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  • Articles  (640)
  • Chemistry  (461)
  • Signal Transduction
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  • 1
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    Neutrophils scan for activated platelets to initiate inflammation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-12-06
    Description: Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils' bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280847/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sreeramkumar, Vinatha -- Adrover, Jose M -- Ballesteros, Ivan -- Cuartero, Maria Isabel -- Rossaint, Jan -- Bilbao, Izaskun -- Nacher, Maria -- Pitaval, Christophe -- Radovanovic, Irena -- Fukui, Yoshinori -- McEver, Rodger P -- Filippi, Marie-Dominique -- Lizasoain, Ignacio -- Ruiz-Cabello, Jesus -- Zarbock, Alexander -- Moro, Maria A -- Hidalgo, Andres -- HL03463/HL/NHLBI NIH HHS/ -- HL085607/HL/NHLBI NIH HHS/ -- HL090676/HL/NHLBI NIH HHS/ -- P01 HL085607/HL/NHLBI NIH HHS/ -- R01 HL034363/HL/NHLBI NIH HHS/ -- R01 HL090676/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1234-8. doi: 10.1126/science.1256478. Epub 2014 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. ; Unidad de Investigacion Neurovascular, Department of Pharmacology, Faculty of Medicine, Universidad Complutense and Instituto de Investigacion Hospital 12 de Octubre (i+12), Madrid, Spain. ; Department of Anesthesiology and Critical Care Medicine, University of Munster and Max Planck Institute Munster, Munster, Germany. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Ciber de Enfermedades Respiratorias (CIBERES), Madrid, Spain. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Faculty of Science, Medicine and Health, University of Wollongong, New South Wales, Australia. ; Division of Immunogenetics, Department of Immunobiology and Neuroscience, Kyushu University, Japan. ; Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. ; Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH, USA. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany. ahidalgo@cnic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Circulation ; Blood Platelets/*immunology ; Cell Movement ; Cell Polarity ; Endothelium, Vascular/immunology ; Inflammation/blood/*immunology ; Male ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Neutrophils/*immunology ; *Platelet Activation ; Signal Transduction ; Thrombosis/*immunology ; Venules/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The genome of the sea urchin Strongylocentrotus purpuratus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-11
    Description: We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159423/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sea Urchin Genome Sequencing Consortium -- Sodergren, Erica -- Weinstock, George M -- Davidson, Eric H -- Cameron, R Andrew -- Gibbs, Richard A -- Angerer, Robert C -- Angerer, Lynne M -- Arnone, Maria Ina -- Burgess, David R -- Burke, Robert D -- Coffman, James A -- Dean, Michael -- Elphick, Maurice R -- Ettensohn, Charles A -- Foltz, Kathy R -- Hamdoun, Amro -- Hynes, Richard O -- Klein, William H -- Marzluff, William -- McClay, David R -- Morris, Robert L -- Mushegian, Arcady -- Rast, Jonathan P -- Smith, L Courtney -- Thorndyke, Michael C -- Vacquier, Victor D -- Wessel, Gary M -- Wray, Greg -- Zhang, Lan -- Elsik, Christine G -- Ermolaeva, Olga -- Hlavina, Wratko -- Hofmann, Gretchen -- Kitts, Paul -- Landrum, Melissa J -- Mackey, Aaron J -- Maglott, Donna -- Panopoulou, Georgia -- Poustka, Albert J -- Pruitt, Kim -- Sapojnikov, Victor -- Song, Xingzhi -- Souvorov, Alexandre -- Solovyev, Victor -- Wei, Zheng -- Whittaker, Charles A -- Worley, Kim -- Durbin, K James -- Shen, Yufeng -- Fedrigo, Olivier -- Garfield, David -- Haygood, Ralph -- Primus, Alexander -- Satija, Rahul -- Severson, Tonya -- Gonzalez-Garay, Manuel L -- Jackson, Andrew R -- Milosavljevic, Aleksandar -- Tong, Mark -- Killian, Christopher E -- Livingston, Brian T -- Wilt, Fred H -- Adams, Nikki -- Belle, Robert -- Carbonneau, Seth -- Cheung, Rocky -- Cormier, Patrick -- Cosson, Bertrand -- Croce, Jenifer -- Fernandez-Guerra, Antonio -- Geneviere, Anne-Marie -- Goel, Manisha -- Kelkar, Hemant -- Morales, Julia -- Mulner-Lorillon, Odile -- Robertson, Anthony J -- Goldstone, Jared V -- Cole, Bryan -- Epel, David -- Gold, Bert -- Hahn, Mark E -- Howard-Ashby, Meredith -- Scally, Mark -- Stegeman, John J -- Allgood, Erin L -- Cool, Jonah -- Judkins, Kyle M -- McCafferty, Shawn S -- Musante, Ashlan M -- Obar, Robert A -- Rawson, Amanda P -- Rossetti, Blair J -- Gibbons, Ian R -- Hoffman, Matthew P -- Leone, Andrew -- Istrail, Sorin -- Materna, Stefan C -- Samanta, Manoj P -- Stolc, Viktor -- Tongprasit, Waraporn -- Tu, Qiang -- Bergeron, Karl-Frederik -- Brandhorst, Bruce P -- Whittle, James -- Berney, Kevin -- Bottjer, David J -- Calestani, Cristina -- Peterson, Kevin -- Chow, Elly -- Yuan, Qiu Autumn -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Bosdet, Ian -- Heesun, Shin -- Marra, Marco A -- Schein, Jacqueline -- Anderson, Michele K -- Brockton, Virginia -- Buckley, Katherine M -- Cohen, Avis H -- Fugmann, Sebastian D -- Hibino, Taku -- Loza-Coll, Mariano -- Majeske, Audrey J -- Messier, Cynthia -- Nair, Sham V -- Pancer, Zeev -- Terwilliger, David P -- Agca, Cavit -- Arboleda, Enrique -- Chen, Nansheng -- Churcher, Allison M -- Hallbook, F -- Humphrey, Glen W -- Idris, Mohammed M -- Kiyama, Takae -- Liang, Shuguang -- Mellott, Dan -- Mu, Xiuqian -- Murray, Greg -- Olinski, Robert P -- Raible, Florian -- Rowe, Matthew -- Taylor, John S -- Tessmar-Raible, Kristin -- Wang, D -- Wilson, Karen H -- Yaguchi, Shunsuke -- Gaasterland, Terry -- Galindo, Blanca E -- Gunaratne, Herath J -- Juliano, Celina -- Kinukawa, Masashi -- Moy, Gary W -- Neill, Anna T -- Nomura, Mamoru -- Raisch, Michael -- Reade, Anna -- Roux, Michelle M -- Song, Jia L -- Su, Yi-Hsien -- Townley, Ian K -- Voronina, Ekaterina -- Wong, Julian L -- Amore, Gabriele -- Branno, Margherita -- Brown, Euan R -- Cavalieri, Vincenzo -- Duboc, Veronique -- Duloquin, Louise -- Flytzanis, Constantin -- Gache, Christian -- Lapraz, Francois -- Lepage, Thierry -- Locascio, Annamaria -- Martinez, Pedro -- Matassi, Giorgio -- Matranga, Valeria -- Range, Ryan -- Rizzo, Francesca -- Rottinger, Eric -- Beane, Wendy -- Bradham, Cynthia -- Byrum, Christine -- Glenn, Tom -- Hussain, Sofia -- Manning, Gerard -- Miranda, Esther -- Thomason, Rebecca -- Walton, Katherine -- Wikramanayke, Athula -- Wu, Shu-Yu -- Xu, Ronghui -- Brown, C Titus -- Chen, Lili -- Gray, Rachel F -- Lee, Pei Yun -- Nam, Jongmin -- Oliveri, Paola -- Smith, Joel -- Muzny, Donna -- Bell, Stephanie -- Chacko, Joseph -- Cree, Andrew -- Curry, Stacey -- Davis, Clay -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Jerry -- Gill, Rachel -- Hamilton, Cerrissa -- Hernandez, Judith -- Hines, Sandra -- Hume, Jennifer -- Jackson, Laronda -- Jolivet, Angela -- Kovar, Christie -- Lee, Sandra -- Lewis, Lora -- Miner, George -- Morgan, Margaret -- Nazareth, Lynne V -- Okwuonu, Geoffrey -- Parker, David -- Pu, Ling-Ling -- Thorn, Rachel -- Wright, Rita -- 2P42 ESO7381/PHS HHS/ -- 5 U54 HG003273/HG/NHGRI NIH HHS/ -- EY11930/EY/NEI NIH HHS/ -- F32 ESO12794/PHS HHS/ -- F32 HD047136/HD/NICHD NIH HHS/ -- F32 HD047136-02/HD/NICHD NIH HHS/ -- F32 HD047136-03/HD/NICHD NIH HHS/ -- F32-HD47136/HD/NICHD NIH HHS/ -- GM058231/GM/NIGMS NIH HHS/ -- GM070840/GM/NIGMS NIH HHS/ -- GM61005/GM/NIGMS NIH HHS/ -- GM61464/GM/NIGMS NIH HHS/ -- HD-37105/HD/NICHD NIH HHS/ -- HD039948/HD/NICHD NIH HHS/ -- HD14483/HD/NICHD NIH HHS/ -- HD66219/HD/NICHD NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 ES006272/ES/NIEHS NIH HHS/ -- R01 ES006272-13/ES/NIEHS NIH HHS/ -- R01 GM070840/GM/NIGMS NIH HHS/ -- R01 HD028152/HD/NICHD NIH HHS/ -- R01ES006272/ES/NIEHS NIH HHS/ -- R37-HD12896/HD/NICHD NIH HHS/ -- RR-15044/RR/NCRR NIH HHS/ -- S19916/Biotechnology and Biological Sciences Research Council/United Kingdom -- T32 GM007601/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):941-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095691" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcification, Physiologic ; Cell Adhesion Molecules/genetics/physiology ; Complement Activation/genetics ; Computational Biology ; Embryonic Development/genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental ; Genes ; *Genome ; Immunity, Innate/genetics ; Immunologic Factors/genetics/physiology ; Male ; Nervous System Physiological Phenomena ; Proteins/genetics/physiology ; *Sequence Analysis, DNA ; Signal Transduction ; Strongylocentrotus purpuratus/embryology/*genetics/immunology/physiology ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Functional impact of global rare copy number variation in autism spectrum disorders (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-10
    Description: The autism spectrum disorders (ASDs) are a group of conditions characterized by impairments in reciprocal social interaction and communication, and the presence of restricted and repetitive behaviours. Individuals with an ASD vary greatly in cognitive development, which can range from above average to intellectual disability. Although ASDs are known to be highly heritable ( approximately 90%), the underlying genetic determinants are still largely unknown. Here we analysed the genome-wide characteristics of rare (〈1% frequency) copy number variation in ASD using dense genotyping arrays. When comparing 996 ASD individuals of European ancestry to 1,287 matched controls, cases were found to carry a higher global burden of rare, genic copy number variants (CNVs) (1.19 fold, P = 0.012), especially so for loci previously implicated in either ASD and/or intellectual disability (1.69 fold, P = 3.4 x 10(-4)). Among the CNVs there were numerous de novo and inherited events, sometimes in combination in a given family, implicating many novel ASD genes such as SHANK2, SYNGAP1, DLGAP2 and the X-linked DDX53-PTCHD1 locus. We also discovered an enrichment of CNVs disrupting functional gene sets involved in cellular proliferation, projection and motility, and GTPase/Ras signalling. Our results reveal many new genetic and functional targets in ASD that may lead to final connected pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021798/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinto, Dalila -- Pagnamenta, Alistair T -- Klei, Lambertus -- Anney, Richard -- Merico, Daniele -- Regan, Regina -- Conroy, Judith -- Magalhaes, Tiago R -- Correia, Catarina -- Abrahams, Brett S -- Almeida, Joana -- Bacchelli, Elena -- Bader, Gary D -- Bailey, Anthony J -- Baird, Gillian -- Battaglia, Agatino -- Berney, Tom -- Bolshakova, Nadia -- Bolte, Sven -- Bolton, Patrick F -- Bourgeron, Thomas -- Brennan, Sean -- Brian, Jessica -- Bryson, Susan E -- Carson, Andrew R -- Casallo, Guillermo -- Casey, Jillian -- Chung, Brian H Y -- Cochrane, Lynne -- Corsello, Christina -- Crawford, Emily L -- Crossett, Andrew -- Cytrynbaum, Cheryl -- Dawson, Geraldine -- de Jonge, Maretha -- Delorme, Richard -- Drmic, Irene -- Duketis, Eftichia -- Duque, Frederico -- Estes, Annette -- Farrar, Penny -- Fernandez, Bridget A -- Folstein, Susan E -- Fombonne, Eric -- Freitag, Christine M -- Gilbert, John -- Gillberg, Christopher -- Glessner, Joseph T -- Goldberg, Jeremy -- Green, Andrew -- Green, Jonathan -- Guter, Stephen J -- Hakonarson, Hakon -- Heron, Elizabeth A -- Hill, Matthew -- Holt, Richard -- Howe, Jennifer L -- Hughes, Gillian -- Hus, Vanessa -- Igliozzi, Roberta -- Kim, Cecilia -- Klauck, Sabine M -- Kolevzon, Alexander -- Korvatska, Olena -- Kustanovich, Vlad -- Lajonchere, Clara M -- Lamb, Janine A -- Laskawiec, Magdalena -- Leboyer, Marion -- Le Couteur, Ann -- Leventhal, Bennett L -- Lionel, Anath C -- Liu, Xiao-Qing -- Lord, Catherine -- Lotspeich, Linda -- Lund, Sabata C -- Maestrini, Elena -- Mahoney, William -- Mantoulan, Carine -- Marshall, Christian R -- McConachie, Helen -- McDougle, Christopher J -- McGrath, Jane -- McMahon, William M -- Merikangas, Alison -- Migita, Ohsuke -- Minshew, Nancy J -- Mirza, Ghazala K -- Munson, Jeff -- Nelson, Stanley F -- Noakes, Carolyn -- Noor, Abdul -- Nygren, Gudrun -- Oliveira, Guiomar -- Papanikolaou, Katerina -- Parr, Jeremy R -- Parrini, Barbara -- Paton, Tara -- Pickles, Andrew -- Pilorge, Marion -- Piven, Joseph -- Ponting, Chris P -- Posey, David J -- Poustka, Annemarie -- Poustka, Fritz -- Prasad, Aparna -- Ragoussis, Jiannis -- Renshaw, Katy -- Rickaby, Jessica -- Roberts, Wendy -- Roeder, Kathryn -- Roge, Bernadette -- Rutter, Michael L -- Bierut, Laura J -- Rice, John P -- Salt, Jeff -- Sansom, Katherine -- Sato, Daisuke -- Segurado, Ricardo -- Sequeira, Ana F -- Senman, Lili -- Shah, Naisha -- Sheffield, Val C -- Soorya, Latha -- Sousa, Ines -- Stein, Olaf -- Sykes, Nuala -- Stoppioni, Vera -- Strawbridge, Christina -- Tancredi, Raffaella -- Tansey, Katherine -- Thiruvahindrapduram, Bhooma -- Thompson, Ann P -- Thomson, Susanne -- Tryfon, Ana -- Tsiantis, John -- Van Engeland, Herman -- Vincent, John B -- Volkmar, Fred -- Wallace, Simon -- Wang, Kai -- Wang, Zhouzhi -- Wassink, Thomas H -- Webber, Caleb -- Weksberg, Rosanna -- Wing, Kirsty -- Wittemeyer, Kerstin -- Wood, Shawn -- Wu, Jing -- Yaspan, Brian L -- Zurawiecki, Danielle -- Zwaigenbaum, Lonnie -- Buxbaum, Joseph D -- Cantor, Rita M -- Cook, Edwin H -- Coon, Hilary -- Cuccaro, Michael L -- Devlin, Bernie -- Ennis, Sean -- Gallagher, Louise -- Geschwind, Daniel H -- Gill, Michael -- Haines, Jonathan L -- Hallmayer, Joachim -- Miller, Judith -- Monaco, Anthony P -- Nurnberger, John I Jr -- Paterson, Andrew D -- Pericak-Vance, Margaret A -- Schellenberg, Gerard D -- Szatmari, Peter -- Vicente, Astrid M -- Vieland, Veronica J -- Wijsman, Ellen M -- Scherer, Stephen W -- Sutcliffe, James S -- Betancur, Catalina -- 075491/Z/04/Wellcome Trust/United Kingdom -- AS2077/Autism Speaks/ -- AS7462/Autism Speaks/ -- G0601030/Medical Research Council/United Kingdom -- HD055751/HD/NICHD NIH HHS/ -- HD055782/HD/NICHD NIH HHS/ -- HD055784/HD/NICHD NIH HHS/ -- HD35465/HD/NICHD NIH HHS/ -- MC_U137761446/Medical Research Council/United Kingdom -- MH061009/MH/NIMH NIH HHS/ -- MH06359/MH/NIMH NIH HHS/ -- MH066673/MH/NIMH NIH HHS/ -- MH080647/MH/NIMH NIH HHS/ -- MH081754/MH/NIMH NIH HHS/ -- MH52708/MH/NIMH NIH HHS/ -- MH55284/MH/NIMH NIH HHS/ -- MH57881/MH/NIMH NIH HHS/ -- MH66766/MH/NIMH NIH HHS/ -- NS026630/NS/NINDS NIH HHS/ -- NS042165/NS/NINDS NIH HHS/ -- NS049261/NS/NINDS NIH HHS/ -- P01 CA089392/CA/NCI NIH HHS/ -- P01 CA089392-08/CA/NCI NIH HHS/ -- P01 HD035465-01S1/HD/NICHD NIH HHS/ -- P01 NS026630/NS/NINDS NIH HHS/ -- P01 NS026630-15/NS/NINDS NIH HHS/ -- P50 HD055748/HD/NICHD NIH HHS/ -- P50 HD055748-01/HD/NICHD NIH HHS/ -- P50 HD055748-02/HD/NICHD NIH HHS/ -- P50 HD055748-03/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- P50 HD055751-01/HD/NICHD NIH HHS/ -- P50 HD055782/HD/NICHD NIH HHS/ -- P50 HD055782-04/HD/NICHD NIH HHS/ -- R01 DA013423/DA/NIDA NIH HHS/ -- R01 DA013423-05/DA/NIDA NIH HHS/ -- R01 DA019963/DA/NIDA NIH HHS/ -- R01 DA019963-01A2/DA/NIDA NIH HHS/ -- R01 DA019963-02/DA/NIDA NIH HHS/ -- R01 DA019963-03/DA/NIDA NIH HHS/ -- R01 MH052708-05/MH/NIMH NIH HHS/ -- R01 MH055284/MH/NIMH NIH HHS/ -- R01 MH055284-04/MH/NIMH NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH057881-02/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH061009-05/MH/NIMH NIH HHS/ -- R01 MH080647/MH/NIMH NIH HHS/ -- R01 MH080647-11/MH/NIMH NIH HHS/ -- R01 MH081754/MH/NIMH NIH HHS/ -- R01 MH081754-01/MH/NIMH NIH HHS/ -- R01 NS042165/NS/NINDS NIH HHS/ -- R01 NS042165-05/NS/NINDS NIH HHS/ -- R01 NS049261/NS/NINDS NIH HHS/ -- R01 NS049261-02/NS/NINDS NIH HHS/ -- U01 HG004422/HG/NHGRI NIH HHS/ -- U01 HG004422-02/HG/NHGRI NIH HHS/ -- U10 MH066766-05/MH/NIMH NIH HHS/ -- U19 HD035469/HD/NICHD NIH HHS/ -- U19 HD035469-06/HD/NICHD NIH HHS/ -- U19 HD035469-07/HD/NICHD NIH HHS/ -- U19 HD035469-08/HD/NICHD NIH HHS/ -- U19 HD035469-09/HD/NICHD NIH HHS/ -- U19 HD035469-10/HD/NICHD NIH HHS/ -- U54 MH066673/MH/NIMH NIH HHS/ -- U54 MH066673-05/MH/NIMH NIH HHS/ -- UL1 TR000448/TR/NCATS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Jul 15;466(7304):368-72. doi: 10.1038/nature09146. Epub 2010 Jun 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Centre for Applied Genomics and Program in Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20531469" target="_blank"〉PubMed〈/a〉
    Keywords: Case-Control Studies ; Cell Movement ; Child ; Child Development Disorders, Pervasive/*genetics/pathology/*physiopathology ; Cytoprotection ; DNA Copy Number Variations/*genetics ; Europe/ethnology ; Gene Dosage/*genetics ; Genetic Predisposition to Disease/*genetics ; Genome-Wide Association Study ; Humans ; Signal Transduction ; Social Behavior
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Derivation of novel human ground state naive pluripotent stem cells (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-01
    Description: Mouse embryonic stem (ES) cells are isolated from the inner cell mass of blastocysts, and can be preserved in vitro in a naive inner-cell-mass-like configuration by providing exogenous stimulation with leukaemia inhibitory factor (LIF) and small molecule inhibition of ERK1/ERK2 and GSK3beta signalling (termed 2i/LIF conditions). Hallmarks of naive pluripotency include driving Oct4 (also known as Pou5f1) transcription by its distal enhancer, retaining a pre-inactivation X chromosome state, and global reduction in DNA methylation and in H3K27me3 repressive chromatin mark deposition on developmental regulatory gene promoters. Upon withdrawal of 2i/LIF, naive mouse ES cells can drift towards a primed pluripotent state resembling that of the post-implantation epiblast. Although human ES cells share several molecular features with naive mouse ES cells, they also share a variety of epigenetic properties with primed murine epiblast stem cells (EpiSCs). These include predominant use of the proximal enhancer element to maintain OCT4 expression, pronounced tendency for X chromosome inactivation in most female human ES cells, increase in DNA methylation and prominent deposition of H3K27me3 and bivalent domain acquisition on lineage regulatory genes. The feasibility of establishing human ground state naive pluripotency in vitro with equivalent molecular and functional features to those characterized in mouse ES cells remains to be defined. Here we establish defined conditions that facilitate the derivation of genetically unmodified human naive pluripotent stem cells from already established primed human ES cells, from somatic cells through induced pluripotent stem (iPS) cell reprogramming or directly from blastocysts. The novel naive pluripotent cells validated herein retain molecular characteristics and functional properties that are highly similar to mouse naive ES cells, and distinct from conventional primed human pluripotent cells. This includes competence in the generation of cross-species chimaeric mouse embryos that underwent organogenesis following microinjection of human naive iPS cells into mouse morulas. Collectively, our findings establish new avenues for regenerative medicine, patient-specific iPS cell disease modelling and the study of early human development in vitro and in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gafni, Ohad -- Weinberger, Leehee -- Mansour, Abed AlFatah -- Manor, Yair S -- Chomsky, Elad -- Ben-Yosef, Dalit -- Kalma, Yael -- Viukov, Sergey -- Maza, Itay -- Zviran, Asaf -- Rais, Yoach -- Shipony, Zohar -- Mukamel, Zohar -- Krupalnik, Vladislav -- Zerbib, Mirie -- Geula, Shay -- Caspi, Inbal -- Schneir, Dan -- Shwartz, Tamar -- Gilad, Shlomit -- Amann-Zalcenstein, Daniela -- Benjamin, Sima -- Amit, Ido -- Tanay, Amos -- Massarwa, Rada -- Novershtern, Noa -- Hanna, Jacob H -- England -- Nature. 2013 Dec 12;504(7479):282-6. doi: 10.1038/nature12745. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel [2]. ; 1] The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel [2] The Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel [3] The Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel [4]. ; 1] Wolfe PGD Stem Cell Lab, Racine IVF Unit, Lis Maternity Hospital, Tel Aviv Sourasky Medical Center, Tel-Aviv, Israel [2] The Department of Cell and Developmental Biology, Sackler Medical School, Tel-Aviv University, Israel. ; Wolfe PGD Stem Cell Lab, Racine IVF Unit, Lis Maternity Hospital, Tel Aviv Sourasky Medical Center, Tel-Aviv, Israel. ; The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. ; 1] The Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel [2] The Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel. ; The Israel National Center for Personalized Medicine (INCPM), Weizmann Institute of Science, Rehovot 76100, Israel. ; The Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; Cellular Reprogramming ; Chimera/embryology ; Chromatin/metabolism ; DNA Methylation ; Embryo, Mammalian/cytology/embryology ; Embryonic Stem Cells/cytology/metabolism ; Epigenesis, Genetic ; Female ; Germ Layers/cytology ; Histones/metabolism ; Humans ; Induced Pluripotent Stem Cells/*cytology/metabolism/transplantation ; Male ; Mice ; Morula/cytology ; Organogenesis ; Promoter Regions, Genetic/genetics ; Regenerative Medicine ; Reproducibility of Results ; Signal Transduction ; X Chromosome Inactivation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Positive regulation of T cell activation and integrin adhesion by the adapter Fyb/Slap (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-22
    Description: The molecular adapter Fyb/Slap regulates signaling downstream of the T cell receptor (TCR), but whether it plays a positive or negative role is controversial. We demonstrate that Fyb/Slap-deficient T cells exhibit defective proliferation and cytokine production in response to TCR stimulation. Fyb/Slap is also required in vivo for T cell-dependent immune responses. Functionally, Fyb/Slap has no apparent role in the activation of known TCR signaling pathways, F-actin polymerization, or TCR clustering. Rather, Fyb/Slap regulates TCR-induced integrin clustering and adhesion. Thus, Fyb/Slap is the first molecular adapter to be identified that couples TCR stimulation to the avidity modulation of integrins governing T cell adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, E K -- Krawczyk, C -- Kong, Y Y -- Raab, M -- Hyduk, S J -- Bouchard, D -- Chan, V S -- Kozieradzki, I -- Oliveira-Dos-Santos, A J -- Wakeham, A -- Ohashi, P S -- Cybulsky, M I -- Rudd, C E -- Penninger, J M -- New York, N.Y. -- Science. 2001 Sep 21;293(5538):2260-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11567140" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/metabolism ; Antigens, CD3/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; B-Lymphocytes/immunology ; Carrier Proteins/genetics/*physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Chimera ; Gene Targeting ; Humans ; Immunization ; Immunoglobulin G/biosynthesis ; Integrins/*metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Lectins, C-Type ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Phosphoproteins/genetics/*physiology ; Receptors, Antigen, T-Cell/immunology/metabolism ; Receptors, Interleukin-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/metabolism/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Rescue of a Drosophila NF1 mutant phenotype by protein kinase A (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: The neurofibromatosis type 1 (NF1) tumor suppressor protein is thought to restrict cell proliferation by functioning as a Ras-specific guanosine triphosphatase-activating protein. However, Drosophila homozygous for null mutations of an NF1 homolog showed no obvious signs of perturbed Ras1-mediated signaling. Loss of NF1 resulted in a reduction in size of larvae, pupae, and adults. This size defect was not modified by manipulating Ras1 signaling but was restored by expression of activated adenosine 3', 5'-monophosphate-dependent protein kinase (PKA). Thus, NF1 and PKA appear to interact in a pathway that controls the overall growth of Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉The, I -- Hannigan, G E -- Cowley, G S -- Reginald, S -- Zhong, Y -- Gusella, J F -- Hariharan, I K -- Bernards, A -- NS22229/NS/NINDS NIH HHS/ -- NS34779/NS/NINDS NIH HHS/ -- NS36084/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 May 2;276(5313):791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Harvard Medical School Building 149, 13th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115203" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Count ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/genetics/*metabolism ; Drosophila/cytology/*genetics/growth & development/metabolism ; *Drosophila Proteins ; GTP Phosphohydrolases/metabolism ; Genes, Insect ; Insect Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Nerve Tissue Proteins ; Neurofibromin 1 ; Phenotype ; Proteins/chemistry/genetics ; Recombinant Fusion Proteins/pharmacology ; Signal Transduction ; *ras GTPase-Activating Proteins ; ras Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Unexpected requirement for ELMO1 in clearance of apoptotic germ cells in vivo (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-17
    Description: Apoptosis and the subsequent clearance of dying cells occurs throughout development and adult life in many tissues. Failure to promptly clear apoptotic cells has been linked to many diseases. ELMO1 is an evolutionarily conserved cytoplasmic engulfment protein that functions downstream of the phosphatidylserine receptor BAI1, and, along with DOCK1 and the GTPase RAC1, promotes internalization of the dying cells. Here we report the generation of ELMO1-deficient mice, which we found to be unexpectedly viable and grossly normal. However, they had a striking testicular pathology, with disrupted seminiferous epithelium, multinucleated giant cells, uncleared apoptotic germ cells and decreased sperm output. Subsequent in vitro and in vivo analyses revealed a crucial role for ELMO1 in the phagocytic clearance of apoptotic germ cells by Sertoli cells lining the seminiferous epithelium. The engulfment receptor BAI1 and RAC1 (upstream and downstream of ELMO1, respectively) were also important for Sertoli-cell-mediated engulfment. Collectively, these findings uncover a selective requirement for ELMO1 in Sertoli-cell-mediated removal of apoptotic germ cells and make a compelling case for a relationship between engulfment and tissue homeostasis in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773546/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elliott, Michael R -- Zheng, Shuqiu -- Park, Daeho -- Woodson, Robin I -- Reardon, Michael A -- Juncadella, Ignacio J -- Kinchen, Jason M -- Zhang, Jun -- Lysiak, Jeffrey J -- Ravichandran, Kodi S -- R01 GM064709/GM/NIGMS NIH HHS/ -- R01 HD057242/HD/NICHD NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):333-7. doi: 10.1038/nature09356.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844538" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/deficiency/genetics/*metabolism ; Angiogenic Proteins/metabolism ; Animals ; *Apoptosis ; Cell Line ; Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Neuropeptides/metabolism ; Phagocytosis/*physiology ; Phosphatidylserines/metabolism ; Seminiferous Epithelium/cytology/pathology ; Sertoli Cells/*cytology/*metabolism/pathology ; Signal Transduction ; Spermatozoa/*cytology/pathology ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Spatial control of EGF receptor activation by reversible dimerization on living cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-09
    Description: Epidermal growth factor receptor (EGFR) is a type I receptor tyrosine kinase, the deregulation of which has been implicated in a variety of human carcinomas. EGFR signalling is preceded by receptor dimerization, typically thought to result from a ligand-induced conformational change in the ectodomain that exposes a loop (dimerization arm) required for receptor association. Ligand binding may also trigger allosteric changes in the cytoplasmic domain of the receptor that is crucial for signalling. Despite these insights, ensemble-averaging approaches have not determined the precise mechanism of receptor activation in situ. Using quantum-dot-based optical tracking of single molecules combined with a novel time-dependent diffusivity analysis, here we present the dimerization dynamics of individual EGFRs on living cells. Before ligand addition, EGFRs spontaneously formed finite-lifetime dimers kinetically stabilized by their dimerization arms. The dimers were primed both for ligand binding and for signalling, such that after EGF addition they rapidly showed a very slow diffusivity state that correlated with activation. Although the kinetic stability of unliganded dimers was in principle sufficient for EGF-independent activation, ligand binding was still required for signalling. Interestingly, dimers were enriched in the cell periphery in an actin- and receptor-expression-dependent fashion, resulting in a peripheral enhancement of EGF-induced signalling that may enable polarized responses to growth factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Inhee -- Akita, Robert -- Vandlen, Richard -- Toomre, Derek -- Schlessinger, Joseph -- Mellman, Ira -- AR 051448/AR/NIAMS NIH HHS/ -- AR 051886/AR/NIAMS NIH HHS/ -- P50 AR 054086/AR/NIAMS NIH HHS/ -- P50 AR054086/AR/NIAMS NIH HHS/ -- R01 AR051448/AR/NIAMS NIH HHS/ -- R01 AR051886/AR/NIAMS NIH HHS/ -- England -- Nature. 2010 Apr 1;464(7289):783-7. doi: 10.1038/nature08827. Epub 2010 Mar 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20208517" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; CHO Cells ; Cell Line, Tumor ; *Cell Polarity ; Cell Survival ; Cricetinae ; Cricetulus ; Diffusion ; Enzyme Activation/drug effects ; Enzyme Stability/drug effects ; Epidermal Growth Factor/metabolism/pharmacology ; GRB2 Adaptor Protein/genetics/metabolism ; Gene Expression Regulation ; Humans ; Kinetics ; Ligands ; *Protein Multimerization/drug effects ; Protein Transport ; Receptor, Epidermal Growth Factor/agonists/*chemistry/genetics/*metabolism ; Signal Transduction ; Thermodynamics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Human intracellular ISG15 prevents interferon-alpha/beta over-amplification and auto-inflammation (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-10-14
    Description: Intracellular ISG15 is an interferon (IFN)-alpha/beta-inducible ubiquitin-like modifier which can covalently bind other proteins in a process called ISGylation; it is an effector of IFN-alpha/beta-dependent antiviral immunity in mice. We previously published a study describing humans with inherited ISG15 deficiency but without unusually severe viral diseases. We showed that these patients were prone to mycobacterial disease and that human ISG15 was non-redundant as an extracellular IFN-gamma-inducing molecule. We show here that ISG15-deficient patients also display unanticipated cellular, immunological and clinical signs of enhanced IFN-alpha/beta immunity, reminiscent of the Mendelian autoinflammatory interferonopathies Aicardi-Goutieres syndrome and spondyloenchondrodysplasia. We further show that an absence of intracellular ISG15 in the patients' cells prevents the accumulation of USP18, a potent negative regulator of IFN-alpha/beta signalling, resulting in the enhancement and amplification of IFN-alpha/beta responses. Human ISG15, therefore, is not only redundant for antiviral immunity, but is a key negative regulator of IFN-alpha/beta immunity. In humans, intracellular ISG15 is IFN-alpha/beta-inducible not to serve as a substrate for ISGylation-dependent antiviral immunity, but to ensure USP18-dependent regulation of IFN-alpha/beta and prevention of IFN-alpha/beta-dependent autoinflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303590/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303590/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xianqin -- Bogunovic, Dusan -- Payelle-Brogard, Beatrice -- Francois-Newton, Veronique -- Speer, Scott D -- Yuan, Chao -- Volpi, Stefano -- Li, Zhi -- Sanal, Ozden -- Mansouri, Davood -- Tezcan, Ilhan -- Rice, Gillian I -- Chen, Chunyuan -- Mansouri, Nahal -- Mahdaviani, Seyed Alireza -- Itan, Yuval -- Boisson, Bertrand -- Okada, Satoshi -- Zeng, Lu -- Wang, Xing -- Jiang, Hui -- Liu, Wenqiang -- Han, Tiantian -- Liu, Delin -- Ma, Tao -- Wang, Bo -- Liu, Mugen -- Liu, Jing-Yu -- Wang, Qing K -- Yalnizoglu, Dilek -- Radoshevich, Lilliana -- Uze, Gilles -- Gros, Philippe -- Rozenberg, Flore -- Zhang, Shen-Ying -- Jouanguy, Emmanuelle -- Bustamante, Jacinta -- Garcia-Sastre, Adolfo -- Abel, Laurent -- Lebon, Pierre -- Notarangelo, Luigi D -- Crow, Yanick J -- Boisson-Dupuis, Stephanie -- Casanova, Jean-Laurent -- Pellegrini, Sandra -- 1P01AI076210-01A1/AI/NIAID NIH HHS/ -- 309449/European Research Council/International -- 8UL1TR000043/TR/NCATS NIH HHS/ -- P01 AI076210/AI/NIAID NIH HHS/ -- P01 AI090935/AI/NIAID NIH HHS/ -- P01AI090935/AI/NIAID NIH HHS/ -- R00 AI106942/AI/NIAID NIH HHS/ -- R00AI106942-02/AI/NIAID NIH HHS/ -- R01 AI035237/AI/NIAID NIH HHS/ -- R37 AI095983/AI/NIAID NIH HHS/ -- R37AI095983/AI/NIAID NIH HHS/ -- U19 AI083025/AI/NIAID NIH HHS/ -- U19AI083025/AI/NIAID NIH HHS/ -- UL1 TR000043/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jan 1;517(7532):89-93. doi: 10.1038/nature13801. Epub 2014 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China. ; 1] St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA [2] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; Institut Pasteur, Cytokine Signaling Unit, CNRS URA 1961, 75724 Paris, France. ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Microbiology Training Area, Graduate School of Biomedical Sciences of Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; 1] Division of Immunology, Children's Hospital Boston, Boston, Massachusetts 02115, USA [2] Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, 16132 Genoa, Italy. ; Immunology Division and Pediatric Neurology Department, Hacettepe University Children's Hospital, 06100 Ankara, Turkey. ; Division of Infectious Diseases and Clinical Immunology, Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, 4739 Teheran, Iran. ; Manchester Academic Health Science Centre, University of Manchester, Genetic Medicine, Manchester, M13 9NT, UK. ; Department of Pediatrics, Third Xiangya Hospital, Central South University, Changsha 410013, China. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA. ; BGI-Shenzhen, Shenzhen 518083, China. ; Sangzhi County People's Hospital, Sangzhi 427100, China. ; Genetics Laboratory, Hubei Maternal and Child Health Hospital, Wuhan, Hubei 430070, China. ; 1] Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China [2] Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA. ; Institut Pasteur, Bacteria-Cell Interactions Unit, 75724 Paris, France. ; CNRS UMR5235, Montpellier II University, Place Eugene Bataillon, 34095 Montpellier, France. ; Department of Biochemistry, McGill University, Montreal, QC H3A 0G4, Canada. ; Paris Descartes University, 75006 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] Center for the Study of Primary Immunodeficiencies, Necker Hospital for Sick Children, 75015 Paris, France. ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; 1] St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA [2] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [3] Paris Descartes University, Imagine Institute, 75015 Paris, France. ; Division of Immunology, Children's Hospital Boston, Boston, Massachusetts 02115, USA. ; 1] Manchester Academic Health Science Centre, University of Manchester, Genetic Medicine, Manchester, M13 9NT, UK [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] INSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, Imagine Institute, 75006 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] Howard Hughes Medical Institute, New York, New York 10065, USA [4] Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children, 75015 Paris, France [5]. ; 1] Institut Pasteur, Cytokine Signaling Unit, CNRS URA 1961, 75724 Paris, France [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25307056" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Alleles ; Child ; Cytokines/deficiency/genetics/*metabolism ; Endopeptidases/chemistry/metabolism ; Female ; Gene Expression Regulation ; Humans ; Inflammation/genetics/immunology/*prevention & control ; Interferon Type I/*immunology/metabolism ; Intracellular Space/*metabolism ; Male ; Pedigree ; S-Phase Kinase-Associated Proteins/metabolism ; Signal Transduction ; Ubiquitination ; Ubiquitins/deficiency/genetics/*metabolism ; Viruses/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    GPI-anchored cell-surface molecules complexed to protein tyrosine kinases (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: Binding of ligand or antibody to certain cell-surface proteins that are anchored to the membrane by glycophosphatidylinositol (GPI) can cause activation of leukocytes. However, it is not known how these molecules, which lack intracellular domains, can transduce signals. The GPI-linked human molecules CD59, CD55, CD48, CD24, and CD14 as well as the mouse molecules Thy-1 and Ly-6 were found to associate with protein tyrosine kinases, key regulators of cell activation and signal transduction. A protein tyrosine kinase associated with the GPI-linked proteins CD59, CD55, and CD48 in human T cells, and with Thy-1 in mouse T cells was identified as p56lck, a protein tyrosine kinase related to Src. This interaction of GPI-linked molecules with protein tyrosine kinases suggests a potential mechanism of signal transduction in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefanova, I -- Horejsi, V -- Ansotegui, I J -- Knapp, W -- Stockinger, H -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1016-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Immunology-Vienna International Research Cooperation Center, University of Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1719635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*physiology ; Antigens, Differentiation/physiology ; Cell Adhesion Molecules/physiology ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; Humans ; Membrane Glycoproteins/physiology ; Membrane Proteins/*physiology ; Mice ; Phosphatidylinositols/physiology ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*physiology ; Receptor Aggregation ; Receptors, Cell Surface/*physiology ; Signal Transduction ; Tyrosine/analogs & derivatives/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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