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  • Cells, Cultured  (9)
  • Nature Publishing Group (NPG)  (9)
  • National Academy of Sciences
  • Wiley
  • 2010-2014  (9)
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  • 1
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    A promoter-level mammalian expression atlas (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: Regulated transcription controls the diversity, developmental pathways and spatial organization of the hundreds of cell types that make up a mammal. Using single-molecule cDNA sequencing, we mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body. We find that few genes are truly 'housekeeping', whereas many mammalian promoters are composite entities composed of several closely separated TSSs, with independent cell-type-specific expression profiles. TSSs specific to different cell types evolve at different rates, whereas promoters of broadly expressed genes are the most conserved. Promoter-based expression analysis reveals key transcription factors defining cell states and links them to binding-site motifs. The functions of identified novel transcripts can be predicted by coexpression and sample ontology enrichment analyses. The functional annotation of the mammalian genome 5 (FANTOM5) project provides comprehensive expression profiles and functional annotation of mammalian cell-type-specific transcriptomes with wide applications in biomedical research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529748/" 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/PMC4529748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉FANTOM Consortium and the RIKEN PMI and CLST (DGT) -- Forrest, Alistair R R -- Kawaji, Hideya -- Rehli, Michael -- Baillie, J Kenneth -- de Hoon, Michiel J L -- Haberle, Vanja -- Lassmann, Timo -- Kulakovskiy, Ivan V -- Lizio, Marina -- Itoh, Masayoshi -- Andersson, Robin -- Mungall, Christopher J -- Meehan, Terrence F -- Schmeier, Sebastian -- Bertin, Nicolas -- Jorgensen, Mette -- Dimont, Emmanuel -- Arner, Erik -- Schmidl, Christian -- Schaefer, Ulf -- Medvedeva, Yulia A -- Plessy, Charles -- Vitezic, Morana -- Severin, Jessica -- Semple, Colin A -- Ishizu, Yuri -- Young, Robert S -- Francescatto, Margherita -- Alam, Intikhab -- Albanese, Davide -- Altschuler, Gabriel M -- Arakawa, Takahiro -- Archer, John A C -- Arner, Peter -- Babina, Magda -- Rennie, Sarah -- Balwierz, Piotr J -- Beckhouse, Anthony G -- Pradhan-Bhatt, Swati -- Blake, Judith A -- Blumenthal, Antje -- Bodega, Beatrice -- Bonetti, Alessandro -- Briggs, James -- Brombacher, Frank -- Burroughs, A Maxwell -- Califano, Andrea -- Cannistraci, Carlo V -- Carbajo, Daniel -- Chen, Yun -- Chierici, Marco -- Ciani, Yari -- Clevers, Hans C -- Dalla, Emiliano -- Davis, Carrie A -- Detmar, Michael -- Diehl, Alexander D -- Dohi, Taeko -- Drablos, Finn -- Edge, Albert S B -- Edinger, Matthias -- Ekwall, Karl -- Endoh, Mitsuhiro -- Enomoto, Hideki -- Fagiolini, Michela -- Fairbairn, Lynsey -- Fang, Hai -- Farach-Carson, Mary C -- Faulkner, Geoffrey J -- Favorov, Alexander V -- Fisher, Malcolm E -- Frith, Martin C -- Fujita, Rie -- Fukuda, Shiro -- Furlanello, Cesare -- Furino, Masaaki -- Furusawa, Jun-ichi -- Geijtenbeek, Teunis B -- Gibson, Andrew P -- Gingeras, Thomas -- Goldowitz, Daniel -- Gough, Julian -- Guhl, Sven -- Guler, Reto -- Gustincich, Stefano -- Ha, Thomas J -- Hamaguchi, Masahide -- Hara, Mitsuko -- Harbers, Matthias -- Harshbarger, Jayson -- Hasegawa, Akira -- Hasegawa, Yuki -- Hashimoto, Takehiro -- Herlyn, Meenhard -- Hitchens, Kelly J -- Ho Sui, Shannan J -- Hofmann, Oliver M -- Hoof, Ilka -- Hori, Furni -- Huminiecki, Lukasz -- Iida, Kei -- Ikawa, Tomokatsu -- Jankovic, Boris R -- Jia, Hui -- Joshi, Anagha -- Jurman, Giuseppe -- Kaczkowski, Bogumil -- Kai, Chieko -- Kaida, Kaoru -- Kaiho, Ai -- Kajiyama, Kazuhiro -- Kanamori-Katayama, Mutsumi -- Kasianov, Artem S -- Kasukawa, Takeya -- Katayama, Shintaro -- Kato, Sachi -- Kawaguchi, Shuji -- Kawamoto, Hiroshi -- Kawamura, Yuki I -- Kawashima, Tsugumi -- Kempfle, Judith S -- Kenna, Tony J -- Kere, Juha -- Khachigian, Levon M -- Kitamura, Toshio -- Klinken, S Peter -- Knox, Alan J -- Kojima, Miki -- Kojima, Soichi -- Kondo, Naoto -- Koseki, Haruhiko -- Koyasu, Shigeo -- Krampitz, Sarah -- Kubosaki, Atsutaka -- Kwon, Andrew T -- Laros, Jeroen F J -- Lee, Weonju -- Lennartsson, Andreas -- Li, Kang -- Lilje, Berit -- Lipovich, Leonard -- Mackay-Sim, Alan -- Manabe, Ri-ichiroh -- Mar, Jessica C -- Marchand, Benoit -- Mathelier, Anthony -- Mejhert, Niklas -- Meynert, Alison -- Mizuno, Yosuke -- de Lima Morais, David A -- Morikawa, Hiromasa -- Morimoto, Mitsuru -- Moro, Kazuyo -- Motakis, Efthymios -- Motohashi, Hozumi -- Mummery, Christine L -- Murata, Mitsuyoshi -- Nagao-Sato, Sayaka -- Nakachi, Yutaka -- Nakahara, Fumio -- Nakamura, Toshiyuki -- Nakamura, Yukio -- Nakazato, Kenichi -- van Nimwegen, Erik -- Ninomiya, Noriko -- Nishiyori, Hiromi -- Noma, Shohei -- Noazaki, Tadasuke -- Ogishima, Soichi -- Ohkura, Naganari -- Ohimiya, Hiroko -- Ohno, Hiroshi -- Ohshima, Mitsuhiro -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry A -- Pain, Arnab -- Passier, Robert -- Patrikakis, Margaret -- Persson, Helena -- Piazza, Silvano -- Prendergast, James G D -- Rackham, Owen J L -- Ramilowski, Jordan A -- Rashid, Mamoon -- Ravasi, Timothy -- Rizzu, Patrizia -- Roncador, Marco -- Roy, Sugata -- Rye, Morten B -- Saijyo, Eri -- Sajantila, Antti -- Saka, Akiko -- Sakaguchi, Shimon -- Sakai, Mizuho -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schneider, Claudio -- Schultes, Erik A -- Schulze-Tanzil, Gundula G -- Schwegmann, Anita -- Sengstag, Thierry -- Sheng, Guojun -- Shimoji, Hisashi -- Shimoni, Yishai -- Shin, Jay W -- Simon, Christophe -- Sugiyama, Daisuke -- Sugiyama, Takaai -- Suzuki, Masanori -- Suzuki, Naoko -- Swoboda, Rolf K -- 't Hoen, Peter A C -- Tagami, Michihira -- Takahashi, Naoko -- Takai, Jun -- Tanaka, Hiroshi -- Tatsukawa, Hideki -- Tatum, Zuotian -- Thompson, Mark -- Toyodo, Hiroo -- Toyoda, Tetsuro -- Valen, Elvind -- van de Wetering, Marc -- van den Berg, Linda M -- Verado, Roberto -- Vijayan, Dipti -- Vorontsov, Ilya E -- Wasserman, Wyeth W -- Watanabe, Shoko -- Wells, Christine A -- Winteringham, Louise N -- Wolvetang, Ernst -- Wood, Emily J -- Yamaguchi, Yoko -- Yamamoto, Masayuki -- Yoneda, Misako -- Yonekura, Yohei -- Yoshida, Shigehiro -- Zabierowski, Susan E -- Zhang, Peter G -- Zhao, Xiaobei -- Zucchelli, Silvia -- Summers, Kim M -- Suzuki, Harukazu -- Daub, Carsten O -- Kawai, Jun -- Heutink, Peter -- Hide, Winston -- Freeman, Tom C -- Lenhard, Boris -- Bajic, Vladimir B -- Taylor, Martin S -- Makeev, Vsevolod J -- Sandelin, Albin -- Hume, David A -- Carninci, Piero -- Hayashizaki, Yoshihide -- BB/F003722/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G022771/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I001107/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_PC_U127597124/Medical Research Council/United Kingdom -- MC_UP_1102/1/Medical Research Council/United Kingdom -- R01 DE022969/DE/NIDCR NIH HHS/ -- R01 GM084875/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):462-70. doi: 10.1038/nature13182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-07-08
    Description: Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer. Normally, ROS levels are tightly controlled by an inducible antioxidant program that responds to cellular stressors and is predominantly regulated by the transcription factor Nrf2 (also known as Nfe2l2) and its repressor protein Keap1 (refs 2-5). In contrast to the acute physiological regulation of Nrf2, in neoplasia there is evidence for increased basal activation of Nrf2. Indeed, somatic mutations that disrupt the Nrf2-Keap1 interaction to stabilize Nrf2 and increase the constitutive transcription of Nrf2 target genes were recently identified, indicating that enhanced ROS detoxification and additional Nrf2 functions may in fact be pro-tumorigenic. Here, we investigated ROS metabolism in primary murine cells following the expression of endogenous oncogenic alleles of Kras, Braf and Myc, and found that ROS are actively suppressed by these oncogenes. K-Ras(G12D), B-Raf(V619E) and Myc(ERT2) each increased the transcription of Nrf2 to stably elevate the basal Nrf2 antioxidant program and thereby lower intracellular ROS and confer a more reduced intracellular environment. Oncogene-directed increased expression of Nrf2 is a new mechanism for the activation of the Nrf2 antioxidant program, and is evident in primary cells and tissues of mice expressing K-Ras(G12D) and B-Raf(V619E), and in human pancreatic cancer. Furthermore, genetic targeting of the Nrf2 pathway impairs K-Ras(G12D)-induced proliferation and tumorigenesis in vivo. Thus, the Nrf2 antioxidant and cellular detoxification program represents a previously unappreciated mediator of oncogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404470/" 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/PMC3404470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeNicola, Gina M -- Karreth, Florian A -- Humpton, Timothy J -- Gopinathan, Aarthi -- Wei, Cong -- Frese, Kristopher -- Mangal, Dipti -- Yu, Kenneth H -- Yeo, Charles J -- Calhoun, Eric S -- Scrimieri, Francesca -- Winter, Jordan M -- Hruban, Ralph H -- Iacobuzio-Donahue, Christine -- Kern, Scott E -- Blair, Ian A -- Tuveson, David A -- CA084291/CA/NCI NIH HHS/ -- CA101973/CA/NCI NIH HHS/ -- CA105490/CA/NCI NIH HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA111294/CA/NCI NIH HHS/ -- CA128920/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- R01 CA101973/CA/NCI NIH HHS/ -- R01 CA101973-05/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jul 6;475(7354):106-9. doi: 10.1038/nature10189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Li Ka Shing Centre, Cancer Research UK Cambridge Institute, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734707" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/metabolism ; Alleles ; Animals ; Antioxidants/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics/*metabolism/*pathology ; Cells, Cultured ; Cytoskeletal Proteins/genetics/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/metabolism ; Genes, myc/genetics ; Humans ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase Kinases/metabolism ; NF-E2-Related Factor 2/deficiency/genetics/*metabolism ; NIH 3T3 Cells ; Oncogenes/*genetics ; Oxidation-Reduction ; Pancreatic Neoplasms/genetics/*metabolism/*pathology ; Proto-Oncogene Proteins B-raf/genetics/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; Reactive Oxygen Species/*metabolism
    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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    Alveolar progenitor and stem cells in lung development, renewal and cancer (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-02-07
    Description: Alveoli are gas-exchange sacs lined by squamous alveolar type (AT) 1 cells and cuboidal, surfactant-secreting AT2 cells. Classical studies suggested that AT1 arise from AT2 cells, but recent studies propose other sources. Here we use molecular markers, lineage tracing and clonal analysis to map alveolar progenitors throughout the mouse lifespan. We show that, during development, AT1 and AT2 cells arise directly from a bipotent progenitor, whereas after birth new AT1 cells derive from rare, self-renewing, long-lived, mature AT2 cells that produce slowly expanding clonal foci of alveolar renewal. This stem-cell function is broadly activated by AT1 injury, and AT2 self-renewal is selectively induced by EGFR (epidermal growth factor receptor) ligands in vitro and oncogenic Kras(G12D) in vivo, efficiently generating multifocal, clonal adenomas. Thus, there is a switch after birth, when AT2 cells function as stem cells that contribute to alveolar renewal, repair and cancer. We propose that local signals regulate AT2 stem-cell activity: a signal transduced by EGFR-KRAS controls self-renewal and is hijacked during oncogenesis, whereas another signal controls reprogramming to AT1 fate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013278/" 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/PMC4013278/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Desai, Tushar J -- Brownfield, Douglas G -- Krasnow, Mark A -- P30 CA124435/CA/NCI NIH HHS/ -- U01 HL099995/HL/NHLBI NIH HHS/ -- U01 HL099999/HL/NHLBI NIH HHS/ -- England -- Nature. 2014 Mar 13;507(7491):190-4. doi: 10.1038/nature12930. Epub 2014 Feb 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biochemistry and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305-5307, USA [2] Department of Internal Medicine, Division of Pulmonary and Critical Care, Stanford University School of Medicine, Stanford, California 94305-5307, USA. ; Department of Biochemistry and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305-5307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24499815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Transformation, Neoplastic/metabolism/pathology ; Cells, Cultured ; Cellular Reprogramming ; Clone Cells/cytology ; Female ; Lung/*cytology/embryology/*growth & development/pathology ; Lung Neoplasms/metabolism/*pathology ; Male ; Mice ; Models, Biological ; Multipotent Stem Cells/*cytology/metabolism/*pathology ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; Pulmonary Alveoli/*cytology ; Receptor, Epidermal Growth Factor/metabolism ; *Regeneration ; Signal Transduction
    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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    Ultrasensitive fluorescent proteins for imaging neuronal activity (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-23
    Description: Fluorescent calcium sensors are widely used to image neural activity. Using structure-based mutagenesis and neuron-based screening, we developed a family of ultrasensitive protein calcium sensors (GCaMP6) that outperformed other sensors in cultured neurons and in zebrafish, flies and mice in vivo. In layer 2/3 pyramidal neurons of the mouse visual cortex, GCaMP6 reliably detected single action potentials in neuronal somata and orientation-tuned synaptic calcium transients in individual dendritic spines. The orientation tuning of structurally persistent spines was largely stable over timescales of weeks. Orientation tuning averaged across spine populations predicted the tuning of their parent cell. Although the somata of GABAergic neurons showed little orientation tuning, their dendrites included highly tuned dendritic segments (5-40-microm long). GCaMP6 sensors thus provide new windows into the organization and dynamics of neural circuits over multiple spatial and temporal scales.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777791/" 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/PMC3777791/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Tsai-Wen -- Wardill, Trevor J -- Sun, Yi -- Pulver, Stefan R -- Renninger, Sabine L -- Baohan, Amy -- Schreiter, Eric R -- Kerr, Rex A -- Orger, Michael B -- Jayaraman, Vivek -- Looger, Loren L -- Svoboda, Karel -- Kim, Douglas S -- T32 GM008042/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jul 18;499(7458):295-300. doi: 10.1038/nature12354.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868258" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Calcium/metabolism ; Calcium-Binding Proteins/*chemistry/genetics ; Cells, Cultured ; Dendritic Spines/metabolism ; Fluorescent Dyes/*chemistry ; GABAergic Neurons/metabolism ; Luminescent Proteins/*chemistry/genetics ; Mice ; Molecular Imaging ; Mutagenesis ; Protein Engineering ; Pyramidal Cells/metabolism/physiology ; Visual Cortex/cytology/physiology
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Brown-fat paucity due to impaired BMP signalling induces compensatory browning of white fat (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-15
    Description: Maintenance of body temperature is essential for the survival of homeotherms. Brown adipose tissue (BAT) is a specialized fat tissue that is dedicated to thermoregulation. Owing to its remarkable capacity to dissipate stored energy and its demonstrated presence in adult humans, BAT holds great promise for the treatment of obesity and metabolic syndrome. Rodent data suggest the existence of two types of brown fat cells: constitutive BAT (cBAT), which is of embryonic origin and anatomically located in the interscapular region of mice; and recruitable BAT (rBAT), which resides within white adipose tissue (WAT) and skeletal muscle, and has alternatively been called beige, brite or inducible BAT. Bone morphogenetic proteins (BMPs) regulate the formation and thermogenic activity of BAT. Here we use mouse models to provide evidence for a systemically active regulatory mechanism that controls whole-body BAT activity for thermoregulation and energy homeostasis. Genetic ablation of the type 1A BMP receptor (Bmpr1a) in brown adipogenic progenitor cells leads to a severe paucity of cBAT. This in turn increases sympathetic input to WAT, thereby promoting the formation of rBAT within white fat depots. This previously unknown compensatory mechanism, aimed at restoring total brown-fat-mediated thermogenic capacity in the body, is sufficient to maintain normal temperature homeostasis and resistance to diet-induced obesity. These data suggest an important physiological cross-talk between constitutive and recruitable brown fat cells. This sophisticated regulatory mechanism of body temperature may participate in the control of energy balance and metabolic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623555/" 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/PMC3623555/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schulz, Tim J -- Huang, Ping -- Huang, Tian Lian -- Xue, Ruidan -- McDougall, Lindsay E -- Townsend, Kristy L -- Cypess, Aaron M -- Mishina, Yuji -- Gussoni, Emanuela -- Tseng, Yu-Hua -- F32 DK091996/DK/NIDDK NIH HHS/ -- K23 DK081604/DK/NIDDK NIH HHS/ -- P30 DK036836/DK/NIDDK NIH HHS/ -- R01 DK077097/DK/NIDDK NIH HHS/ -- R01 NS047727/NS/NINDS NIH HHS/ -- T32 DK007260/DK/NIDDK NIH HHS/ -- England -- Nature. 2013 Mar 21;495(7441):379-83. doi: 10.1038/nature11943. Epub 2013 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23485971" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/*cytology/innervation/metabolism ; Adipose Tissue, White/*cytology/metabolism ; Animals ; Body Temperature ; Body Temperature Regulation ; Bone Morphogenetic Protein Receptors, Type I/genetics/metabolism ; Bone Morphogenetic Proteins/genetics/*metabolism ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Energy Metabolism ; Mice ; *Signal Transduction ; Stem Cells/cytology
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  • 6
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    IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-22
    Description: Both genome-wide genetic and epigenetic alterations are fundamentally important for the development of cancers, but the interdependence of these aberrations is poorly understood. Glioblastomas and other cancers with the CpG island methylator phenotype (CIMP) constitute a subset of tumours with extensive epigenomic aberrations and a distinct biology. Glioma CIMP (G-CIMP) is a powerful determinant of tumour pathogenicity, but the molecular basis of G-CIMP remains unresolved. Here we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), establishes G-CIMP by remodelling the methylome. This remodelling results in reorganization of the methylome and transcriptome. Examination of the epigenome of a large set of intermediate-grade gliomas demonstrates a distinct G-CIMP phenotype that is highly dependent on the presence of IDH mutation. Introduction of mutant IDH1 into primary human astrocytes alters specific histone marks, induces extensive DNA hypermethylation, and reshapes the methylome in a fashion that mirrors the changes observed in G-CIMP-positive lower-grade gliomas. Furthermore, the epigenomic alterations resulting from mutant IDH1 activate key gene expression programs, characterize G-CIMP-positive proneural glioblastomas but not other glioblastomas, and are predictive of improved survival. Our findings demonstrate that IDH mutation is the molecular basis of CIMP in gliomas, provide a framework for understanding oncogenesis in these gliomas, and highlight the interplay between genomic and epigenomic changes in human cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351699/" 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/PMC3351699/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turcan, Sevin -- Rohle, Daniel -- Goenka, Anuj -- Walsh, Logan A -- Fang, Fang -- Yilmaz, Emrullah -- Campos, Carl -- Fabius, Armida W M -- Lu, Chao -- Ward, Patrick S -- Thompson, Craig B -- Kaufman, Andrew -- Guryanova, Olga -- Levine, Ross -- Heguy, Adriana -- Viale, Agnes -- Morris, Luc G T -- Huse, Jason T -- Mellinghoff, Ingo K -- Chan, Timothy A -- R01 CA154767/CA/NCI NIH HHS/ -- R01CA154767-01/CA/NCI NIH HHS/ -- U54 CA143798/CA/NCI NIH HHS/ -- U54-CA143798/CA/NCI NIH HHS/ -- England -- Nature. 2012 Feb 15;483(7390):479-83. doi: 10.1038/nature10866.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Oncology and Pathogenesis Program, 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/22343889" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/cytology/metabolism ; Cell Survival/genetics ; Cells, Cultured ; CpG Islands/genetics ; DNA Methylation/*genetics ; Epigenesis, Genetic ; Epigenomics ; Gene Expression Regulation ; Glioblastoma/genetics/pathology ; Glioma/*genetics/pathology ; HEK293 Cells ; Histones/metabolism ; Humans ; Isocitrate Dehydrogenase/*genetics/metabolism ; Metabolome/genetics ; Mutation/*genetics ; *Phenotype ; Tumor Cells, Cultured
    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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  • 7
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    A draft map of the human proteome (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-05-30
    Description: The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides does not exist yet. Here we present a draft map of the human proteome using high-resolution Fourier-transform mass spectrometry. In-depth proteomic profiling of 30 histologically normal human samples, including 17 adult tissues, 7 fetal tissues and 6 purified primary haematopoietic cells, resulted in identification of proteins encoded by 17,294 genes accounting for approximately 84% of the total annotated protein-coding genes in humans. A unique and comprehensive strategy for proteogenomic analysis enabled us to discover a number of novel protein-coding regions, which includes translated pseudogenes, non-coding RNAs and upstream open reading frames. This large human proteome catalogue (available as an interactive web-based resource at http://www.humanproteomemap.org) will complement available human genome and transcriptome data to accelerate biomedical research in health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403737/" 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/PMC4403737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Min-Sik -- Pinto, Sneha M -- Getnet, Derese -- Nirujogi, Raja Sekhar -- Manda, Srikanth S -- Chaerkady, Raghothama -- Madugundu, Anil K -- Kelkar, Dhanashree S -- Isserlin, Ruth -- Jain, Shobhit -- Thomas, Joji K -- Muthusamy, Babylakshmi -- Leal-Rojas, Pamela -- Kumar, Praveen -- Sahasrabuddhe, Nandini A -- Balakrishnan, Lavanya -- Advani, Jayshree -- George, Bijesh -- Renuse, Santosh -- Selvan, Lakshmi Dhevi N -- Patil, Arun H -- Nanjappa, Vishalakshi -- Radhakrishnan, Aneesha -- Prasad, Samarjeet -- Subbannayya, Tejaswini -- Raju, Rajesh -- Kumar, Manish -- Sreenivasamurthy, Sreelakshmi K -- Marimuthu, Arivusudar -- Sathe, Gajanan J -- Chavan, Sandip -- Datta, Keshava K -- Subbannayya, Yashwanth -- Sahu, Apeksha -- Yelamanchi, Soujanya D -- Jayaram, Savita -- Rajagopalan, Pavithra -- Sharma, Jyoti -- Murthy, Krishna R -- Syed, Nazia -- Goel, Renu -- Khan, Aafaque A -- Ahmad, Sartaj -- Dey, Gourav -- Mudgal, Keshav -- Chatterjee, Aditi -- Huang, Tai-Chung -- Zhong, Jun -- Wu, Xinyan -- Shaw, Patrick G -- Freed, Donald -- Zahari, Muhammad S -- Mukherjee, Kanchan K -- Shankar, Subramanian -- Mahadevan, Anita -- Lam, Henry -- Mitchell, Christopher J -- Shankar, Susarla Krishna -- Satishchandra, Parthasarathy -- Schroeder, John T -- Sirdeshmukh, Ravi -- Maitra, Anirban -- Leach, Steven D -- Drake, Charles G -- Halushka, Marc K -- Prasad, T S Keshava -- Hruban, Ralph H -- Kerr, Candace L -- Bader, Gary D -- Iacobuzio-Donahue, Christine A -- Gowda, Harsha -- Pandey, Akhilesh -- HHSN268201000032C/HL/NHLBI NIH HHS/ -- HHSN268201000032C/PHS HHS/ -- P41 GM103504/GM/NIGMS NIH HHS/ -- P41GM103504/GM/NIGMS NIH HHS/ -- T32 GM007814/GM/NIGMS NIH HHS/ -- U24 CA160036/CA/NCI NIH HHS/ -- U24CA160036/CA/NCI NIH HHS/ -- U54 GM103520/GM/NIGMS NIH HHS/ -- U54GM103520/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 May 29;509(7502):575-81. doi: 10.1038/nature13302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Institute of Bioinformatics, International Tech Park, Bangalore 560066, India. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA. ; The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Pathology, Universidad de La Frontera, Center of Genetic and Immunological Studies-Scientific and Technological Bioresource Nucleus, Temuco 4811230, Chile. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; School of Medicine, Imperial College London, South Kensington Campus, London SW7 2AZ, UK. ; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Department of Neurosurgery, Postgraduate Institute of Medical Education & Research, Chandigarh 160012, India. ; Department of Internal Medicine Armed Forces Medical College, Pune 411040, India. ; 1] Department of Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India [2] Human Brain Tissue Repository, Neurobiology Research Centre, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Chemical and Biomolecular Engineering and Division of Biomedical Engineering, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong. ; Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Departments of Immunology and Urology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Obstetrics and Gynecology, Johns Hopkins University School of Medicine Baltimore, Maryland 21205, USA [2] Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [3] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [3] Institute of Bioinformatics, International Tech Park, Bangalore 560066, India [4] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA [5] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [6] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [7] Diana Helis Henry Medical Research Foundation, New Orleans, Louisiana 70130, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870542" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cells, Cultured ; Databases, Protein ; Fetus/metabolism ; Fourier Analysis ; Gene Expression Profiling ; Genome, Human/genetics ; Hematopoietic Stem Cells/cytology/metabolism ; Humans ; Internet ; Mass Spectrometry ; Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Protein Biosynthesis ; Protein Isoforms/analysis/genetics/metabolism ; Protein Sorting Signals ; Protein Transport ; Proteome/analysis/chemistry/genetics/*metabolism ; *Proteomics ; Pseudogenes/genetics ; RNA, Untranslated/genetics ; Reproducibility of Results ; Untranslated Regions/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Dynamic regulatory network controlling TH17 cell differentiation (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-08
    Description: Despite their importance, the molecular circuits that control the differentiation of naive T cells remain largely unknown. Recent studies that reconstructed regulatory networks in mammalian cells have focused on short-term responses and relied on perturbation-based approaches that cannot be readily applied to primary T cells. Here we combine transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based perturbation tools to systematically derive and experimentally validate a model of the dynamic regulatory network that controls the differentiation of mouse TH17 cells, a proinflammatory T-cell subset that has been implicated in the pathogenesis of multiple autoimmune diseases. The TH17 transcriptional network consists of two self-reinforcing, but mutually antagonistic, modules, with 12 novel regulators, the coupled action of which may be essential for maintaining the balance between TH17 and other CD4(+) T-cell subsets. Our study identifies and validates 39 regulatory factors, embeds them within a comprehensive temporal network and reveals its organizational principles; it also highlights novel drug targets for controlling TH17 cell differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637864/" 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/PMC3637864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yosef, Nir -- Shalek, Alex K -- Gaublomme, Jellert T -- Jin, Hulin -- Lee, Youjin -- Awasthi, Amit -- Wu, Chuan -- Karwacz, Katarzyna -- Xiao, Sheng -- Jorgolli, Marsela -- Gennert, David -- Satija, Rahul -- Shakya, Arvind -- Lu, Diana Y -- Trombetta, John J -- Pillai, Meenu R -- Ratcliffe, Peter J -- Coleman, Mathew L -- Bix, Mark -- Tantin, Dean -- Park, Hongkun -- Kuchroo, Vijay K -- Regev, Aviv -- 1P50HG006193-01/HG/NHGRI NIH HHS/ -- 5DP1OD003893-03/OD/NIH HHS/ -- AI073748/AI/NIAID NIH HHS/ -- AI45757/AI/NIAID NIH HHS/ -- DP1 OD003893/OD/NIH HHS/ -- DP1 OD003958/OD/NIH HHS/ -- DP1OD003958-01/OD/NIH HHS/ -- F32 HD075541/HD/NICHD NIH HHS/ -- K01 DK090105/DK/NIDDK NIH HHS/ -- NS 30843/NS/NINDS NIH HHS/ -- NS045937/NS/NINDS NIH HHS/ -- P01 AI045757/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P50 HG006193/HG/NHGRI NIH HHS/ -- R01 AI100873/AI/NIAID NIH HHS/ -- R01 NS030843/NS/NINDS NIH HHS/ -- R01 NS045937/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 25;496(7446):461-8. doi: 10.1038/nature11981. Epub 2013 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23467089" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; Cell Differentiation/*genetics ; Cells, Cultured ; DNA/genetics/metabolism ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; Gene Regulatory Networks/*genetics ; Genome/genetics ; Interferon-gamma/biosynthesis ; Interleukin-2/genetics ; Mice ; Mice, Inbred C57BL ; Nanowires ; Neoplasm Proteins/metabolism ; Nuclear Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Reproducibility of Results ; Silicon ; Th17 Cells/*cytology/immunology/*metabolism ; Time Factors ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    mTORC1 controls the adaptive transition of quiescent stem cells from G0 to G(Alert) (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-05-30
    Description: A unique property of many adult stem cells is their ability to exist in a non-cycling, quiescent state. Although quiescence serves an essential role in preserving stem cell function until the stem cell is needed in tissue homeostasis or repair, defects in quiescence can lead to an impairment in tissue function. The extent to which stem cells can regulate quiescence is unknown. Here we show that the stem cell quiescent state is composed of two distinct functional phases, G0 and an 'alert' phase we term G(Alert). Stem cells actively and reversibly transition between these phases in response to injury-induced systemic signals. Using genetic mouse models specific to muscle stem cells (or satellite cells), we show that mTORC1 activity is necessary and sufficient for the transition of satellite cells from G0 into G(Alert) and that signalling through the HGF receptor cMet is also necessary. We also identify G0-to-G(Alert) transitions in several populations of quiescent stem cells. Quiescent stem cells that transition into G(Alert) possess enhanced tissue regenerative function. We propose that the transition of quiescent stem cells into G(Alert) functions as an 'alerting' mechanism, an adaptive response that positions stem cells to respond rapidly under conditions of injury and stress, priming them for cell cycle entry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065227/" 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/PMC4065227/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodgers, Joseph T -- King, Katherine Y -- Brett, Jamie O -- Cromie, Melinda J -- Charville, Gregory W -- Maguire, Katie K -- Brunson, Christopher -- Mastey, Namrata -- Liu, Ling -- Tsai, Chang-Ru -- Goodell, Margaret A -- Rando, Thomas A -- F30 AG035521/AG/NIA NIH HHS/ -- I01 BX002324/BX/BLRD VA/ -- K08 HL098898/HL/NHLBI NIH HHS/ -- P01 AG036695/AG/NIA NIH HHS/ -- R01 AG023806/AG/NIA NIH HHS/ -- R01 AG047820/AG/NIA NIH HHS/ -- R01 AG23806/AG/NIA NIH HHS/ -- R01 AR062185/AR/NIAMS NIH HHS/ -- R01 DK092883/DK/NIDDK NIH HHS/ -- R37 AG023806/AG/NIA NIH HHS/ -- England -- Nature. 2014 Jun 19;510(7505):393-6. doi: 10.1038/nature13255. Epub 2014 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, California 94305, USA [2] Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA. ; Department of Pediatrics and Program in Developmental Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, California 94305, USA [2] Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA [3] Neurology Service and Rehabilitation Research and Development Center of Excellence, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870234" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/genetics/*physiology ; Cells, Cultured ; G0 Phase/genetics/*physiology ; Gene Expression Profiling ; Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes/genetics/*metabolism ; Muscle, Skeletal/*cytology/injuries/metabolism ; Regeneration/physiology ; Satellite Cells, Skeletal Muscle/*cytology/metabolism ; TOR Serine-Threonine Kinases/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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