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  • Lunar and Planetary Science and Exploration  (66)
  • Signal Transduction  (41)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • 2010-2014  (107)
  • 1950-1954  (14)
  • 2010  (107)
  • 1954  (14)
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  • 2010-2014  (107)
  • 1950-1954  (14)
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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 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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  • 3
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    ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-22
    Description: Elevated leukocyte cell numbers (leukocytosis), and monocytes in particular, promote atherosclerosis; however, how they become increased is poorly understood. Mice deficient in the adenosine triphosphate-binding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow. Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis. The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoietic stem and multipotential progenitor cells and connect expansion of these populations with leukocytosis and accelerated atherosclerosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032591/" 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/PMC3032591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yvan-Charvet, Laurent -- Pagler, Tamara -- Gautier, Emmanuel L -- Avagyan, Serine -- Siry, Read L -- Han, Seongah -- Welch, Carrie L -- Wang, Nan -- Randolph, Gwendalyn J -- Snoeck, Hans W -- Tall, Alan R -- HL54591/HL/NHLBI NIH HHS/ -- R01 AG029626/AG/NIA NIH HHS/ -- R01 AI049653/AI/NIAID NIH HHS/ -- R01 AI049653-09/AI/NIAID NIH HHS/ -- R01 AI049653-10/AI/NIAID NIH HHS/ -- R01 AI061741/AI/NIAID NIH HHS/ -- R01 AI061741-03/AI/NIAID NIH HHS/ -- R01 AI061741-04/AI/NIAID NIH HHS/ -- R01A1061741/PHS HHS/ -- R01AG016327/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1689-93. doi: 10.1126/science.1189731. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA. ly2159@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488992" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Apolipoprotein A-I/genetics/metabolism ; Atherosclerosis/metabolism/*physiopathology/therapy ; Bone Marrow Transplantation ; Cell Proliferation ; Cells, Cultured ; Cholesterol/*metabolism ; Hematopoietic Stem Cells/*physiology ; Hypercholesterolemia/metabolism ; Leukocytosis/metabolism/*physiopathology/therapy ; Lipoproteins/genetics/*metabolism ; Lipoproteins, HDL/*metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Multipotent Stem Cells/physiology ; Myeloid Progenitor Cells/*physiology ; Myeloproliferative Disorders/metabolism/physiopathology/therapy ; Phenotype ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Receptors, Interleukin-3/metabolism ; Signal Transduction
    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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  • 4
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    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" 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/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
    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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    Vascular endothelial growth factor B controls endothelial fatty acid uptake (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-17
    Description: The vascular endothelial growth factors (VEGFs) are major angiogenic regulators and are involved in several aspects of endothelial cell physiology. However, the detailed role of VEGF-B in blood vessel function has remained unclear. Here we show that VEGF-B has an unexpected role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation have to be transported through the vascular endothelium to be metabolized by tissue cells, a mechanism that is poorly understood. Bioinformatic analysis showed that Vegfb was tightly co-expressed with nuclear-encoded mitochondrial genes across a large variety of physiological conditions in mice, pointing to a role for VEGF-B in metabolism. VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb(-/-) mice showed less uptake and accumulation of lipids in muscle, heart and brown adipose tissue, and instead shunted lipids to white adipose tissue. This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium. The co-expression of VEGF-B and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated. The involvement of VEGF-B in lipid uptake may open up the possibility for novel strategies to modulate pathological lipid accumulation in diabetes, obesity and cardiovascular diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagberg, Carolina E -- Falkevall, Annelie -- Wang, Xun -- Larsson, Erik -- Huusko, Jenni -- Nilsson, Ingrid -- van Meeteren, Laurens A -- Samen, Erik -- Lu, Li -- Vanwildemeersch, Maarten -- Klar, Joakim -- Genove, Guillem -- Pietras, Kristian -- Stone-Elander, Sharon -- Claesson-Welsh, Lena -- Yla-Herttuala, Seppo -- Lindahl, Per -- Eriksson, Ulf -- England -- Nature. 2010 Apr 8;464(7290):917-21. doi: 10.1038/nature08945. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tissue Biology Group, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228789" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Biological Transport ; Cell Line ; Cell Nucleus/genetics ; Cells, Cultured ; Endothelium/cytology/*metabolism ; Fatty Acid Transport Proteins/genetics ; Fatty Acids/*metabolism ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/genetics/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Neuropilin-1/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Signal Transduction ; Transcription, Genetic ; Vascular Endothelial Growth Factor B/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor Receptor-1/metabolism
    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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    Oncogenically active MYD88 mutations in human lymphoma (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: 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〉
    Keywords: 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
    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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    Altered histone acetylation is associated with age-dependent memory impairment in mice (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peleg, Shahaf -- Sananbenesi, Farahnaz -- Zovoilis, Athanasios -- Burkhardt, Susanne -- Bahari-Javan, Sanaz -- Agis-Balboa, Roberto Carlos -- Cota, Perla -- Wittnam, Jessica Lee -- Gogol-Doering, Andreas -- Opitz, Lennart -- Salinas-Riester, Gabriella -- Dettenhofer, Markus -- Kang, Hui -- Farinelli, Laurent -- Chen, Wei -- Fischer, Andre -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):753-6. doi: 10.1126/science.1186088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Aging and Cognitive Diseases, European Neuroscience Institute, Grisebach Str. 5, D-37077 Goettingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448184" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Aging/*genetics ; Animals ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; Conditioning (Psychology) ; Epigenesis, Genetic ; Fear ; Gene Expression Profiling ; *Gene Expression Regulation ; Hippocampus/*metabolism ; Histone Deacetylase Inhibitors/metabolism/pharmacology ; Histones/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Lysine/metabolism ; Memory/drug effects ; Memory Disorders/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/genetics/metabolism ; Nuclear Proteins/genetics/metabolism ; Signal Transduction ; Transcription Initiation Site ; Transcription, Genetic ; Up-Regulation
    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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    Evidence for Hesperian Impact-Induced Hydrothermalism on Mars (2010)
    In:  Other Sources
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    Publication Date: 2019-07-13
    Description: Several hydrated silicate deposits on Mars are observed within craters and are interpreted as excavated Noachian material. Toro crater (71.8 deg E, 17.0 deg N), located on the northern edge of the Syrtis Major Volcanic Plains, shows spectral and morphologic evidence of impact-induced hydrothermal activity. Spectroscopic observations were used to identify extensive hydrated silicate deposits, including prehnite, chlorites, smectites, and opaline material, a suite of phases that frequently results from hydrothermal alteration in terrestrial craters and also expected on Mars from geochemical modeling of hydrothermal environments. When combined with altimetry and high-resolution imaging data, these deposits appear associated predominantly with the central uplift and with portions of the northern part of the crater floor. Detailed geologic mapping of these deposits reveals geomorphic features that are consistent with hydrothermal activity that followed the impact event, including vent-like and conical mound structures, and a complex network of tectonic structures caused by fluid interactions such as fractures and joints. The crater age has been calculated from the cumulative crater size-frequency distributions and is found to be Early Hesperian. The evidence presented here provides support for impact-induced hydrothermal activity in Toro crater, that extends phyllosilicate formation processes beyond the Noachian era.
    Keywords: Lunar and Planetary Science and Exploration
    Type: Icarus; 208; 667-683
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    Sub-10-Micron and Respirable Particles in Lunar Soils (2010)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: Based on published lunar soil grain size distribution data, we estimate that 1-3% of the mass of typical mature lunar soils is comprised of grains less than 2.5 micrometers in diameter. These particles are in the respirable range (small enough to be inhaled). Estimates are used because the early methods of obtaining grain size distributions did not give reliable results below about 10 micrometers. Grain size analyses of Apollo 11 soil 10084 by a laser diffraction technique shows that this soil contains roughly 2% by volume in the respirable grain size, in agreement with our prior estimate.
    Keywords: Lunar and Planetary Science and Exploration
    Type: JSC-CN-19518 , Lunar and Planetary Science Conference; Mar 01, 2010 - Mar 05, 2010; The Woodlands, TX; United States
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    Lunar Dust Separation for Toxicology Studies (2010)
    In:  CASI
    Details
    Publication Date: 2019-07-13
    Description: During the Apollo missions, crewmembers were briefly exposed to dust in the lunar module, brought in after extravehicular activity. When the lunar ascent module returned to micro-gravity, the dust that had settled on the floor now floated into the air, causing eye discomfort and occasional respiratory symptoms. Because our goal is to set an exposure standard for 6 months of episodic exposure to lunar dust for crew on the lunar surface, these brief exposures of a few days are not conclusive. Based on experience with industrial minerals such as sandblasting quartz, an exposure of several months may cause serious damage, while a short exposure may cause none. The detailed characteristics of sub-micrometer lunar dust are only poorly known, and this is the size range of particles that are of greatest concern. We have developed a method for extracting respirable dust (〈2.5 micron) from Apollo lunar soils. This method meets stringent requirements that the soil must be kept dry, exposed only to pure nitrogen, and must conserve and recover the maximum amount of both respirable dust and coarser soil. In addition, we have developed a method for grinding coarser lunar soil to produce sufficient respirable soil for animal toxicity testing while preserving the freshly exposed grain surfaces in a pristine state.
    Keywords: Lunar and Planetary Science and Exploration
    Type: JSC-CN-19517 , Lunar and Planetary Science Conference; Mar 01, 2010 - Mar 05, 2010; The Woodlands, TX; United States
    Format: application/pdf
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