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  • Articles  (6,679)
  • Mice  (5,420)
  • Cell Line  (2,037)
  • American Association for the Advancement of Science (AAAS)  (6,679)
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  • Articles  (6,679)
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  • 11
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    Retrograde viral delivery of IGF-1 prolongs survival in a mouse ALS model (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: Amyotrophic lateral sclerosis (ALS) is a progressive, lethal neuromuscular disease that is associated with the degeneration of spinal and brainstem motor neurons, leading to atrophy of limb, axial, and respiratory muscles. The cause of ALS is unknown, and there is no effective therapy. Neurotrophic factors are candidates for therapeutic evaluation in ALS. Although chronic delivery of molecules to the central nervous system has proven difficult, we recently discovered that adeno-associated virus can be retrogradely transported efficiently from muscle to motor neurons of the spinal cord. We report that insulin-like growth factor 1 prolongs life and delays disease progression, even when delivered at the time of overt disease symptoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaspar, Brian K -- Llado, Jeronia -- Sherkat, Nushin -- Rothstein, Jeffrey D -- Gage, Fred H -- AG12992/AG/NIA NIH HHS/ -- AG21876/AG/NIA NIH HHS/ -- NS33958/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907804" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/physiopathology/*therapy ; Animals ; Apoptosis ; Base Sequence ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Dependovirus/*genetics ; Disease Models, Animal ; Disease Progression ; Gene Transfer Techniques ; *Genetic Therapy ; *Genetic Vectors/administration & dosage ; Glial Cell Line-Derived Neurotrophic Factor ; Green Fluorescent Proteins ; Insulin-Like Growth Factor I/*genetics ; Luminescent Proteins/genetics ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Motor Neurons/pathology/virology ; Muscle, Skeletal/virology ; Nerve Growth Factors/genetics ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Random Allocation ; Spinal Cord/chemistry/pathology/virology ; Superoxide Dismutase/genetics/metabolism ; Ubiquitin/analysis
    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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  • 12
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    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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  • 13
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    Generation of an LFA-1 antagonist by the transfer of the ICAM-1 immunoregulatory epitope to a small molecule (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-09
    Description: The protein-protein interaction between leukocyte functional antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) is critical to lymphocyte and immune system function. Here, we report on the transfer of the contiguous, nonlinear epitope of ICAM-1, responsible for its association with LFA-1, to a small-molecule framework. These LFA-1 antagonists bound LFA-1, blocked binding of ICAM-1, and inhibited a mixed lymphocyte reaction (MLR) with potency significantly greater than that of cyclosporine A. Furthermore, in comparison to an antibody to LFA-1, they exhibited significant anti-inflammatory effects in vivo. These results demonstrate the utility of small-molecule mimics of nonlinear protein epitopes and the protein epitopes themselves as leads in the identification of novel pharmaceutical agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gadek, T R -- Burdick, D J -- McDowell, R S -- Stanley, M S -- Marsters, J C Jr -- Paris, K J -- Oare, D A -- Reynolds, M E -- Ladner, C -- Zioncheck, K A -- Lee, W P -- Gribling, P -- Dennis, M S -- Skelton, N J -- Tumas, D B -- Clark, K R -- Keating, S M -- Beresini, M H -- Tilley, J W -- Presta, L G -- Bodary, S C -- New York, N.Y. -- Science. 2002 Feb 8;295(5557):1086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioorganic Chemistry, Genentech, One DNA Way, South San Francisco, CA 94080, USA. trg@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11834839" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/metabolism/pharmacology ; Cyclosporine/pharmacology ; Dermatitis, Irritant/drug therapy ; Dinitrofluorobenzene ; Drug Design ; Enzyme-Linked Immunosorbent Assay ; Epitopes ; Female ; Humans ; Immunoglobulin Fab Fragments/immunology/pharmacology ; Immunosuppressive Agents/chemical synthesis/chemistry/metabolism/*pharmacology ; Intercellular Adhesion Molecule-1/chemistry/*immunology/*metabolism ; Lymphocyte Culture Test, Mixed ; Lymphocyte Function-Associated Antigen-1/immunology/*metabolism ; Mice ; Mice, Inbred BALB C ; Molecular Mimicry ; Mutagenesis ; Protein Structure, Secondary ; Structure-Activity Relationship ; Thiophenes/*chemical synthesis/chemistry/metabolism/*pharmacology ; beta-Alanine/analogs & derivatives/*chemical ; synthesis/chemistry/metabolism/*pharmacology
    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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  • 14
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    Critical roles of activation-induced cytidine deaminase in the homeostasis of gut flora (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-16
    Description: Activation-induced cytidine deaminase (AID) plays an essential role in class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes. We report here that deficiency in AID results in the development of hyperplasia of isolated lymphoid follicles (ILFs) associated with a 100-fold expansion of anaerobic flora in the small intestine. Reduction of bacterial flora by antibiotic treatment of AID-/- mice abolished ILF hyperplasia as well as the germinal center enlargement seen in secondary lymphoid tissues. Because an inability to switch to immunoglobulin A on its own does not lead to a similar phenotype, these results suggest that SHM of ILF B cells plays a critical role in regulating intestinal microflora.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagarasan, Sidonia -- Muramatsu, Masamichi -- Suzuki, Keiichiro -- Nagaoka, Hitoshi -- Hiai, Hiroshi -- Honjo, Tasuku -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12434060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents ; B-Lymphocytes/immunology ; Bacteria, Aerobic/*growth & development ; Bacteria, Anaerobic/*growth & development ; Cell Division ; Colony Count, Microbial ; Cytidine Deaminase/genetics/*metabolism ; Dendritic Cells, Follicular/immunology ; Drug Therapy, Combination/pharmacology ; Genes, Immunoglobulin ; Germinal Center/immunology ; Homeostasis ; Hyperplasia ; Immunization ; Immunoglobulin Class Switching ; Immunoglobulin Variable Region/genetics ; Intestine, Small/immunology/*microbiology ; Lymphocyte Activation ; Lymphoid Tissue/immunology/*pathology ; Metronidazole/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Peyer's Patches/pathology ; Somatic Hypermutation, Immunoglobulin ; T-Lymphocytes/immunology
    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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  • 15
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    Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: The formation and patterning of mesoderm during mammalian gastrulation require the activity of Nodal, a secreted mesoderm-inducing factor of the transforming growth factor-beta (TGF-beta) family. Here we show that the transcriptional corepressor DRAP1 has a very specific role in regulation of Nodal activity during mouse embryogenesis. We find that loss of Drap1 leads to severe gastrulation defects that are consistent with increased expression of Nodal and can be partially suppressed by Nodal heterozygosity. Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity. We propose that DRAP1 limits the spread of a morphogenetic signal by down-modulating the response to the Nodal autoregulatory loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iratni, Rabah -- Yan, Yu-Ting -- Chen, Canhe -- Ding, Jixiang -- Zhang, Yi -- Price, Sandy M -- Reinberg, Danny -- Shen, Michael M -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471260" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Line ; Crosses, Genetic ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; *Embryonic and Fetal Development ; Female ; Forkhead Transcription Factors ; Gastrula/*physiology ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heterozygote ; In Situ Hybridization ; Left-Right Determination Factors ; Male ; Mesoderm/cytology/physiology ; Mice ; Morphogenesis ; Mutation ; Nodal Protein ; Phenotype ; Protein Binding ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; *Signal Transduction ; Transcription Factors/metabolism ; Transforming Growth Factor beta/genetics/*metabolism
    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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  • 16
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    Historical essay. The early years of HIV/AIDS (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, Robert C -- New York, N.Y. -- Science. 2002 Nov 29;298(5599):1728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Virology and Department of Microbiology and Immunology, University of Maryland, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12459576" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/history ; Acquired Immunodeficiency Syndrome/diagnosis/*history/immunology/virology ; CD4-Positive T-Lymphocytes/virology ; Cell Line ; Cells, Cultured ; France ; *HIV/classification/isolation & purification/physiology ; History, 20th Century ; Human T-lymphotropic virus 1/isolation & purification/physiology ; Human T-lymphotropic virus 2/isolation & purification/physiology ; Humans ; Interleukin-2/history/isolation & purification/physiology ; Patents as Topic/history ; RNA-Directed DNA Polymerase/history/isolation & purification/metabolism ; United States ; Virus Cultivation
    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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  • 17
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    Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (II) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Martin -- Bristow, Robert -- Glazer, Peter -- Hill, Richard -- McBride, William -- McKenna, Gillies -- Muschel, Ruth -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1894; author reply 1894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Disease Models, Animal ; Endothelium, Vascular/*pathology/radiation effects ; Melanoma, Experimental/blood supply/immunology/pathology/*radiotherapy ; Mice ; Radiation Tolerance ; Sphingomyelin Phosphodiesterase/genetics/metabolism
    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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  • 18
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    Genomics. Mmu 16--comparative genomic highlights (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, Neal G -- Jenkins, Nancy A -- O'Brien, Stephen J -- New York, N.Y. -- Science. 2002 May 31;296(5573):1617-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, 21702, USA. copeland@ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Biological Evolution ; Chromosome Aberrations ; Chromosomes/*genetics ; Chromosomes, Human/genetics ; Computational Biology ; Conserved Sequence ; Evolution, Molecular ; Gene Duplication ; Gene Rearrangement ; Genes ; Genome ; *Genome, Human ; Genomics ; Humans ; Mice ; Mice, Inbred Strains/*genetics ; Multigene Family ; *Sequence Analysis, DNA ; Species Specificity ; Synteny
    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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  • 19
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    Altered patterns of sleep and behavioral adaptability in NPAS2-deficient mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: Animal behavior is synchronized to the 24-hour light:dark (LD) cycle by regulatory programs that produce circadian fluctuations in gene expression throughout the body. In mammals, the transcription factor CLOCK controls circadian oscillation in the suprachiasmatic nucleus of the brain; its paralog, neuronal PAS domain protein 2 (NPAS2), performs a similar function in other forebrain sites. To investigate the role of NPAS2 in behavioral manifestations of circadian rhythm, we studied locomotor activity, sleep patterns, and adaptability to both light- and restricted food-driven entrainment in NPAS2-deficient mice. Our results indicate that NPAS2 plays a substantive role in maintaining circadian behaviors in normal LD and feeding conditions and that NPAS2 is critical for adaptability to food restriction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudley, Carol A -- Erbel-Sieler, Claudia -- Estill, Sandi Jo -- Reick, Martin -- Franken, Paul -- Pitts, SiNae -- McKnight, Steven L -- 37919/PHS HHS/ -- 4R37 MH59388/MH/NIMH NIH HHS/ -- 5T3DK07328/DK/NIDDK NIH HHS/ -- HL 64148/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):379-83. Epub 2003 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843397" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Behavior, Animal ; Biological Clocks/*physiology ; Body Weight ; CLOCK Proteins ; Circadian Rhythm/*physiology ; Crosses, Genetic ; Darkness ; Eating ; Electroencephalography ; Electromyography ; Female ; Food ; Gene Targeting ; Light ; Male ; Mice ; Mice, Inbred C57BL ; *Motor Activity ; Nerve Tissue Proteins/genetics/*physiology ; Prosencephalon/physiology ; *Sleep ; Suprachiasmatic Nucleus/physiology ; Trans-Activators/genetics/physiology ; Transcription Factors/genetics/*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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  • 20
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    Aging and genome maintenance: lessons from the mouse? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasty, Paul -- Campisi, Judith -- Hoeijmakers, Jan -- van Steeg, Harry -- Vijg, Jan -- AG17242/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1355-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA. hastye@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610296" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging/genetics ; Aging, Premature/*genetics ; Animals ; Apoptosis ; Cell Aging ; *DNA Damage ; DNA Helicases/genetics/metabolism ; *DNA Repair/genetics ; Exodeoxyribonucleases ; *Genome ; Genome, Human ; Humans ; Longevity/genetics ; Mice ; Mutation ; Reactive Oxygen Species/metabolism ; RecQ Helicases ; Syndrome ; Telomere/physiology ; Transcription, Genetic
    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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