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  • Articles  (77)
  • Signal Transduction  (77)
  • 2010-2014  (77)
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  • 2010-2014  (77)
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  • 1
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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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  • 2
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    The genetic landscape of the childhood cancer medulloblastoma (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: Medulloblastoma (MB) is the most common malignant brain tumor of children. To identify the genetic alterations in this tumor type, we searched for copy number alterations using high-density microarrays and sequenced all known protein-coding genes and microRNA genes using Sanger sequencing in a set of 22 MBs. We found that, on average, each tumor had 11 gene alterations, fewer by a factor of 5 to 10 than in the adult solid tumors that have been sequenced to date. In addition to alterations in the Hedgehog and Wnt pathways, our analysis led to the discovery of genes not previously known to be altered in MBs. Most notably, inactivating mutations of the histone-lysine N-methyltransferase genes MLL2 or MLL3 were identified in 16% of MB patients. These results demonstrate key differences between the genetic landscapes of adult and childhood cancers, highlight dysregulation of developmental pathways as an important mechanism underlying MBs, and identify a role for a specific type of histone methylation in human tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110744/" 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/PMC3110744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Li, Meng -- Zhang, Xiaosong -- Jones, Sian -- Leary, Rebecca J -- Lin, Jimmy Cheng-Ho -- Boca, Simina M -- Carter, Hannah -- Samayoa, Josue -- Bettegowda, Chetan -- Gallia, Gary L -- Jallo, George I -- Binder, Zev A -- Nikolsky, Yuri -- Hartigan, James -- Smith, Doug R -- Gerhard, Daniela S -- Fults, Daniel W -- VandenBerg, Scott -- Berger, Mitchel S -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Clara, Carlos -- Phillips, Peter C -- Minturn, Jane E -- Biegel, Jaclyn A -- Judkins, Alexander R -- Resnick, Adam C -- Storm, Phillip B -- Curran, Tom -- He, Yiping -- Rasheed, B Ahmed -- Friedman, Henry S -- Keir, Stephen T -- McLendon, Roger -- Northcott, Paul A -- Taylor, Michael D -- Burger, Peter C -- Riggins, Gregory J -- Karchin, Rachel -- Parmigiani, Giovanni -- Bigner, Darell D -- Yan, Hai -- Papadopoulos, Nick -- Vogelstein, Bert -- Kinzler, Kenneth W -- Velculescu, Victor E -- CA057345/CA/NCI NIH HHS/ -- CA096832/CA/NCI NIH HHS/ -- CA118822/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA135877/CA/NCI NIH HHS/ -- GM074906-01A1/GM/NIGMS NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-03/CA/NCI NIH HHS/ -- R01 CA108622/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-05/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-20/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):435-9. doi: 10.1126/science.1198056. Epub 2010 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163964" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cerebellar Neoplasms/*genetics/metabolism ; Child ; DNA Copy Number Variations ; DNA-Binding Proteins/genetics/metabolism ; *Genes, Neoplasm ; Genes, Tumor Suppressor ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Histones/metabolism ; Humans ; Medulloblastoma/*genetics/metabolism ; Methylation ; MicroRNAs/genetics ; *Mutation ; Neoplasm Proteins/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Sequence Analysis, DNA ; Signal Transduction
    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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  • 3
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    The landscape of somatic copy-number alteration across human cancers (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-19
    Description: A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826709/" 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/PMC2826709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beroukhim, Rameen -- Mermel, Craig H -- Porter, Dale -- Wei, Guo -- Raychaudhuri, Soumya -- Donovan, Jerry -- Barretina, Jordi -- Boehm, Jesse S -- Dobson, Jennifer -- Urashima, Mitsuyoshi -- Mc Henry, Kevin T -- Pinchback, Reid M -- Ligon, Azra H -- Cho, Yoon-Jae -- Haery, Leila -- Greulich, Heidi -- Reich, Michael -- Winckler, Wendy -- Lawrence, Michael S -- Weir, Barbara A -- Tanaka, Kumiko E -- Chiang, Derek Y -- Bass, Adam J -- Loo, Alice -- Hoffman, Carter -- Prensner, John -- Liefeld, Ted -- Gao, Qing -- Yecies, Derek -- Signoretti, Sabina -- Maher, Elizabeth -- Kaye, Frederic J -- Sasaki, Hidefumi -- Tepper, Joel E -- Fletcher, Jonathan A -- Tabernero, Josep -- Baselga, Jose -- Tsao, Ming-Sound -- Demichelis, Francesca -- Rubin, Mark A -- Janne, Pasi A -- Daly, Mark J -- Nucera, Carmelo -- Levine, Ross L -- Ebert, Benjamin L -- Gabriel, Stacey -- Rustgi, Anil K -- Antonescu, Cristina R -- Ladanyi, Marc -- Letai, Anthony -- Garraway, Levi A -- Loda, Massimo -- Beer, David G -- True, Lawrence D -- Okamoto, Aikou -- Pomeroy, Scott L -- Singer, Samuel -- Golub, Todd R -- Lander, Eric S -- Getz, Gad -- Sellers, William R -- Meyerson, Matthew -- K08 AR055688/AR/NIAMS NIH HHS/ -- K08 AR055688-03/AR/NIAMS NIH HHS/ -- K08 AR055688-04/AR/NIAMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 CA122833-01A1/CA/NCI NIH HHS/ -- K08 CA122833-02/CA/NCI NIH HHS/ -- K08 CA122833-03/CA/NCI NIH HHS/ -- K08 CA134931/CA/NCI NIH HHS/ -- K08CA122833/CA/NCI NIH HHS/ -- P01CA 098101/CA/NCI NIH HHS/ -- P01CA085859/CA/NCI NIH HHS/ -- P50CA90578/CA/NCI NIH HHS/ -- R01 CA109038/CA/NCI NIH HHS/ -- R01 GM074024/GM/NIGMS NIH HHS/ -- R01CA109038/CA/NCI NIH HHS/ -- R01CA109467/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA126546/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 18;463(7283):899-905. doi: 10.1038/nature08822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Program and Medical and Population Genetics Group, The Broad Institute of M.I.T. and Harvard, 7 Cambridge Center.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164920" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis/genetics ; Cell Line, Tumor ; Cell Survival/genetics ; DNA Copy Number Variations/*genetics ; Gene Amplification/genetics ; Gene Dosage/*genetics ; Genomics ; Humans ; Multigene Family/genetics ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/classification/*genetics/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Signal Transduction ; bcl-X Protein/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Dietary restriction: standing up for sirtuins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985480/" 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/PMC3985480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baur, Joseph A -- Chen, Danica -- Chini, Eduardo N -- Chua, Katrin -- Cohen, Haim Y -- de Cabo, Rafael -- Deng, Chuxia -- Dimmeler, Stefanie -- Gius, David -- Guarente, Leonard P -- Helfand, Stephen L -- Imai, Shin-Ichiro -- Itoh, Hiroshi -- Kadowaki, Takashi -- Koya, Daisuke -- Leeuwenburgh, Christiaan -- McBurney, Michael -- Nabeshima, Yo-Ichi -- Neri, Christian -- Oberdoerffer, Philipp -- Pestell, Richard G -- Rogina, Blanka -- Sadoshima, Junichi -- Sartorelli, Vittorio -- Serrano, Manuel -- Sinclair, David A -- Steegborn, Clemens -- Tatar, Marc -- Tissenbaum, Heidi A -- Tong, Qiang -- Tsubota, Kazuo -- Vaquero, Alejandro -- Verdin, Eric -- P01 AG027916/AG/NIA NIH HHS/ -- R00 AG031182/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG023039/AG/NIA NIH HHS/ -- R01 AG023088/AG/NIA NIH HHS/ -- R01 AG023088-08/AG/NIA NIH HHS/ -- R01 AG024360/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 AG028730-05/AG/NIA NIH HHS/ -- R01 HL067724/HL/NHLBI NIH HHS/ -- R01 HL091469/HL/NHLBI NIH HHS/ -- R01 HL102738/HL/NHLBI NIH HHS/ -- R37 AG024360/AG/NIA NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1012-3; author reply 1013-4. doi: 10.1126/science.329.5995.1012.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798296" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Humans ; *Longevity ; Signal Transduction ; Sirtuins/*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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  • 5
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    Rewiring of genetic networks in response to DNA damage (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping, we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases, and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3 phosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized. Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006187/" 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/PMC3006187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandyopadhyay, Sourav -- Mehta, Monika -- Kuo, Dwight -- Sung, Min-Kyung -- Chuang, Ryan -- Jaehnig, Eric J -- Bodenmiller, Bernd -- Licon, Katherine -- Copeland, Wilbert -- Shales, Michael -- Fiedler, Dorothea -- Dutkowski, Janusz -- Guenole, Aude -- van Attikum, Haico -- Shokat, Kevan M -- Kolodner, Richard D -- Huh, Won-Ki -- Aebersold, Ruedi -- Keogh, Michael-Christopher -- Krogan, Nevan J -- Ideker, Trey -- P30CA013330/CA/NCI NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- R01 ES014811/ES/NIEHS NIH HHS/ -- R01 ES014811-01A1/ES/NIEHS NIH HHS/ -- R01 ES014811-02/ES/NIEHS NIH HHS/ -- R01 ES014811-02S1/ES/NIEHS NIH HHS/ -- R01 ES014811-03/ES/NIEHS NIH HHS/ -- R01 ES014811-04/ES/NIEHS NIH HHS/ -- R01 ES014811-05/ES/NIEHS NIH HHS/ -- R01 ES014811-05S1/ES/NIEHS NIH HHS/ -- R01 ES014811-06/ES/NIEHS NIH HHS/ -- R01 GM026017/GM/NIGMS NIH HHS/ -- R01 GM084279/GM/NIGMS NIH HHS/ -- R01 GM084279-01A1/GM/NIGMS NIH HHS/ -- R01 GM084279-02/GM/NIGMS NIH HHS/ -- R01 GM084279-02S1/GM/NIGMS NIH HHS/ -- R01 GM084279-03/GM/NIGMS NIH HHS/ -- R01 GM084279-04/GM/NIGMS NIH HHS/ -- R01 GM084448/GM/NIGMS NIH HHS/ -- R01-ES14811/ES/NIEHS NIH HHS/ -- R01-GM084279/GM/NIGMS NIH HHS/ -- R37 GM026017/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1385-9. doi: 10.1126/science.1195618.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127252" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/metabolism ; *DNA Damage ; DNA Repair/*genetics ; DNA, Fungal/genetics ; *Epistasis, Genetic ; *Gene Regulatory Networks ; Genes, Fungal ; Histones/genetics/metabolism ; Methyl Methanesulfonate/pharmacology ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Mutagens/pharmacology ; Mutation ; Phosphoprotein Phosphatases/genetics/metabolism ; Protein Interaction Mapping ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Saccharomyces cerevisiae/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Signal Transduction ; Transcription Factors/genetics/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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    Minimal "Self" peptides that inhibit phagocytic clearance and enhance delivery of nanoparticles (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-23
    Description: Foreign particles and cells are cleared from the body by phagocytes that must also recognize and avoid clearance of "self" cells. The membrane protein CD47 is reportedly a "marker of self" in mice that impedes phagocytosis of self by signaling through the phagocyte receptor CD172a. Minimal "Self" peptides were computationally designed from human CD47 and then synthesized and attached to virus-size particles for intravenous injection into mice that express a CD172a variant compatible with hCD47. Self peptides delay macrophage-mediated clearance of nanoparticles, which promotes persistent circulation that enhances dye and drug delivery to tumors. Self-peptide affinity for CD172a is near the optimum measured for human CD172a variants, and Self peptide also potently inhibits nanoparticle uptake mediated by the contractile cytoskeleton. The reductionist approach reveals the importance of human Self peptides and their utility in enhancing drug delivery and imaging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966479/" 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/PMC3966479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez, Pia L -- Harada, Takamasa -- Christian, David A -- Pantano, Diego A -- Tsai, Richard K -- Discher, Dennis E -- 8UL1TR000003/TR/NCATS NIH HHS/ -- P01-DK032094/DK/NIDDK NIH HHS/ -- P30-DK090969/DK/NIDDK NIH HHS/ -- R01 EB007049/EB/NIBIB NIH HHS/ -- R01 HL062352/HL/NHLBI NIH HHS/ -- R01-EB007049/EB/NIBIB NIH HHS/ -- R01-HL062352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):971-5. doi: 10.1126/science.1229568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biophysics and NanoBioPolymers Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD47/chemistry/immunology/metabolism ; Antigens, Differentiation/*metabolism ; Antineoplastic Agents/administration & dosage ; Autoantigens ; Blood Circulation ; Diagnostic Imaging/methods ; Drug Delivery Systems/*methods ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; *Nanoparticles/administration & dosage/analysis ; Neoplasms/chemistry/diagnosis/drug therapy ; Paclitaxel/administration & dosage ; Particle Size ; Peptide Fragments/chemical synthesis/chemistry/immunology/*metabolism ; Phagocytes/immunology/metabolism ; *Phagocytosis ; Receptors, Immunologic/immunology/*metabolism ; Signal Transduction
    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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    Measurement of single-cell dynamics (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-11
    Description: Populations of cells are almost always heterogeneous in function and fate. To understand the plasticity of cells, it is vital to measure quantitatively and dynamically the molecular processes that underlie cell-fate decisions in single cells. Early events in cell signalling often occur within seconds of the stimulus, whereas intracellular signalling processes and transcriptional changes can take minutes or hours. By contrast, cell-fate decisions, such as whether a cell divides, differentiates or dies, can take many hours or days. Multiparameter experimental and computational methods that integrate quantitative measurement and mathematical simulation of these noisy and complex processes are required to understand the highly dynamic mechanisms that control cell plasticity and fate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spiller, David G -- Wood, Christopher D -- Rand, David A -- White, Michael R H -- 67252/Wellcome Trust/United Kingdom -- BB/D010748/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E004210/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E012965/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E013600/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F005814/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F005938/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013725/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBD0107481/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0042101/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0129651/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0136001/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0052611/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0053181/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0058061/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0059381/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500346/Medical Research Council/United Kingdom -- England -- Nature. 2010 Jun 10;465(7299):736-45. doi: 10.1038/nature09232.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Imaging, School of Biological Sciences, Bioscience Research Building, Crown Street, Liverpool L69 7ZB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535203" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; *Cell Physiological Phenomena/genetics/physiology ; Cytological Techniques/*methods ; Microfluidics/methods ; Protein Binding ; Protein Transport ; Signal Transduction ; Transcription, Genetic
    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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    Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-05
    Description: The development and severity of inflammatory bowel diseases and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that mice with an intestinal epithelial cell (IEC)-specific deletion of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3(DeltaIEC) mice) exhibited extensive dysregulation of IEC-intrinsic gene expression, including decreased basal expression of genes associated with antimicrobial defence. Critically, conventionally housed HDAC3(DeltaIEC) mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3(DeltaIEC) mice showed significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 has a central role in maintaining intestinal homeostasis. Re-derivation of HDAC3(DeltaIEC) mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function were largely restored in the absence of commensal bacteria. Although the specific mechanisms through which IEC-intrinsic HDAC3 expression regulates these complex phenotypes remain to be determined, these data indicate that HDAC3 is a critical factor that integrates commensal-bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949438/" 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/PMC3949438/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alenghat, Theresa -- Osborne, Lisa C -- Saenz, Steven A -- Kobuley, Dmytro -- Ziegler, Carly G K -- Mullican, Shannon E -- Choi, Inchan -- Grunberg, Stephanie -- Sinha, Rohini -- Wynosky-Dolfi, Meghan -- Snyder, Annelise -- Giacomin, Paul R -- Joyce, Karen L -- Hoang, Tram B -- Bewtra, Meenakshi -- Brodsky, Igor E -- Sonnenberg, Gregory F -- Bushman, Frederic D -- Won, Kyoung-Jae -- Lazar, Mitchell A -- Artis, David -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- DK043806/DK/NIDDK NIH HHS/ -- DP5 OD012116/OD/NIH HHS/ -- DP5OD012116/OD/NIH HHS/ -- F31-GM082187/GM/NIGMS NIH HHS/ -- K08 DK084347/DK/NIDDK NIH HHS/ -- K08 DK093784/DK/NIDDK NIH HHS/ -- K08-DK084347/DK/NIDDK NIH HHS/ -- K08-DK093784/DK/NIDDK NIH HHS/ -- P01 AI106697/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- P30-DK19525/DK/NIDDK NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- R21 AI105346/AI/NIAID NIH HHS/ -- R21-AI105346/AI/NIAID NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- T32-RR007063/RR/NCRR NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Dec 5;504(7478):153-7. doi: 10.1038/nature12687. Epub 2013 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2] Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [3] Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24185009" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Bacteria/genetics ; Colitis, Ulcerative/enzymology/genetics/microbiology ; Crohn Disease/enzymology/genetics/microbiology ; Female ; Gene Deletion ; Gene Expression Profiling ; *Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; *Homeostasis ; Humans ; Intestinal Mucosa/*enzymology/pathology ; Intestines/*microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Paneth Cells/cytology/metabolism ; RNA, Ribosomal, 16S/genetics ; Signal Transduction ; *Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    In vivo cardiac reprogramming contributes to zebrafish heart regeneration (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-21
    Description: Despite current treatment regimens, heart failure remains the leading cause of morbidity and mortality in the developed world due to the limited capacity of adult mammalian ventricular cardiomyocytes to divide and replace ventricular myocardium lost from ischaemia-induced infarct. Hence there is great interest to identify potential cellular sources and strategies to generate new ventricular myocardium. Past studies have shown that fish and amphibians and early postnatal mammalian ventricular cardiomyocytes can proliferate to help regenerate injured ventricles; however, recent studies have suggested that additional endogenous cellular sources may contribute to this overall ventricular regeneration. Here we have developed, in the zebrafish (Danio rerio), a combination of fluorescent reporter transgenes, genetic fate-mapping strategies and a ventricle-specific genetic ablation system to discover that differentiated atrial cardiomyocytes can transdifferentiate into ventricular cardiomyocytes to contribute to zebrafish cardiac ventricular regeneration. Using in vivo time-lapse and confocal imaging, we monitored the dynamic cellular events during atrial-to-ventricular cardiomyocyte transdifferentiation to define intermediate cardiac reprogramming stages. We observed that Notch signalling becomes activated in the atrial endocardium following ventricular ablation, and discovered that inhibiting Notch signalling blocked the atrial-to-ventricular transdifferentiation and cardiac regeneration. Overall, these studies not only provide evidence for the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abundant new potential cardiac resident cellular source for cardiac ventricular regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090927/" 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/PMC4090927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Ruilin -- Han, Peidong -- Yang, Hongbo -- Ouyang, Kunfu -- Lee, Derek -- Lin, Yi-Fan -- Ocorr, Karen -- Kang, Guson -- Chen, Ju -- Stainier, Didier Y R -- Yelon, Deborah -- Chi, Neil C -- DP2 OD007464/OD/NIH HHS/ -- HL104239/HL/NHLBI NIH HHS/ -- HL54737/HL/NHLBI NIH HHS/ -- OD007464/OD/NIH HHS/ -- R01 HD069305/HD/NICHD NIH HHS/ -- R01 HL054737/HL/NHLBI NIH HHS/ -- R01 HL069594/HL/NHLBI NIH HHS/ -- R01 HL104239/HL/NHLBI NIH HHS/ -- R01 HL108599/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Jun 27;498(7455):497-501. doi: 10.1038/nature12322. Epub 2013 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23783515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; *Cell Transdifferentiation ; *Cellular Reprogramming ; Heart/embryology/*physiology ; Heart Atria/cytology/embryology ; Heart Ventricles/cytology ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/cytology/metabolism ; Receptor, Notch1/metabolism ; Regeneration/*physiology ; Signal Transduction ; Zebrafish/embryology/*physiology
    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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    Stability and function of regulatory T cells is maintained by a neuropilin-1-semaphorin-4a axis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-08-06
    Description: Regulatory T cells (Treg cells) have a crucial role in the immune system by preventing autoimmunity, limiting immunopathology, and maintaining immune homeostasis. However, they also represent a major barrier to effective anti-tumour immunity and sterilizing immunity to chronic viral infections. The transcription factor Foxp3 has a major role in the development and programming of Treg cells. The relative stability of Treg cells at inflammatory disease sites has been a highly contentious subject. There is considerable interest in identifying pathways that control the stability of Treg cells as many immune-mediated diseases are characterized by either exacerbated or limited Treg-cell function. Here we show that the immune-cell-expressed ligand semaphorin-4a (Sema4a) and the Treg-cell-expressed receptor neuropilin-1 (Nrp1) interact both in vitro, to potentiate Treg-cell function and survival, and in vivo, at inflammatory sites. Using mice with a Treg-cell-restricted deletion of Nrp1, we show that Nrp1 is dispensable for suppression of autoimmunity and maintenance of immune homeostasis, but is required by Treg cells to limit anti-tumour immune responses and to cure established inflammatory colitis. Sema4a ligation of Nrp1 restrained Akt phosphorylation cellularly and at the immunologic synapse by phosphatase and tensin homologue (PTEN), which increased nuclear localization of the transcription factor Foxo3a. The Nrp1-induced transcriptome promoted Treg-cell stability by enhancing quiescence and survival factors while inhibiting programs that promote differentiation. Importantly, this Nrp1-dependent molecular program is evident in intra-tumoral Treg cells. Our data support a model in which Treg-cell stability can be subverted in certain inflammatory sites, but is maintained by a Sema4a-Nrp1 axis, highlighting this pathway as a potential therapeutic target that could limit Treg-cell-mediated tumour-induced tolerance without inducing autoimmunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3867145/" 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/PMC3867145/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delgoffe, Greg M -- Woo, Seng-Ryong -- Turnis, Meghan E -- Gravano, David M -- Guy, Cliff -- Overacre, Abigail E -- Bettini, Matthew L -- Vogel, Peter -- Finkelstein, David -- Bonnevier, Jody -- Workman, Creg J -- Vignali, Dario A A -- AI039480/AI/NIAID NIH HHS/ -- CA21765/CA/NCI NIH HHS/ -- F32 AI098383/AI/NIAID NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- R01 AI039480/AI/NIAID NIH HHS/ -- R01 AI091977/AI/NIAID NIH HHS/ -- T32 AI007610/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Sep 12;501(7466):252-6. doi: 10.1038/nature12428. Epub 2013 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23913274" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity/immunology ; Cell Survival ; Colitis/immunology ; Female ; Forkhead Transcription Factors/metabolism ; HEK293 Cells ; Homeostasis/immunology ; Humans ; Immune Tolerance/immunology ; Immunological Synapses ; Lymphocytes, Tumor-Infiltrating/cytology/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasms/genetics/immunology/pathology ; Neuropilin-1/deficiency/*metabolism ; PTEN Phosphohydrolase/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Semaphorins/*metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/cytology/*immunology/*metabolism ; TOR Serine-Threonine Kinases/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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