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  • Articles  (11)
  • Animals  (11)
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  • Articles  (11)
  • 1
    Publication Date: 2000-06-24
    Description: Longisquama insignis was an unusual archosaur from the Late Triassic of central Asia. Along its dorsal axis Longisquama bore a series of paired integumentary appendages that resembled avian feathers in many details, especially in the anatomy of the basal region. The latter is sufficiently similar to the calamus of modern feathers that each probably represents the culmination of virtually identical morphogenetic processes. The exact relationship of Longisquama to birds is uncertain. Nevertheless, we interpret Longisquama's elongate integumentary appendages as nonavian feathers and suggest that they are probably homologous with avian feathers. If so, they antedate the feathers of Archaeopteryx, the first known bird from the Late Jurassic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, T D -- Ruben, J A -- Martin, L D -- Kurochkin, E N -- Feduccia, A -- Maderson, P F -- Hillenius, W J -- Geist, N R -- Alifanov, V -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Oregon State University, Corvallis, OR 97331, USA. tdjones@sfasu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864867" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Birds/anatomy & histology ; *Feathers/anatomy & histology ; *Fossils ; Reptiles/*anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1991-04-26
    Description: The trk proto-oncogene encodes a 140-kilodalton, membrane-spanning protein tyrosine kinase (p140prototrk) that is expressed only in neural tissues. Nerve growth factor (NGF) stimulates phosphorylation of p140prototrk in neural cell lines and in embryonic dorsal root ganglia. Affinity cross-linking and equilibrium binding experiments with 125I-labeled NGF indicate that p140prototrk binds NGF specifically in cultured cells with a dissociation constant of 10(-9) molar. The identification of p140prototrk as an NGF receptor indicates that this protein participates in the primary signal transduction mechanism of NGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, D R -- Hempstead, B L -- Martin-Zanca, D -- Chao, M V -- Parada, L F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):554-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eukaryotic Signal Transduction Group, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Cross-Linking Reagents ; Embryo, Mammalian ; Ganglia, Spinal/*metabolism ; Humans ; Kinetics ; Mice ; Nerve Growth Factors/metabolism/*physiology ; Neuroblastoma ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; *Proto-Oncogenes ; Receptor, trkA ; Receptors, Cell Surface/metabolism/*physiology ; Receptors, Nerve Growth Factor ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1991-04-26
    Description: The effect of nerve growth factor (NGF) was assessed in Xenopus oocytes expressing the human trk proto-oncogene product, p140prototrk. Oocytes injected with trk messenger RNA expressed polypeptides recognized by antibodies to the trk gene product. Exposure of these oocytes to nanomolar amounts of NGF resulted in specific surface binding of 125I-labeled NGF, tyrosine phosphorylation of p140prototrk, and meiotic maturation, as determined by germinal vesicle breakdown and maturation promoting factor (p34cdc2) kinase activation. Thus the trk proto-oncogene product can act as a receptor for NGF in a functionally productive manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nebreda, A R -- Martin-Zanca, D -- Kaplan, D R -- Parada, L F -- Santos, E -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Female ; Humans ; In Vitro Techniques ; Kinetics ; Meiosis/*drug effects ; Microinjections ; Nerve Growth Factors/metabolism/*pharmacology ; Oocytes/cytology/drug effects/*physiology ; Progesterone/pharmacology ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/*genetics/metabolism ; *Proto-Oncogenes ; RNA, Messenger/administration & dosage/genetics ; Receptor, trkA ; Receptors, Cell Surface/drug effects/metabolism ; Receptors, Nerve Growth Factor ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1992-08-03
    Description: Fourteen strains of eastern equine encephalitis (EEE) virus were isolated from Aedes albopictus mosquitoes collected in Polk County, Florida. These are the first isolations of an arbovirus of proven public health and veterinary importance from naturally infected Ae. albopictus in the United States since established populations of this introduced mosquito were first discovered in 1985. The widespread distribution of Ae. albopictus in Florida and in other areas of the United States where EEE is endemic raises concern that this species may become an epizootic and epidemic vector of EEE virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, C J -- Niebylski, M L -- Smith, G C -- Karabatsos, N -- Martin, D -- Mutebi, J P -- Craig, G B Jr -- Mahler, M J -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):526-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Vector-Borne Infectious Diseases, Centers for Disease Control, U.S. Public Health Service, Fort Collins, CO 80522.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321985" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*microbiology ; Animals ; Centers for Disease Control and Prevention (U.S.) ; Encephalitis Virus, Eastern Equine/*isolation & purification ; Florida ; Mice ; United States ; Vero Cells
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2004-11-30
    Description: The widespread extinctions of large mammals at the end of the Pleistocene epoch have often been attributed to the depredations of humans; here we present genetic evidence that questions this assumption. We used ancient DNA and Bayesian techniques to reconstruct a detailed genetic history of bison throughout the late Pleistocene and Holocene epochs. Our analyses depict a large diverse population living throughout Beringia until around 37,000 years before the present, when the population's genetic diversity began to decline dramatically. The timing of this decline correlates with environmental changes associated with the onset of the last glacial cycle, whereas archaeological evidence does not support the presence of large populations of humans in Eastern Beringia until more than 15,000 years later.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, Beth -- Drummond, Alexei J -- Rambaut, Andrew -- Wilson, Michael C -- Matheus, Paul E -- Sher, Andrei V -- Pybus, Oliver G -- Gilbert, M Thomas P -- Barnes, Ian -- Binladen, Jonas -- Willerslev, Eske -- Hansen, Anders J -- Baryshnikov, Gennady F -- Burns, James A -- Davydov, Sergei -- Driver, Jonathan C -- Froese, Duane G -- Harington, C Richard -- Keddie, Grant -- Kosintsev, Pavel -- Kunz, Michael L -- Martin, Larry D -- Stephenson, Robert O -- Storer, John -- Tedford, Richard -- Zimov, Sergei -- Cooper, Alan -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1561-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Henry Wellcome Ancient Biomolecules Centre, Oxford University, South Parks Road, Oxford OX13PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567864" target="_blank"〉PubMed〈/a〉
    Keywords: Alaska ; Animals ; Bayes Theorem ; *Bison/classification/genetics ; Canada ; China ; *Climate ; DNA, Mitochondrial/genetics ; Environment ; *Fossils ; Genetic Variation ; Genetics, Population ; Human Activities ; Humans ; North America ; Phylogeny ; Population Dynamics ; Sequence Analysis, DNA ; Time
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2011-11-04
    Description: Despite decades of research, the roles of climate and humans in driving the dramatic extinctions of large-bodied mammals during the Late Quaternary period remain contentious. Here we use ancient DNA, species distribution models and the human fossil record to elucidate how climate and humans shaped the demographic history of woolly rhinoceros, woolly mammoth, wild horse, reindeer, bison and musk ox. We show that climate has been a major driver of population change over the past 50,000 years. However, each species responds differently to the effects of climatic shifts, habitat redistribution and human encroachment. Although climate change alone can explain the extinction of some species, such as Eurasian musk ox and woolly rhinoceros, a combination of climatic and anthropogenic effects appears to be responsible for the extinction of others, including Eurasian steppe bison and wild horse. We find no genetic signature or any distinctive range dynamics distinguishing extinct from surviving species, emphasizing the challenges associated with predicting future responses of extant mammals to climate and human-mediated habitat change.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070744/" 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/PMC4070744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorenzen, Eline D -- Nogues-Bravo, David -- Orlando, Ludovic -- Weinstock, Jaco -- Binladen, Jonas -- Marske, Katharine A -- Ugan, Andrew -- Borregaard, Michael K -- Gilbert, M Thomas P -- Nielsen, Rasmus -- Ho, Simon Y W -- Goebel, Ted -- Graf, Kelly E -- Byers, David -- Stenderup, Jesper T -- Rasmussen, Morten -- Campos, Paula F -- Leonard, Jennifer A -- Koepfli, Klaus-Peter -- Froese, Duane -- Zazula, Grant -- Stafford, Thomas W Jr -- Aaris-Sorensen, Kim -- Batra, Persaram -- Haywood, Alan M -- Singarayer, Joy S -- Valdes, Paul J -- Boeskorov, Gennady -- Burns, James A -- Davydov, Sergey P -- Haile, James -- Jenkins, Dennis L -- Kosintsev, Pavel -- Kuznetsova, Tatyana -- Lai, Xulong -- Martin, Larry D -- McDonald, H Gregory -- Mol, Dick -- Meldgaard, Morten -- Munch, Kasper -- Stephan, Elisabeth -- Sablin, Mikhail -- Sommer, Robert S -- Sipko, Taras -- Scott, Eric -- Suchard, Marc A -- Tikhonov, Alexei -- Willerslev, Rane -- Wayne, Robert K -- Cooper, Alan -- Hofreiter, Michael -- Sher, Andrei -- Shapiro, Beth -- Rahbek, Carsten -- Willerslev, Eske -- R01 HG003229/HG/NHGRI NIH HHS/ -- England -- Nature. 2011 Nov 2;479(7373):359-64. doi: 10.1038/nature10574.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for GeoGenetics, University of Copenhagen, Oster Voldgade 5-7, DK-1350 Copenhagen K, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22048313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bayes Theorem ; *Biota ; Bison ; Climate Change/*history ; DNA, Mitochondrial/analysis/genetics ; Europe ; *Extinction, Biological ; Fossils ; Genetic Variation ; Geography ; History, Ancient ; Horses ; Human Activities/*history ; Humans ; Mammals/genetics/*physiology ; Mammoths ; Molecular Sequence Data ; Population Dynamics ; Reindeer ; Siberia ; Species Specificity ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
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  • 7
    Publication Date: 2014-07-22
    Description: Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow microenvironment might contribute to the clinical outcomes of this common event. We previously showed that bone marrow nestin(+) mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. Here we demonstrate that abrogation of this regulatory circuit is essential for MPN pathogenesis. Sympathetic nerve fibres, supporting Schwann cells and nestin(+) MSCs are consistently reduced in the bone marrow of MPN patients and mice expressing the human JAK2(V617F) mutation in HSCs. Unexpectedly, MSC reduction is not due to differentiation but is caused by bone marrow neural damage and Schwann cell death triggered by interleukin-1beta produced by mutant HSCs. In turn, in vivo depletion of nestin(+) cells or their production of CXCL12 expanded mutant HSC number and accelerated MPN progression. In contrast, administration of neuroprotective or sympathomimetic drugs prevented mutant HSC expansion. Treatment with beta3-adrenergic agonists that restored the sympathetic regulation of nestin(+) MSCs prevented the loss of these cells and blocked MPN progression by indirectly reducing the number of leukaemic stem cells. Our results demonstrate that mutant-HSC-driven niche damage critically contributes to disease manifestation in MPN and identify niche-forming MSCs and their neural regulation as promising therapeutic targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arranz, Lorena -- Sanchez-Aguilera, Abel -- Martin-Perez, Daniel -- Isern, Joan -- Langa, Xavier -- Tzankov, Alexandar -- Lundberg, Pontus -- Muntion, Sandra -- Tzeng, Yi-Shiuan -- Lai, Dar-Ming -- Schwaller, Jurg -- Skoda, Radek C -- Mendez-Ferrer, Simon -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 7;512(7512):78-81. doi: 10.1038/nature13383. Epub 2014 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Niche Pathophysiology Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain. ; University Hospital Basel, CH-4031 Basel, Switzerland. ; Department of Haematology, IBSAL-Hospital Universitario de Salamanca, 37007 Salamanca, Spain. ; National Taiwan University, Taipei 10002, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043017" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-3 Receptor Agonists/pharmacology/therapeutic use ; Animals ; Apoptosis/drug effects ; Disease Progression ; Female ; Hematopoietic Stem Cells/drug effects/*pathology ; Humans ; Interleukin-1beta/metabolism ; Janus Kinase 2/genetics ; Mesenchymal Stromal Cells/drug effects/pathology ; Mice ; Myeloproliferative Disorders/drug therapy/*pathology ; Neoplasms/drug therapy/*pathology ; Neoplastic Stem Cells/drug effects/pathology ; Nerve Fibers/drug effects/*pathology ; Nestin/metabolism ; Neuroprotective Agents/pharmacology/therapeutic use ; Receptors, Adrenergic, beta-3/metabolism ; Schwann Cells/drug effects/pathology ; *Stem Cell Niche ; Sympathetic Nervous System/drug effects/*pathology/physiopathology
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    Electronic ISSN: 1476-4687
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  • 8
    Publication Date: 2006-05-20
    Description: Endocast analysis of the brain Homo floresiensis by Falk et al. (Reports, 8 April 2005, p. 242) implies that the hominid is an insular dwarf derived from H. erectus, but its tiny cranial capacity cannot result from normal dwarfing. Consideration of more appropriate microcephalic syndromes and specimens supports the hypothesis of modern human microcephaly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, R D -- Maclarnon, A M -- Phillips, J L -- Dussubieux, L -- Williams, P R -- Dobyns, W B -- New York, N.Y. -- Science. 2006 May 19;312(5776):999; author reply 999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Field Museum, Chicago, IL 60605-2496, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709768" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Body Size ; Brain/*anatomy & histology/*pathology ; Cephalometry ; Fossils ; History, Ancient ; Hominidae/*anatomy & histology/classification ; Humans ; Microcephaly/history/*pathology ; Organ Size ; Paleopathology ; Skull/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2010-02-20
    Description: Large-bodied suspension feeders (planktivores), which include the most massive animals to have ever lived, are conspicuously absent from Mesozoic marine environments. The only clear representatives of this trophic guild in the Mesozoic have been an enigmatic and apparently short-lived Jurassic group of extinct pachycormid fishes. Here, we report several new examples of these giant bony fishes from Asia, Europe, and North America. These fossils provide the first detailed anatomical information on this poorly understood clade and extend its range from the lower Middle Jurassic to the end of the Cretaceous, showing that this group persisted for more than 100 million years. Modern large-bodied, planktivorous vertebrates diversified after the extinction of pachycormids at the Cretaceous-Paleogene boundary, which is consistent with an opportunistic refilling of vacated ecospace.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedman, Matt -- Shimada, Kenshu -- Martin, Larry D -- Everhart, Michael J -- Liston, Jeff -- Maltese, Anthony -- Triebold, Michael -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):990-3. doi: 10.1126/science.1184743.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, 1025 East 57th Street, Chicago, IL 60637, USA. mattf@earth.ox.ac.uk [corrected]〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asia ; Biological Evolution ; Body Size ; Bone and Bones/anatomy & histology ; *Ecosystem ; Europe ; Extinction, Biological ; Feeding Behavior ; *Fishes/anatomy & histology/classification/physiology ; Fossils ; Jaw/anatomy & histology ; North America ; Oceans and Seas ; Phylogeny ; *Plankton ; *Seawater ; Skull/anatomy & histology ; Time
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2015-09-26
    Description: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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