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  • Male  (86)
  • American Association for the Advancement of Science (AAAS)  (86)
  • American Association for the Advancement of Science
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  • Springer Nature
  • 2000-2004  (86)
  • 1995-1999
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  • American Association for the Advancement of Science (AAAS)  (86)
  • American Association for the Advancement of Science
  • Oxford University Press
  • Springer Nature
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  • 2000-2004  (86)
  • 1995-1999
  • 1980-1984
  • 1940-1944
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  • 1
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    No major schizophrenia locus detected on chromosome 1q in a large multicenter sample (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: Reports of substantial evidence for genetic linkage of schizophrenia to chromosome 1q were evaluated by genotyping 16 DNA markers across 107 centimorgans of this chromosome in a multicenter sample of 779 informative schizophrenia pedigrees. No significant evidence was observed for such linkage, nor for heterogeneity in allele sharing among the eight individual samples. Separate analyses of European-origin families, recessive models of inheritance, and families with larger numbers of affected cases also failed to produce significant evidence for linkage. If schizophrenia susceptibility genes are present on chromosome 1q, their population-wide genetic effects are likely to be small.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levinson, Douglas F -- Holmans, Peter A -- Laurent, Claudine -- Riley, Brien -- Pulver, Ann E -- Gejman, Pablo V -- Schwab, Sibylle G -- Williams, Nigel M -- Owen, Michael J -- Wildenauer, Dieter B -- Sanders, Alan R -- Nestadt, Gerald -- Mowry, Bryan J -- Wormley, Brandon -- Bauche, Stephanie -- Soubigou, Stephane -- Ribble, Robert -- Nertney, Deborah A -- Liang, Kung Yee -- Martinolich, Laura -- Maier, Wolfgang -- Norton, Nadine -- Williams, Hywel -- Albus, Margot -- Carpenter, Eric B -- DeMarchi, Nicola -- Ewen-White, Kelly R -- Walsh, Dermot -- Jay, Maurice -- Deleuze, Jean-Francois -- O'Neill, F Anthony -- Papadimitriou, George -- Weilbaecher, Ann -- Lerer, Bernard -- O'Donovan, Michael C -- Dikeos, Dimitris -- Silverman, Jeremy M -- Kendler, Kenneth S -- Mallet, Jacques -- Crowe, Raymond R -- Walters, Marilyn -- G9309834/Medical Research Council/United Kingdom -- G9810900/Medical Research Council/United Kingdom -- K24-MH64197/MH/NIMH NIH HHS/ -- KO2-01207/PHS HHS/ -- MH 41953/MH/NIMH NIH HHS/ -- MH 45390/MH/NIMH NIH HHS/ -- MH 52537/MH/NIMH NIH HHS/ -- MH61602/MH/NIMH NIH HHS/ -- R01-MH57314/MH/NIMH NIH HHS/ -- U01 MH46289/MH/NIMH NIH HHS/ -- U01 MH46318/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):739-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA. dfl@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976456" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Alleles ; Australia ; Canada ; Chromosomes, Human, Pair 1/*genetics ; Europe ; Female ; Genes, Recessive ; *Genetic Linkage ; *Genetic Predisposition to Disease ; Genotype ; Humans ; Lod Score ; Male ; Microsatellite Repeats ; Pedigree ; Schizophrenia/ethnology/*genetics ; United States
    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
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    Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, D W -- Varley, J M -- Szydlo, T E -- Kang, D H -- Wahrer, D C -- Shannon, K E -- Lubratovich, M -- Verselis, S J -- Isselbacher, K J -- Fraumeni, J F -- Birch, J M -- Li, F P -- Garber, J E -- Haber, D A -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Center for Cancer Risk Analysis and Harvard Medical School, Building 149, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; G1 Phase ; *G2 Phase ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Li-Fraumeni Syndrome/enzymology/*genetics/pathology ; Male ; Pedigree ; Polymorphism, Genetic ; Protein Kinases/genetics ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; Sarcoma/genetics ; Signal Transduction ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Biomarkers of caloric restriction may predict longevity in humans (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, George S -- Lane, Mark A -- Ingram, Donald K -- Mattison, Julie A -- Elahi, Dariush -- Tobin, Jordan D -- Muller, Denis -- Metter, E Jeffrey -- New York, N.Y. -- Science. 2002 Aug 2;297(5582):811.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12161648" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Aging/blood ; Animals ; Biomarkers/blood ; *Body Temperature ; Dehydroepiandrosterone Sulfate/*blood ; Diet ; Energy Intake/*physiology ; Humans ; Insulin/*blood ; Life Expectancy ; Longevity/*physiology ; Longitudinal Studies ; Macaca mulatta/*blood/*physiology ; Male ; Middle Aged
    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
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    Mast cells: a cellular link between autoantibodies and inflammatory arthritis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-07
    Description: Previous studies have revealed that autoantibodies, complement components, and Fc receptors each participate in the pathogenesis of erosive arthritis in K/BxN mice. However, it is not known which cellular populations are responsive to these inflammatory signals. We find that two strains of mice deficient in mast cells, W/Wv and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored in the W/Wv strain by mast cell engraftment. Thus, mast cells may function as a cellular link between autoantibodies, soluble mediators, and other effector populations in inflammatory arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, David M -- Friend, Daniel S -- Gurish, Michael F -- Benoist, Christophe -- Mathis, Diane -- Brenner, Michael B -- 1R01 AR/AI46580-01/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 6;297(5587):1689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12215644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*immunology/pathology ; Autoantibodies/*immunology ; Blood Transfusion ; Bone Marrow Transplantation ; Cell Degranulation ; Joints/*immunology/pathology ; Male ; Mast Cells/*immunology/transplantation ; Mice ; Mice, Inbred C57BL
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Role of brain insulin receptor in control of body weight and reproduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruning, J C -- Gautam, D -- Burks, D J -- Gillette, J -- Schubert, M -- Orban, P C -- Klein, R -- Krone, W -- Muller-Wieland, D -- Kahn, C R -- DK31036/DK/NIDDK NIH HHS/ -- DK55326-01A2/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Klinik II und Poliklinik fur Innere Medizin and Center of Molecular Medicine (ZMMK) der Universitat zu Koln, Joseph Stelzmann Strasse 9, 50931 Cologne, Germany. jens.bruening@uni-koeln.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000114" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Blood Glucose/analysis ; *Body Weight ; Brain/*metabolism ; Eating ; Female ; Hypertriglyceridemia/etiology ; Insulin/blood/*physiology ; Insulin Resistance ; Leptin/blood ; Leuprolide/pharmacology ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; Neurons/metabolism ; Obesity/etiology ; Ovarian Follicle/physiology ; Receptor, Insulin/genetics/*physiology ; *Reproduction ; Sex Characteristics ; Signal Transduction ; Spermatogenesis
    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
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    Genomic instability in mice lacking histone H2AX (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-06
    Description: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" 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/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/physiology ; Base Sequence ; Cell Aging ; Cell Cycle ; Cells, Cultured ; *Chromosome Aberrations ; DNA Damage ; *DNA Repair ; Female ; Gene Targeting ; Histones/chemistry/*genetics/*physiology ; Immunoglobulin Class Switching ; Infertility, Male/genetics/physiopathology ; Lymphocyte Count ; Male ; Meiosis ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Phosphorylation ; *Recombination, Genetic ; Spermatocytes/physiology ; T-Lymphocytes/immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Insect population control using a dominant, repressible, lethal genetic system (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: A major modification to the sterile insect technique is described, in which transgenic insects homozygous for a dominant, repressible, female-specific lethal gene system are used. We demonstrate two methods that give the required genetic characteristics in an otherwise wild-type genetic background. The first system uses a sex-specific promoter or enhancer to drive the expression of a repressible transcription factor, which in turn controls the expression of a toxic gene product. The second system uses non-sex-specific expression of the repressible transcription factor to regulate a selectively lethal gene product. Both methods work efficiently in Drosophila melanogaster, and we expect these principles to be widely applicable to more economically important organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, D D -- Donnelly, C A -- Wood, R J -- Alphey, L S -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2474-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741964" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Crosses, Genetic ; DNA-Binding Proteins ; *Drosophila Proteins ; Drosophila melanogaster/*genetics ; Egg Proteins/genetics ; Enhancer Elements, Genetic ; Fat Body/metabolism ; Female ; Gene Expression Regulation ; *Genes, Dominant ; *Genes, Insect ; *Genes, Lethal ; Genes, ras ; Homozygote ; Male ; Models, Biological ; Nuclear Proteins/genetics ; *Pest Control, Biological ; Promoter Regions, Genetic ; Tetracycline/pharmacology ; Trans-Activators/genetics ; Transcription Factors/genetics
    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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  • 8
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    Hematopoietic stem cell quiescence maintained by p21cip1/waf1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Relative quiescence is a defining characteristic of hematopoietic stem cells, while their progeny have dramatic proliferative ability and inexorably move toward terminal differentiation. The quiescence of stem cells has been conjectured to be of critical biologic importance in protecting the stem cell compartment, which we directly assessed using mice engineered to be deficient in the G1 checkpoint regulator, cyclin-dependent kinase inhibitor, p21cip1/waf1 (p21). In the absence of p21, hematopoietic stem cell proliferation and absolute number were increased under normal homeostatic conditions. Exposing the animals to cell cycle-specific myelotoxic injury resulted in premature death due to hematopoietic cell depletion. Further, self-renewal of primitive cells was impaired in serially transplanted bone marrow from p21-/- mice, leading to hematopoietic failure. Therefore, p21 is the molecular switch governing the entry of stem cells into the cell cycle, and in its absence, increased cell cycling leads to stem cell exhaustion. Under conditions of stress, restricted cell cycling is crucial to prevent premature stem cell depletion and hematopoietic death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, T -- Rodrigues, N -- Shen, H -- Yang, Y -- Dombkowski, D -- Sykes, M -- Scadden, D T -- AI07387/AI/NIAID NIH HHS/ -- DK50234/DK/NIDDK NIH HHS/ -- HL44851/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1804-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Hematology, AIDS Research Center, Massachusetts General Hospital Cancer Center, Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimetabolites/pharmacology ; Blood Cell Count ; Bone Marrow Transplantation ; Cell Count ; *Cell Cycle ; Cell Death ; Cell Differentiation ; Cell Division ; Coculture Techniques ; Colony-Forming Units Assay ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/*physiology ; Female ; Fluorouracil/pharmacology ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Homeostasis ; Male ; Mice ; Mice, Inbred Strains
    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
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    Requirement for RORgamma in thymocyte survival and lymphoid organ development (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
    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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  • 10
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    Mitotic misregulation and human aging (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: Messenger RNA levels were measured in actively dividing fibroblasts isolated from young, middle-age, and old-age humans and humans with progeria, a rare genetic disorder characterized by accelerated aging. Genes whose expression is associated with age-related phenotypes and diseases were identified. The data also suggest that an underlying mechanism of the aging process involves increasing errors in the mitotic machinery of dividing cells in the postreproductive stage of life. We propose that this dysfunction leads to chromosomal pathologies that result in misregulation of genes involved in the aging process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ly, D H -- Lockhart, D J -- Lerner, R A -- Schultz, P G -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2486-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741968" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Aging/*genetics/pathology ; Biochemical Phenomena ; Cell Division ; Cell Line ; Cell Nucleus/ultrastructure ; Child ; Chromosome Segregation/genetics ; Disease/etiology ; Extracellular Matrix/metabolism ; Female ; Fibroblasts/cytology/*metabolism ; *Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Male ; Middle Aged ; *Mitosis/genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Progeria/*genetics/pathology ; RNA, Messenger/genetics/metabolism ; Spindle Apparatus/metabolism ; Transcription Factors/genetics
    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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