first_name":"Carlos","last_name":"Caldas"},{"full_name":"van Diest, Paul J.","first_name":"Paul J.","last_name":"van Diest"},{"last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","first_name":"Martin W"},{"first_name":"Erik","full_name":"Sahai, Erik","last_name":"Sahai"},{"last_name":"Derksen","full_name":"Derksen, Patrick W.B.","first_name":"Patrick W.B."}],"volume":7,"date_published":"2016-12-22T00:00:00Z","intvolume":"         7","_id":"11072","quality_controlled":"1","abstract":[{"text":"Spatiotemporal activation of RhoA and actomyosin contraction underpins cellular adhesion and division. Loss of cell–cell adhesion and chromosomal instability are cardinal events that drive tumour progression. Here, we show that p120-catenin (p120) not only controls cell–cell adhesion, but also acts as a critical regulator of cytokinesis. We find that p120 regulates actomyosin contractility through concomitant binding to RhoA and the centralspindlin component MKLP1, independent of cadherin association. In anaphase, p120 is enriched at the cleavage furrow where it binds MKLP1 to spatially control RhoA GTPase cycling. Binding of p120 to MKLP1 during cytokinesis depends on the N-terminal coiled-coil domain of p120 isoform 1A. Importantly, clinical data show that loss of p120 expression is a common event in breast cancer that strongly correlates with multinucleation and adverse patient survival. In summary, our study identifies p120 loss as a driver event of chromosomal instability in cancer.\r\n","lang":"eng"}],"date_created":"2022-04-07T07:48:34Z","publication_status":"published","external_id":{"pmid":["28004812"]},"scopus_import":"1","day":"22","publication":"Nature Communications","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1038/ncomms13874","publication_identifier":{"issn":["2041-1723"]},"language":[{"iso":"eng"}],"oa":1,"keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry"],"article_type":"original","article_number":"13874","pmid":1,"extern":"1","year":"2016","title":"p120-catenin prevents multinucleation through control of MKLP1-dependent RhoA activity during cytokinesis","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/ncomms13874"}]},{"title":"The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity","acknowledgement":"This work was supported by the National Sciences and Engineering Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles Copeland for critical reading of the manuscript.","department":[{"_id":"XiFe"}],"year":"2015","extern":"1","pmid":1,"article_type":"original","keyword":["Cell Biology","Plant Science","Physiology","General Medicine"],"publication_identifier":{"issn":["0032-0781","1471-9053"]},"language":[{"iso":"eng"}],"doi":"10.1093/pcp/pcv087","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Plant and Cell Physiology","scopus_import":"1","date_created":"2023-01-16T09:20:22Z","external_id":{"pmid":["26063389"]},"publication_status":"published","abstract":[{"lang":"eng","text":"SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in the induction of defense responses. However, the molecular mechanisms underlying NLR activation and the subsequent provocation of immune responses are only partially characterized. To identify negative regulators of NLR-mediated immunity, a forward genetic screen was undertaken to search for enhancers of the dwarf, autoimmune gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism, the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display wild-type-like morphology and resistance. M2 progeny were screened for mutant, snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes. The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated expression of the pPR2-GUS defense marker reporter gene and enhanced resistance to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning and Illumina sequencing, it was determined that the muse9 mutation is in the gene encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10. The syd-10 single mutant has no observable alteration from wild-type-like resistance, although the syd-4 T-DNA insertion allele displays enhanced resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated immunity. SYD may work with other proteins at the chromatin level to repress SNC1 transcription; such regulation is important for fine-tuning the expression of NLR-encoding genes to prevent unpropitious autoimmunity."}],"quality_controlled":"1","issue":"8","_id":"12196","author":[{"last_name":"Johnson","full_name":"Johnson, Kaeli C.M.","first_name":"Kaeli C.M."},{"last_name":"Xia","full_name":"Xia, Shitou","first_name":"Shitou"},{"id":"e0164712-22ee-11ed-b12a-d80fcdf35958","orcid":"0000-0002-4008-1234","first_name":"Xiaoqi","full_name":"Feng, Xiaoqi","last_name":"Feng"},{"last_name":"Li","first_name":"Xin","full_name":"Li, Xin"}],"page":"1616-1623","volume":56,"intvolume":"        56","date_published":"2015-08-01T00:00:00Z","type":"journal_article","article_processing_charge":"No","publisher":"Oxford University Press","citation":{"ieee":"K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity,” <i>Plant and Cell Physiology</i>, vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015.","apa":"Johnson, K. C. M., Xia, S., Feng, X., &#38; Li, X. (2015). The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/pcp/pcv087\">https://doi.org/10.1093/pcp/pcv087</a>","chicago":"Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” <i>Plant and Cell Physiology</i>. Oxford University Press, 2015. <a href=\"https://doi.org/10.1093/pcp/pcv087\">https://doi.org/10.1093/pcp/pcv087</a>.","mla":"Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” <i>Plant and Cell Physiology</i>, vol. 56, no. 8, Oxford University Press, 2015, pp. 1616–23, doi:<a href=\"https://doi.org/10.1093/pcp/pcv087\">10.1093/pcp/pcv087</a>.","short":"K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015) 1616–1623.","ista":"Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.","ama":"Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>. 2015;56(8):1616-1623. doi:<a href=\"https://doi.org/10.1093/pcp/pcv087\">10.1093/pcp/pcv087</a>"},"oa_version":"None","date_updated":"2023-05-08T11:03:23Z","month":"08","status":"public"},{"article_processing_charge":"No","keyword":["General Biochemistry","Genetics and Molecular Biology","General Physics and Astronomy","General Chemistry"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-1723"]},"publisher":"Springer Nature","citation":{"chicago":"Ma, Peixiang, Yi Xue, Nicolas Coquelle, Jens D. Haller, Tairan Yuwen, Isabel Ayala, Oleg Mikhailovskii, et al. “Observing the Overall Rocking Motion of a Protein in a Crystal.” <i>Nature Communications</i>. Springer Nature, 2015. <a href=\"https://doi.org/10.1038/ncomms9361\">https://doi.org/10.1038/ncomms9361</a>.","apa":"Ma, P., Xue, Y., Coquelle, N., Haller, J. D., Yuwen, T., Ayala, I., … Schanda, P. (2015). Observing the overall rocking motion of a protein in a crystal. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/ncomms9361\">https://doi.org/10.1038/ncomms9361</a>","ieee":"P. Ma <i>et al.</i>, “Observing the overall rocking motion of a protein in a crystal,” <i>Nature Communications</i>, vol. 6. Springer Nature, 2015.","ista":"Ma P, Xue Y, Coquelle N, Haller JD, Yuwen T, Ayala I, Mikhailovskii O, Willbold D, Colletier J-P, Skrynnikov NR, Schanda P. 2015. Observing the overall rocking motion of a protein in a crystal. Nature Communications. 6, 8361.","ama":"Ma P, Xue Y, Coquelle N, et al. Observing the overall rocking motion of a protein in a crystal. <i>Nature Communications</i>. 2015;6. doi:<a href=\"https://doi.org/10.1038/ncomms9361\">10.1038/ncomms9361</a>","short":"P. Ma, Y. Xue, N. Coquelle, J.D. Haller, T. Yuwen, I. Ayala, O. Mikhailovskii, D. Willbold, J.-P. Colletier, N.R. Skrynnikov, P. Schanda, Nature Communications 6 (2015).","mla":"Ma, Peixiang, et al. “Observing the Overall Rocking Motion of a Protein in a Crystal.” <i>Nature Communications</i>, vol. 6, 8361, Springer Nature, 2015, doi:<a href=\"https://doi.org/10.1038/ncomms9361\">10.1038/ncomms9361</a>."},"article_number":"8361","type":"journal_article","article_type":"original","day":"05","publication":"Nature Communications","oa_version":"Published Version","doi":"10.1038/ncomms9361","date_updated":"2021-01-12T08:19:24Z","status":"public","month":"10","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_created":"2020-09-18T10:07:36Z","publication_status":"published","title":"Observing the overall rocking motion of a protein in a crystal","abstract":[{"text":"The large majority of three-dimensional structures of biological macromolecules have been determined by X-ray diffraction of crystalline samples. High-resolution structure determination crucially depends on the homogeneity of the protein crystal. Overall ‘rocking’ motion of molecules in the crystal is expected to influence diffraction quality, and such motion may therefore affect the process of solving crystal structures. Yet, so far overall molecular motion has not directly been observed in protein crystals, and the timescale of such dynamics remains unclear. Here we use solid-state NMR, X-ray diffraction methods and μs-long molecular dynamics simulations to directly characterize the rigid-body motion of a protein in different crystal forms. For ubiquitin crystals investigated in this study we determine the range of possible correlation times of rocking motion, 0.1–100 μs. The amplitude of rocking varies from one crystal form to another and is correlated with the resolution obtainable in X-ray diffraction experiments.","lang":"eng"}],"volume":6,"author":[{"last_name":"Ma","full_name":"Ma, Peixiang","first_name":"Peixiang"},{"last_name":"Xue","full_name":"Xue, Yi","first_name":"Yi"},{"last_name":"Coquelle","first_name":"Nicolas","full_name":"Coquelle, Nicolas"},{"first_name":"Jens D.","full_name":"Haller, Jens D.","last_name":"Haller"},{"first_name":"Tairan","full_name":"Yuwen, Tairan","last_name":"Yuwen"},{"last_name":"Ayala","full_name":"Ayala, Isabel","first_name":"Isabel"},{"last_name":"Mikhailovskii","first_name":"Oleg","full_name":"Mikhailovskii, Oleg"},{"full_name":"Willbold, Dieter","first_name":"Dieter","last_name":"Willbold"},{"last_name":"Colletier","full_name":"Colletier, Jacques-Philippe","first_name":"Jacques-Philippe"},{"first_name":"Nikolai R.","full_name":"Skrynnikov, Nikolai R.","last_name":"Skrynnikov"},{"first_name":"Paul","full_name":"Schanda, Paul","orcid":"0000-0002-9350-7606","id":"7B541462-FAF6-11E9-A490-E8DFE5697425","last_name":"Schanda"}],"intvolume":"         6","date_published":"2015-10-05T00:00:00Z","extern":"1","quality_controlled":"1","_id":"8456","year":"2015"},{"type":"journal_article","citation":{"ieee":"P. M. Kraus <i>et al.</i>, “Observation of laser-induced electronic structure in oriented polyatomic molecules,” <i>Nature Communications</i>, vol. 6. Springer Nature, 2015.","apa":"Kraus, P. M., Tolstikhin, O. I., Baykusheva, D. R., Rupenyan, A., Schneider, J., Bisgaard, C. Z., … Wörner, H. J. (2015). Observation of laser-induced electronic structure in oriented polyatomic molecules. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/ncomms8039\">https://doi.org/10.1038/ncomms8039</a>","chicago":"Kraus, P. M., O. I. Tolstikhin, Denitsa Rangelova Baykusheva, A. Rupenyan, J. Schneider, C. Z. Bisgaard, T. Morishita, F. Jensen, L. B. Madsen, and H. J. Wörner. “Observation of Laser-Induced Electronic Structure in Oriented Polyatomic Molecules.” <i>Nature Communications</i>. Springer Nature, 2015. <a href=\"https://doi.org/10.1038/ncomms8039\">https://doi.org/10.1038/ncomms8039</a>.","mla":"Kraus, P. M., et al. “Observation of Laser-Induced Electronic Structure in Oriented Polyatomic Molecules.” <i>Nature Communications</i>, vol. 6, 7039, Springer Nature, 2015, doi:<a href=\"https://doi.org/10.1038/ncomms8039\">10.1038/ncomms8039</a>.","short":"P.M. Kraus, O.I. Tolstikhin, D.R. Baykusheva, A. Rupenyan, J. Schneider, C.Z. Bisgaard, T. Morishita, F. Jensen, L.B. Madsen, H.J. Wörner, Nature Communications 6 (2015).","ista":"Kraus PM, Tolstikhin OI, Baykusheva DR, Rupenyan A, Schneider J, Bisgaard CZ, Morishita T, Jensen F, Madsen LB, Wörner HJ. 2015. Observation of laser-induced electronic structure in oriented polyatomic molecules. Nature Communications. 6, 7039.","ama":"Kraus PM, Tolstikhin OI, Baykusheva DR, et al. Observation of laser-induced electronic structure in oriented polyatomic molecules. <i>Nature Communications</i>. 2015;6. doi:<a href=\"https://doi.org/10.1038/ncomms8039\">10.1038/ncomms8039</a>"},"publisher":"Springer Nature","article_processing_charge":"No","status":"public","month":"05","date_updated":"2023-08-22T08:52:56Z","oa_version":"Published Version","scopus_import":"1","abstract":[{"text":"All attosecond time-resolved measurements have so far relied on the use of intense near-infrared laser pulses. In particular, attosecond streaking, laser-induced electron diffraction and high-harmonic generation all make use of non-perturbative light–matter interactions. Remarkably, the effect of the strong laser field on the studied sample has often been neglected in previous studies. Here we use high-harmonic spectroscopy to measure laser-induced modifications of the electronic structure of molecules. We study high-harmonic spectra of spatially oriented CH3F and CH3Br as generic examples of polar polyatomic molecules. We accurately measure intensity ratios of even and odd-harmonic orders, and of the emission from aligned and unaligned molecules. We show that these robust observables reveal a substantial modification of the molecular electronic structure by the external laser field. Our insights offer new challenges and opportunities for a range of emerging strong-field attosecond spectroscopies.","lang":"eng"}],"date_created":"2023-08-10T06:38:01Z","publication_status":"published","external_id":{"pmid":["25940229"]},"_id":"14016","quality_controlled":"1","date_published":"2015-05-05T00:00:00Z","intvolume":"         6","volume":6,"author":[{"last_name":"Kraus","first_name":"P. M.","full_name":"Kraus, P. M."},{"last_name":"Tolstikhin","first_name":"O. I.","full_name":"Tolstikhin, O. I."},{"id":"71b4d059-2a03-11ee-914d-dfa3beed6530","first_name":"Denitsa Rangelova","full_name":"Baykusheva, Denitsa Rangelova","last_name":"Baykusheva"},{"full_name":"Rupenyan, A.","first_name":"A.","last_name":"Rupenyan"},{"full_name":"Schneider, J.","first_name":"J.","last_name":"Schneider"},{"full_name":"Bisgaard, C. Z.","first_name":"C. Z.","last_name":"Bisgaard"},{"first_name":"T.","full_name":"Morishita, T.","last_name":"Morishita"},{"last_name":"Jensen","full_name":"Jensen, F.","first_name":"F."},{"last_name":"Madsen","full_name":"Madsen, L. B.","first_name":"L. B."},{"full_name":"Wörner, H. J.","first_name":"H. J.","last_name":"Wörner"}],"article_type":"original","article_number":"7039","language":[{"iso":"eng"}],"publication_identifier":{"eissn":["2041-1723"]},"keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry","Multidisciplinary"],"oa":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1038/ncomms8039","publication":"Nature Communications","day":"05","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1038/ncomms8039"}],"title":"Observation of laser-induced electronic structure in oriented polyatomic molecules","year":"2015","pmid":1,"extern":"1"},{"publication_status":"published","date_created":"2022-04-07T07:48:49Z","external_id":{"pmid":["26091034"]},"abstract":[{"lang":"eng","text":"Human cancer cells bear complex chromosome rearrangements that can be potential drivers of cancer development. However, the molecular mechanisms underlying these rearrangements have been unclear. Zhang et al. use a new technique combining live-cell imaging and single-cell sequencing to demonstrate that chromosomes mis-segregated to micronuclei frequently undergo chromothripsis-like rearrangements in the subsequent cell cycle."}],"scopus_import":"1","volume":161,"author":[{"last_name":"Hatch","full_name":"Hatch, Emily M.","first_name":"Emily M."},{"first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER"}],"page":"1502-1504","date_published":"2015-06-18T00:00:00Z","intvolume":"       161","quality_controlled":"1","issue":"7","_id":"11073","article_processing_charge":"No","publisher":"Elsevier","citation":{"ama":"Hatch EM, Hetzer M. Linking micronuclei to chromosome fragmentation. <i>Cell</i>. 2015;161(7):1502-1504. doi:<a href=\"https://doi.org/10.1016/j.cell.2015.06.005\">10.1016/j.cell.2015.06.005</a>","ista":"Hatch EM, Hetzer M. 2015. Linking micronuclei to chromosome fragmentation. Cell. 161(7), 1502–1504.","short":"E.M. Hatch, M. Hetzer, Cell 161 (2015) 1502–1504.","mla":"Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” <i>Cell</i>, vol. 161, no. 7, Elsevier, 2015, pp. 1502–04, doi:<a href=\"https://doi.org/10.1016/j.cell.2015.06.005\">10.1016/j.cell.2015.06.005</a>.","chicago":"Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” <i>Cell</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.cell.2015.06.005\">https://doi.org/10.1016/j.cell.2015.06.005</a>.","apa":"Hatch, E. M., &#38; Hetzer, M. (2015). Linking micronuclei to chromosome fragmentation. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cell.2015.06.005\">https://doi.org/10.1016/j.cell.2015.06.005</a>","ieee":"E. M. Hatch and M. Hetzer, “Linking micronuclei to chromosome fragmentation,” <i>Cell</i>, vol. 161, no. 7. Elsevier, pp. 1502–1504, 2015."},"type":"journal_article","oa_version":"Published Version","date_updated":"2022-07-18T08:34:33Z","month":"06","status":"public","title":"Linking micronuclei to chromosome fragmentation","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.cell.2015.06.005"}],"extern":"1","pmid":1,"year":"2015","keyword":["General Biochemistry","Genetics and Molecular Biology"],"oa":1,"publication_identifier":{"issn":["0092-8674"]},"language":[{"iso":"eng"}],"article_type":"original","day":"18","publication":"Cell","doi":"10.1016/j.cell.2015.06.005","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd"},{"publisher":"Elsevier","citation":{"mla":"Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” <i>Current Biology</i>, vol. 25, no. 10, Elsevier, 2015, pp. PR397-R399, doi:<a href=\"https://doi.org/10.1016/j.cub.2015.02.033\">10.1016/j.cub.2015.02.033</a>.","short":"E.M. Hatch, M. Hetzer, Current Biology 25 (2015) PR397-R399.","ama":"Hatch EM, Hetzer M. Chromothripsis. <i>Current Biology</i>. 2015;25(10):PR397-R399. doi:<a href=\"https://doi.org/10.1016/j.cub.2015.02.033\">10.1016/j.cub.2015.02.033</a>","ista":"Hatch EM, Hetzer M. 2015. Chromothripsis. Current Biology. 25(10), PR397-R399.","apa":"Hatch, E. M., &#38; Hetzer, M. (2015). Chromothripsis. <i>Current Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cub.2015.02.033\">https://doi.org/10.1016/j.cub.2015.02.033</a>","ieee":"E. M. Hatch and M. Hetzer, “Chromothripsis,” <i>Current Biology</i>, vol. 25, no. 10. Elsevier, pp. PR397-R399, 2015.","chicago":"Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” <i>Current Biology</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.cub.2015.02.033\">https://doi.org/10.1016/j.cub.2015.02.033</a>."},"article_processing_charge":"No","type":"journal_article","status":"public","month":"05","oa_version":"Published Version","date_updated":"2022-07-18T08:34:34Z","date_created":"2022-04-07T07:49:00Z","publication_status":"published","external_id":{"pmid":["25989073"]},"scopus_import":"1","volume":25,"page":"PR397-R399","author":[{"first_name":"Emily M.","full_name":"Hatch, Emily M.","last_name":"Hatch"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","first_name":"Martin W","full_name":"HETZER, Martin W","last_name":"HETZER"}],"intvolume":"        25","date_published":"2015-05-18T00:00:00Z","_id":"11074","quality_controlled":"1","issue":"10","publication_identifier":{"issn":["0960-9822"]},"language":[{"iso":"eng"}],"oa":1,"keyword":["General Agricultural and Biological Sciences","General Biochemistry","Genetics and Molecular Biology"],"article_type":"original","day":"18","publication":"Current Biology","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1016/j.cub.2015.02.033","title":"Chromothripsis","main_file_link":[{"url":"https://doi.org/10.1016/j.cub.2015.02.033","open_access":"1"}],"pmid":1,"extern":"1","year":"2015"},{"year":"2015","pmid":1,"extern":"1","title":"The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1083/jcb.201410047","publication":"Journal of Cell Biology","day":"16","article_type":"original","language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"keyword":["Cell Biology"],"_id":"11075","quality_controlled":"1","issue":"6","intvolume":"       208","date_published":"2015-03-16T00:00:00Z","page":"671-681","volume":208,"author":[{"first_name":"J. Sebastian","full_name":"Gomez-Cavazos, J. Sebastian","last_name":"Gomez-Cavazos"},{"last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"scopus_import":"1","abstract":[{"lang":"eng","text":"Previously, we identified the nucleoporin gp210/Nup210 as a critical regulator of muscle and neuronal differentiation, but how this nucleoporin exerts its function and whether it modulates nuclear pore complex (NPC) activity remain unknown. Here, we show that gp210/Nup210 mediates muscle cell differentiation in vitro via its conserved N-terminal domain that extends into the perinuclear space. Removal of the C-terminal domain, which partially mislocalizes gp210/Nup210 away from NPCs, efficiently rescues the differentiation defect caused by the knockdown of endogenous gp210/Nup210. Unexpectedly, a gp210/Nup210 mutant lacking the NPC-targeting transmembrane and C-terminal domains is sufficient for C2C12 myoblast differentiation. We demonstrate that the endoplasmic reticulum (ER) stress-specific caspase cascade is exacerbated during Nup210 depletion and that blocking ER stress-mediated apoptosis rescues differentiation of Nup210-deficient cells. Our results suggest that the role of gp210/Nup210 in cell differentiation is mediated by its large luminal domain, which can act independently of NPC association and appears to play a pivotal role in the maintenance of nuclear envelope/ER homeostasis."}],"external_id":{"pmid":["25778917"]},"date_created":"2022-04-07T07:49:10Z","publication_status":"published","month":"03","status":"public","date_updated":"2022-07-18T08:43:00Z","oa_version":"Published Version","type":"journal_article","citation":{"apa":"Gomez-Cavazos, J. S., &#38; Hetzer, M. (2015). The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.201410047\">https://doi.org/10.1083/jcb.201410047</a>","ieee":"J. S. Gomez-Cavazos and M. Hetzer, “The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis,” <i>Journal of Cell Biology</i>, vol. 208, no. 6. Rockefeller University Press, pp. 671–681, 2015.","chicago":"Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210 Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2015. <a href=\"https://doi.org/10.1083/jcb.201410047\">https://doi.org/10.1083/jcb.201410047</a>.","mla":"Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210 Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.” <i>Journal of Cell Biology</i>, vol. 208, no. 6, Rockefeller University Press, 2015, pp. 671–81, doi:<a href=\"https://doi.org/10.1083/jcb.201410047\">10.1083/jcb.201410047</a>.","short":"J.S. Gomez-Cavazos, M. Hetzer, Journal of Cell Biology 208 (2015) 671–681.","ista":"Gomez-Cavazos JS, Hetzer M. 2015. The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology. 208(6), 671–681.","ama":"Gomez-Cavazos JS, Hetzer M. The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. <i>Journal of Cell Biology</i>. 2015;208(6):671-681. doi:<a href=\"https://doi.org/10.1083/jcb.201410047\">10.1083/jcb.201410047</a>"},"publisher":"Rockefeller University Press","article_processing_charge":"No"},{"external_id":{"pmid":["25691464"]},"date_created":"2022-04-07T07:49:21Z","publication_status":"published","abstract":[{"text":"Nuclear pore complexes (NPCs) are composed of several copies of ∼30 different proteins called nucleoporins (Nups). NPCs penetrate the nuclear envelope (NE) and regulate the nucleocytoplasmic trafficking of macromolecules. Beyond this vital role, NPC components influence genome functions in a transport-independent manner. Nups play an evolutionarily conserved role in gene expression regulation that, in metazoans, extends into the nuclear interior. Additionally, in proliferative cells, Nups play a crucial role in genome integrity maintenance and mitotic progression. Here we discuss genome-related functions of Nups and their impact on essential DNA metabolism processes such as transcription, chromosome duplication, and segregation.","lang":"eng"}],"scopus_import":"1","page":"337-349","volume":29,"author":[{"first_name":"Arkaitz","full_name":"Ibarra, Arkaitz","last_name":"Ibarra"},{"last_name":"HETZER","first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"date_published":"2015-02-01T00:00:00Z","intvolume":"        29","quality_controlled":"1","issue":"4","_id":"11076","article_processing_charge":"No","publisher":"Cold Spring Harbor Laboratory","citation":{"apa":"Ibarra, A., &#38; Hetzer, M. (2015). Nuclear pore proteins and the control of genome functions. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.256495.114\">https://doi.org/10.1101/gad.256495.114</a>","ieee":"A. Ibarra and M. Hetzer, “Nuclear pore proteins and the control of genome functions,” <i>Genes &#38; Development</i>, vol. 29, no. 4. Cold Spring Harbor Laboratory, pp. 337–349, 2015.","chicago":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2015. <a href=\"https://doi.org/10.1101/gad.256495.114\">https://doi.org/10.1101/gad.256495.114</a>.","short":"A. Ibarra, M. Hetzer, Genes &#38; Development 29 (2015) 337–349.","mla":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” <i>Genes &#38; Development</i>, vol. 29, no. 4, Cold Spring Harbor Laboratory, 2015, pp. 337–49, doi:<a href=\"https://doi.org/10.1101/gad.256495.114\">10.1101/gad.256495.114</a>.","ista":"Ibarra A, Hetzer M. 2015. Nuclear pore proteins and the control of genome functions. Genes &#38; Development. 29(4), 337–349.","ama":"Ibarra A, Hetzer M. Nuclear pore proteins and the control of genome functions. <i>Genes &#38; Development</i>. 2015;29(4):337-349. doi:<a href=\"https://doi.org/10.1101/gad.256495.114\">10.1101/gad.256495.114</a>"},"type":"journal_article","oa_version":"Published Version","date_updated":"2022-07-18T08:43:20Z","status":"public","month":"02","title":"Nuclear pore proteins and the control of genome functions","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.256495.114"}],"extern":"1","pmid":1,"year":"2015","oa":1,"keyword":["Developmental Biology","Genetics"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"article_type":"original","day":"01","publication":"Genes & Development","doi":"10.1101/gad.256495.114","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd"},{"intvolume":"        29","date_published":"2015-06-16T00:00:00Z","page":"1224-1238","volume":29,"author":[{"first_name":"Filipe V.","full_name":"Jacinto, Filipe V.","last_name":"Jacinto"},{"last_name":"Benner","first_name":"Chris","full_name":"Benner, Chris"},{"last_name":"HETZER","full_name":"HETZER, Martin W","first_name":"Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"quality_controlled":"1","issue":"12","_id":"11077","date_created":"2022-04-07T07:49:31Z","external_id":{"pmid":["26080816"]},"publication_status":"published","abstract":[{"lang":"eng","text":"Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), membrane-embedded channels that mediate nuclear transport across the nuclear envelope. Recent evidence suggests that several Nups have additional roles in controlling the activation and silencing of developmental genes; however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the derepression of developmental genes and induction of early differentiation. This loss of stem cell identity is not associated with defects in the nuclear import of key pluripotency factors. Rather, Nup153 binds around the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb-repressive complex 1 (PRC1) to a subset of its target loci. Our results demonstrate a chromatin-associated role of Nup153 in maintaining stem cell pluripotency by functioning in mammalian epigenetic gene silencing."}],"scopus_import":"1","date_updated":"2022-07-18T08:43:51Z","oa_version":"Published Version","status":"public","month":"06","article_processing_charge":"No","citation":{"short":"F.V. Jacinto, C. Benner, M. Hetzer, Genes &#38; Development 29 (2015) 1224–1238.","mla":"Jacinto, Filipe V., et al. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” <i>Genes &#38; Development</i>, vol. 29, no. 12, Cold Spring Harbor Laboratory, 2015, pp. 1224–38, doi:<a href=\"https://doi.org/10.1101/gad.260919.115\">10.1101/gad.260919.115</a>.","ama":"Jacinto FV, Benner C, Hetzer M. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. <i>Genes &#38; Development</i>. 2015;29(12):1224-1238. doi:<a href=\"https://doi.org/10.1101/gad.260919.115\">10.1101/gad.260919.115</a>","ista":"Jacinto FV, Benner C, Hetzer M. 2015. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. Genes &#38; Development. 29(12), 1224–1238.","ieee":"F. V. Jacinto, C. Benner, and M. Hetzer, “The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing,” <i>Genes &#38; Development</i>, vol. 29, no. 12. Cold Spring Harbor Laboratory, pp. 1224–1238, 2015.","apa":"Jacinto, F. V., Benner, C., &#38; Hetzer, M. (2015). The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.260919.115\">https://doi.org/10.1101/gad.260919.115</a>","chicago":"Jacinto, Filipe V., Chris Benner, and Martin Hetzer. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2015. <a href=\"https://doi.org/10.1101/gad.260919.115\">https://doi.org/10.1101/gad.260919.115</a>."},"publisher":"Cold Spring Harbor Laboratory","type":"journal_article","extern":"1","pmid":1,"year":"2015","title":"The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing","main_file_link":[{"url":"https://doi.org/10.1101/gad.260919.115","open_access":"1"}],"publication":"Genes & Development","day":"16","doi":"10.1101/gad.260919.115","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","oa":1,"keyword":["Developmental Biology","Genetics"],"publication_identifier":{"eissn":["1549-5477"],"issn":["0890-9369"]},"language":[{"iso":"eng"}],"article_type":"original"},{"scopus_import":"1","external_id":{"pmid":["27135913"]},"date_created":"2022-04-07T07:49:39Z","publication_status":"published","abstract":[{"text":"Aging is associated with the decline of protein, cell, and organ function. Here, we use an integrated approach to characterize gene expression, bulk translation, and cell biology in the brains and livers of young and old rats. We identify 468 differences in protein abundance between young and old animals. The majority are a consequence of altered translation output, that is, the combined effect of changes in transcript abundance and translation efficiency. In addition, we identify 130 proteins whose overall abundance remains unchanged but whose sub-cellular localization, phosphorylation state, or splice-form varies. While some protein-level differences appear to be a generic property of the rats’ chronological age, the majority are specific to one organ. These may be a consequence of the organ’s physiology or the chronological age of the cells within the tissue. Taken together, our study provides an initial view of the proteome at the molecular, sub-cellular, and organ level in young and old rats.","lang":"eng"}],"quality_controlled":"1","issue":"3","_id":"11078","intvolume":"         1","date_published":"2015-09-23T00:00:00Z","page":"P224-237","volume":1,"author":[{"last_name":"Ori","full_name":"Ori, Alessandro","first_name":"Alessandro"},{"last_name":"Toyama","first_name":"Brandon H.","full_name":"Toyama, Brandon H."},{"first_name":"Michael S.","full_name":"Harris, Michael S.","last_name":"Harris"},{"last_name":"Bock","full_name":"Bock, Thomas","first_name":"Thomas"},{"last_name":"Iskar","full_name":"Iskar, Murat","first_name":"Murat"},{"last_name":"Bork","full_name":"Bork, Peer","first_name":"Peer"},{"last_name":"Ingolia","full_name":"Ingolia, Nicholas T.","first_name":"Nicholas T."},{"last_name":"HETZER","first_name":"Martin W","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"},{"last_name":"Beck","first_name":"Martin","full_name":"Beck, Martin"}],"type":"journal_article","article_processing_charge":"No","citation":{"ieee":"A. Ori <i>et al.</i>, “Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats,” <i>Cell Systems</i>, vol. 1, no. 3. Elsevier, pp. P224-237, 2015.","apa":"Ori, A., Toyama, B. H., Harris, M. S., Bock, T., Iskar, M., Bork, P., … Beck, M. (2015). Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. <i>Cell Systems</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cels.2015.08.012\">https://doi.org/10.1016/j.cels.2015.08.012</a>","chicago":"Ori, Alessandro, Brandon H. Toyama, Michael S. Harris, Thomas Bock, Murat Iskar, Peer Bork, Nicholas T. Ingolia, Martin Hetzer, and Martin Beck. “Integrated Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration in Old Rats.” <i>Cell Systems</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.cels.2015.08.012\">https://doi.org/10.1016/j.cels.2015.08.012</a>.","mla":"Ori, Alessandro, et al. “Integrated Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration in Old Rats.” <i>Cell Systems</i>, vol. 1, no. 3, Elsevier, 2015, pp. P224-237, doi:<a href=\"https://doi.org/10.1016/j.cels.2015.08.012\">10.1016/j.cels.2015.08.012</a>.","short":"A. Ori, B.H. Toyama, M.S. Harris, T. Bock, M. Iskar, P. Bork, N.T. Ingolia, M. Hetzer, M. Beck, Cell Systems 1 (2015) P224-237.","ama":"Ori A, Toyama BH, Harris MS, et al. Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. <i>Cell Systems</i>. 2015;1(3):P224-237. doi:<a href=\"https://doi.org/10.1016/j.cels.2015.08.012\">10.1016/j.cels.2015.08.012</a>","ista":"Ori A, Toyama BH, Harris MS, Bock T, Iskar M, Bork P, Ingolia NT, Hetzer M, Beck M. 2015. Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. Cell Systems. 1(3), P224-237."},"publisher":"Elsevier","date_updated":"2022-07-18T08:44:07Z","oa_version":"Published Version","status":"public","month":"09","main_file_link":[{"url":"https://doi.org/10.1016/j.cels.2015.08.012","open_access":"1"}],"title":"Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats","year":"2015","extern":"1","pmid":1,"article_type":"original","keyword":["Cell Biology","Histology","Pathology and Forensic Medicine"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2405-4712"]},"doi":"10.1016/j.cels.2015.08.012","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","publication":"Cell Systems","day":"23"}]