ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    facet.materialart.
    Unbekannt
    Functional impact of global rare copy number variation in autism spectrum disorders (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-06-10
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 2
    facet.materialart.
    Unbekannt
    The genetic landscape of the childhood cancer medulloblastoma (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-12-18
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 3
    facet.materialart.
    Unbekannt
    The landscape of somatic copy-number alteration across human cancers (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-02-19
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 4
    facet.materialart.
    Unbekannt
    Dietary restriction: standing up for sirtuins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-08-28
    Beschreibung: 〈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〉
    Schlagwort(e): Aging/*physiology ; Animals ; *Caloric Restriction ; Humans ; *Longevity ; Signal Transduction ; Sirtuins/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 5
    facet.materialart.
    Unbekannt
    Rewiring of genetic networks in response to DNA damage (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-12-04
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 6
    facet.materialart.
    Unbekannt
    Measurement of single-cell dynamics (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-06-11
    Beschreibung: 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〉
    Schlagwort(e): Cell Differentiation ; *Cell Physiological Phenomena/genetics/physiology ; Cytological Techniques/*methods ; Microfluidics/methods ; Protein Binding ; Protein Transport ; Signal Transduction ; Transcription, Genetic
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 7
    facet.materialart.
    Unbekannt
    Oncogenically active MYD88 mutations in human lymphoma (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-12-24
    Beschreibung: The activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) remains the least curable form of this malignancy despite recent advances in therapy. Constitutive nuclear factor (NF)-kappaB and JAK kinase signalling promotes malignant cell survival in these lymphomas, but the genetic basis for this signalling is incompletely understood. Here we describe the dependence of ABC DLBCLs on MYD88, an adaptor protein that mediates toll and interleukin (IL)-1 receptor signalling, and the discovery of highly recurrent oncogenic mutations affecting MYD88 in ABC DLBCL tumours. RNA interference screening revealed that MYD88 and the associated kinases IRAK1 and IRAK4 are essential for ABC DLBCL survival. High-throughput RNA resequencing uncovered MYD88 mutations in ABC DLBCL lines. Notably, 29% of ABC DLBCL tumours harboured the same amino acid substitution, L265P, in the MYD88 Toll/IL-1 receptor (TIR) domain at an evolutionarily invariant residue in its hydrophobic core. This mutation was rare or absent in other DLBCL subtypes and Burkitt's lymphoma, but was observed in 9% of mucosa-associated lymphoid tissue lymphomas. At a lower frequency, additional mutations were observed in the MYD88 TIR domain, occurring in both the ABC and germinal centre B-cell-like (GCB) DLBCL subtypes. Survival of ABC DLBCL cells bearing the L265P mutation was sustained by the mutant but not the wild-type MYD88 isoform, demonstrating that L265P is a gain-of-function driver mutation. The L265P mutant promoted cell survival by spontaneously assembling a protein complex containing IRAK1 and IRAK4, leading to IRAK4 kinase activity, IRAK1 phosphorylation, NF-kappaB signalling, JAK kinase activation of STAT3, and secretion of IL-6, IL-10 and interferon-beta. Hence, the MYD88 signalling pathway is integral to the pathogenesis of ABC DLBCL, supporting the development of inhibitors of IRAK4 kinase and other components of this pathway for the treatment of tumours bearing oncogenic MYD88 mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ngo, Vu N -- Young, Ryan M -- Schmitz, Roland -- Jhavar, Sameer -- Xiao, Wenming -- Lim, Kian-Huat -- Kohlhammer, Holger -- Xu, Weihong -- Yang, Yandan -- Zhao, Hong -- Shaffer, Arthur L -- Romesser, Paul -- Wright, George -- Powell, John -- Rosenwald, Andreas -- Muller-Hermelink, Hans Konrad -- Ott, German -- Gascoyne, Randy D -- Connors, Joseph M -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Delabie, Jan -- Smeland, Erlend B -- Fisher, Richard I -- Braziel, Rita M -- Tubbs, Raymond R -- Cook, J R -- Weisenburger, Denny D -- Chan, Wing C -- Staudt, Louis M -- U01-CA 114778/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2011 Feb 3;470(7332):115-9. doi: 10.1038/nature09671. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179087" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Amino Acid Substitution ; Burkitt Lymphoma/genetics ; Cell Line, Tumor ; Cell Survival ; Cytokines/metabolism/secretion ; High-Throughput Nucleotide Sequencing ; Humans ; Hydrophobic and Hydrophilic Interactions ; Interleukin-1 Receptor-Associated Kinases/biosynthesis/genetics/metabolism ; Janus Kinases/metabolism ; Lymphoma, B-Cell, Marginal Zone/genetics ; Lymphoma, Large B-Cell, Diffuse/classification/*genetics/*pathology ; Molecular Sequence Data ; Mutant Proteins/chemistry/genetics/metabolism ; Mutation/*genetics ; Myeloid Differentiation Factor 88/chemistry/*genetics/*metabolism ; NF-kappa B/metabolism ; Oncogenes/*genetics ; Phosphorylation ; Protein Structure, Tertiary ; RNA Interference ; Receptors, Interleukin-1/metabolism ; STAT3 Transcription Factor/metabolism ; Sequence Analysis, RNA ; Signal Transduction ; Toll-Like Receptors/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 8
    facet.materialart.
    Unbekannt
    ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-10-12
    Beschreibung: Gastrointestinal stromal tumour (GIST) is the most common human sarcoma and is primarily defined by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. KIT is highly expressed in interstitial cells of Cajal (ICCs)-the presumed cell of origin for GIST-as well as in haematopoietic stem cells, melanocytes, mast cells and germ cells. Yet, families harbouring germline activating KIT mutations and mice with knock-in Kit mutations almost exclusively develop ICC hyperplasia and GIST, suggesting that the cellular context is important for KIT to mediate oncogenesis. Here we show that the ETS family member ETV1 is highly expressed in the subtypes of ICCs sensitive to oncogenic KIT mediated transformation, and is required for their development. In addition, ETV1 is universally highly expressed in GISTs and is required for growth of imatinib-sensitive and resistant GIST cell lines. Transcriptome profiling and global analyses of ETV1-binding sites suggest that ETV1 is a master regulator of an ICC-GIST-specific transcription network mainly through enhancer binding. The ETV1 transcriptional program is further regulated by activated KIT, which prolongs ETV1 protein stability and cooperates with ETV1 to promote tumorigenesis. We propose that GIST arises from ICCs with high levels of endogenous ETV1 expression that, when coupled with an activating KIT mutation, drives an oncogenic ETS transcriptional program. This differs from other ETS-dependent tumours such as prostate cancer, melanoma and Ewing sarcoma where genomic translocation or amplification drives aberrant ETS expression. It also represents a novel mechanism of oncogenic transcription factor activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955195/" 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/PMC2955195/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Ping -- Chen, Yu -- Zhang, Lei -- Guo, Xingyi -- Wongvipat, John -- Shamu, Tambudzai -- Fletcher, Jonathan A -- Dewell, Scott -- Maki, Robert G -- Zheng, Deyou -- Antonescu, Cristina R -- Allis, C David -- Sawyers, Charles L -- 5F32CA130372/CA/NCI NIH HHS/ -- CA148260/CA/NCI NIH HHS/ -- CA47179/CA/NCI NIH HHS/ -- F32 CA130372/CA/NCI NIH HHS/ -- F32 CA130372-02/CA/NCI NIH HHS/ -- GM40922/GM/NIGMS NIH HHS/ -- K08 CA140946/CA/NCI NIH HHS/ -- K08 CA140946-02/CA/NCI NIH HHS/ -- K08CA140946/CA/NCI NIH HHS/ -- P01 CA047179/CA/NCI NIH HHS/ -- P01 CA047179-169002/CA/NCI NIH HHS/ -- P01CA47179/CA/NCI NIH HHS/ -- R21 MH087840/MH/NIMH NIH HHS/ -- R21 MH087840-01/MH/NIMH NIH HHS/ -- R21MH087840/MH/NIMH NIH HHS/ -- RC2 CA148260-02/CA/NCI NIH HHS/ -- England -- Nature. 2010 Oct 14;467(7317):849-53. doi: 10.1038/nature09409. Epub 2010 Oct 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20927104" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Benzamides ; Binding Sites ; Biomarkers, Tumor/genetics/metabolism ; Cell Line, Tumor ; *Cell Lineage ; Cell Survival/drug effects ; *Cell Transformation, Neoplastic ; DNA-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Disease Progression ; Enhancer Elements, Genetic/genetics ; Gastrointestinal Stromal Tumors/*metabolism/*pathology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Imatinib Mesylate ; Interstitial Cells of Cajal/metabolism/pathology ; Mice ; Mutant Proteins/genetics/metabolism ; Mutation ; NIH 3T3 Cells ; Oncogenes/genetics/*physiology ; Piperazines/pharmacology ; Protein Stability ; Proto-Oncogene Proteins c-kit/genetics/*metabolism ; Pyrimidines/pharmacology ; Signal Transduction ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 9
    facet.materialart.
    Unbekannt
    An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-08-21
    Beschreibung: Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis, is a major cause of morbidity and mortality worldwide. Efforts to control it are hampered by difficulties with diagnosis, prevention and treatment. Most people infected with M. tuberculosis remain asymptomatic, termed latent TB, with a 10% lifetime risk of developing active TB disease. Current tests, however, cannot identify which individuals will develop disease. The immune response to M. tuberculosis is complex and incompletely characterized, hindering development of new diagnostics, therapies and vaccines. Here we identify a whole-blood 393 transcript signature for active TB in intermediate and high-burden settings, correlating with radiological extent of disease and reverting to that of healthy controls after treatment. A subset of patients with latent TB had signatures similar to those in patients with active TB. We also identify a specific 86-transcript signature that discriminates active TB from other inflammatory and infectious diseases. Modular and pathway analysis revealed that the TB signature was dominated by a neutrophil-driven interferon (IFN)-inducible gene profile, consisting of both IFN-gamma and type I IFN-alphabeta signalling. Comparison with transcriptional signatures in purified cells and flow cytometric analysis suggest that this TB signature reflects changes in cellular composition and altered gene expression. Although an IFN-inducible signature was also observed in whole blood of patients with systemic lupus erythematosus (SLE), their complete modular signature differed from TB, with increased abundance of plasma cell transcripts. Our studies demonstrate a hitherto underappreciated role of type I IFN-alphabeta signalling in the pathogenesis of TB, which has implications for vaccine and therapeutic development. Our study also provides a broad range of transcriptional biomarkers with potential as diagnostic and prognostic tools to combat the TB epidemic.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492754/" 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/PMC3492754/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berry, Matthew P R -- Graham, Christine M -- McNab, Finlay W -- Xu, Zhaohui -- Bloch, Susannah A A -- Oni, Tolu -- Wilkinson, Katalin A -- Banchereau, Romain -- Skinner, Jason -- Wilkinson, Robert J -- Quinn, Charles -- Blankenship, Derek -- Dhawan, Ranju -- Cush, John J -- Mejias, Asuncion -- Ramilo, Octavio -- Kon, Onn M -- Pascual, Virginia -- Banchereau, Jacques -- Chaussabel, Damien -- O'Garra, Anne -- 088316/Wellcome Trust/United Kingdom -- 1 U19 AI082715-01/AI/NIAID NIH HHS/ -- MC_U117565642/Medical Research Council/United Kingdom -- MC_U117588499/Medical Research Council/United Kingdom -- P01 CA084512/CA/NCI NIH HHS/ -- P50 ARO54083/PHS HHS/ -- R01 AR050770-01/AR/NIAMS NIH HHS/ -- U01 AI082110/AI/NIAID NIH HHS/ -- U117565642/Medical Research Council/United Kingdom -- U117588499(88499)/Medical Research Council/United Kingdom -- U19 AI082715/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- England -- Nature. 2010 Aug 19;466(7309):973-7. doi: 10.1038/nature09247.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunoregulation, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20725040" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Blood/metabolism ; Case-Control Studies ; *Gene Expression Profiling ; Gene Expression Regulation/*immunology ; Humans ; Interferon Type I/*immunology ; Latent Tuberculosis/blood/diagnosis/genetics/immunology ; Lupus Erythematosus, Systemic/blood/genetics ; Mycobacterium tuberculosis/immunology ; Neutrophils/*immunology ; Signal Transduction ; Transcription, Genetic/*genetics ; Tuberculosis/*blood/diagnosis/*genetics/immunology ; Tuberculosis, Pulmonary/blood/diagnosis/genetics/immunology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 10
    facet.materialart.
    Unbekannt
    Dopaminergic network differences in human impulsivity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-07-31
    Beschreibung: Dopamine (DA) has long been implicated in impulsivity, but the precise mechanisms linking human variability in DA signaling to differences in impulsive traits remain largely unknown. By using a dual-scan positron emission tomography approach in healthy human volunteers with amphetamine and the D2/D3 ligand [18F]fallypride, we found that higher levels of trait impulsivity were predicted by diminished midbrain D2/D3 autoreceptor binding and greater amphetamine-induced DA release in the striatum, which was in turn associated with stimulant craving. Path analysis confirmed that the impact of decreased midbrain D2/D3 autoreceptor availability on trait impulsivity is mediated in part through its effect on stimulated striatal DA release.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3161413/" 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/PMC3161413/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buckholtz, Joshua W -- Treadway, Michael T -- Cowan, Ronald L -- Woodward, Neil D -- Li, Rui -- Ansari, M Sib -- Baldwin, Ronald M -- Schwartzman, Ashley N -- Shelby, Evan S -- Smith, Clarence E -- Kessler, Robert M -- Zald, David H -- R01 DA019670/DA/NIDA NIH HHS/ -- R01 DA019670-04/DA/NIDA NIH HHS/ -- R01DA019670-04/DA/NIDA NIH HHS/ -- T32 MH018921/MH/NIMH NIH HHS/ -- T32 MH018921-22/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):532. doi: 10.1126/science.1185778.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Vanderbilt University, Nashville, TN 37240, USA. joshua.buckholtz@vanderbilt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671181" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Amphetamine-Related Disorders/etiology/metabolism ; Autoreceptors/metabolism ; Benzamides/metabolism ; Corpus Striatum/*metabolism ; Dextroamphetamine/*administration & dosage ; Dopamine/*metabolism ; Female ; Humans ; Impulsive Behavior/*metabolism ; Ligands ; Male ; Positron-Emission Tomography ; Pyrrolidines/metabolism ; Receptors, Dopamine D2/metabolism ; Receptors, Dopamine D3/*metabolism ; Signal Transduction ; Substantia Nigra/metabolism ; Tegmentum Mesencephali/*metabolism ; Ventral Tegmental Area/metabolism ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...