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  • 1
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    Regulation of longevity and stress resistance by Sch9 in yeast (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-04-09
    Description: The protein kinase Akt/protein kinase B (PKB) is implicated in insulin signaling in mammals and functions in a pathway that regulates longevity and stress resistance in Caenorhabditis elegans. We screened for long-lived mutants in nondividing yeast Saccharomyces cerevisiae and identified mutations in adenylate cyclase and SCH9, which is homologous to Akt/PKB, that increase resistance to oxidants and extend life-span by up to threefold. Stress-resistance transcription factors Msn2/Msn4 and protein kinase Rim15 were required for this life-span extension. These results indicate that longevity is associated with increased investment in maintenance and show that highly conserved genes play similar roles in life-span regulation in S. cerevisiae and higher eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fabrizio, P -- Pozza, F -- Pletcher, S D -- Gendron, C M -- Longo, V D -- AG 08761-10/AG/NIA NIH HHS/ -- AG09793/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2001 Apr 13;292(5515):288-90. Epub 2001 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biogerontology, Andrus Gerontology Center, and Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089-0191, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11292860" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/metabolism ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/genetics/physiology ; Culture Media ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA Transposable Elements ; DNA-Binding Proteins/genetics/metabolism ; Drosophila/genetics/physiology ; Drug Resistance, Microbial ; Gene Deletion ; Hot Temperature ; Longevity ; Molecular Sequence Data ; Mutagenesis, Insertional ; Oxidants/pharmacology ; Paraquat/pharmacology ; Phenotype ; Protein Kinases/chemistry/genetics/*metabolism ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transformation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Evolutionary medicine: from dwarf model systems to healthy centenarians? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Restriction of the number of calories consumed extends longevity in many organisms. In rodents, caloric restriction decreases the levels of plasma glucose and insulin-like growth factor I (IGF-1) and postpones or attenuates cancer, immunosenescence, and inflammation without irreversible side effects. In organisms ranging from yeast to mice, mutations in glucose or IGF-I-like signaling pathways extend life-span but also cause glycogen or fat accumulation and dwarfism. This information suggests a new category of drugs that could prevent or postpone diseases of aging with few adverse effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Longo, Valter D -- Finch, Caleb E -- AG 01028/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1342-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Andrus Gerontology Center, Division of Biogerontology, and Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. vlongo@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610293" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Biological Evolution ; Caenorhabditis elegans/genetics/physiology ; Caloric Restriction ; Drosophila/genetics/physiology ; Dwarfism/physiopathology ; Gene Expression Regulation ; Glucose/*metabolism ; Growth Hormone/metabolism ; Human Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/*metabolism ; *Longevity/genetics ; Mice ; Models, Animal ; Mutation ; Signal Transduction ; Yeasts/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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  • 3
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    Defective lymphotoxin-beta receptor-induced NF-kappaB transcriptional activity in NIK-deficient mice (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-17
    Description: The role of NF-kappaB-inducing kinase (NIK) in cytokine signaling remains controversial. To identify the physiologic functions of NIK, we disrupted the NIK locus by gene targeting. Although NIK-/- mice displayed abnormalities in both lymphoid tissue development and antibody responses, NIK-/- cells manifested normal NF-kappaB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-beta (LTbeta). However, NIK was selectively required for gene transcription induced through ligation of LTbeta receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-kappaB in a receptor-restricted manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, L -- Wu, L -- Wesche, H -- Arthur, C D -- White, J M -- Goeddel, D V -- Schreiber, R D -- New York, N.Y. -- Science. 2001 Mar 16;291(5511):2162-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11251123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/metabolism ; Cells, Cultured ; DNA/metabolism ; Fibroblasts/metabolism ; Gene Targeting ; Genes, Reporter ; Interleukin-1/metabolism/pharmacology ; Ligands ; Lymphoid Tissue/abnormalities ; Lymphotoxin beta Receptor ; Mice ; Mice, Inbred C57BL ; NF-kappa B/genetics/*metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/immunology/*metabolism ; Signal Transduction ; *Transcription, Genetic ; Tumor Necrosis Factor-alpha/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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  • 4
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    Ascent of dinosaurs linked to an iridium anomaly at the Triassic-Jurassic boundary (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: Analysis of tetrapod footprints and skeletal material from more than 70 localities in eastern North America shows that large theropod dinosaurs appeared less than 10,000 years after the Triassic-Jurassic boundary and less than 30,000 years after the last Triassic taxa, synchronous with a terrestrial mass extinction. This extraordinary turnover is associated with an iridium anomaly (up to 285 parts per trillion, with an average maximum of 141 parts per trillion) and a fern spore spike, suggesting that a bolide impact was the cause. Eastern North American dinosaurian diversity reached a stable maximum less than 100,000 years after the boundary, marking the establishment of dinosaur-dominated communities that prevailed for the next 135 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olsen, P E -- Kent, D V -- Sues, H-D -- Koeberl, C -- Huber, H -- Montanari, A -- Rainforth, E C -- Fowell, S J -- Szajna, M J -- Hartline, B W -- New York, N.Y. -- Science. 2002 May 17;296(5571):1305-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lamont-Doherty Earth Observatory of Columbia University, Palisades, NY 10964, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Dinosaurs ; *Ecosystem ; Ferns ; *Fossils ; Geologic Sediments/chemistry ; Iridium/*analysis ; Meteoroids ; Minor Planets ; North America ; Spores ; 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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  • 5
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    TNF-R1 signaling: a beautiful pathway (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    Description: Tumor necrosis factor (TNF) is a major mediator of apoptosis as well as inflammation and immunity, and it has been implicated in the pathogenesis of a wide spectrum of human diseases, including sepsis, diabetes, cancer, osteoporosis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases. The interaction of TNF with TNF receptor-1 (TNF-R1) activates several signal transduction pathways. A common feature of each pathway is the TNF-induced formation of a multiprotein signaling complex at the cell membrane. Over the past decade, many of the components and mechanisms of these signaling pathways have been elucidated. We provide an overview of current knowledge of TNF signaling and introduce an STKE Connections Map that depicts a canonical view of this process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Guoqing -- Goeddel, David V -- New York, N.Y. -- Science. 2002 May 31;296(5573):1634-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik Inc., Two Corporate Drive, South San Francisco, CA 94080, USA. goeddel@tularik.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Apoptosis ; Cell Membrane/metabolism ; Humans ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/metabolism ; Models, Biological ; Multiprotein Complexes ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Receptors, Tumor Necrosis Factor, Type I ; *Signal Transduction ; Tumor Necrosis Factor-alpha/chemistry/*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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  • 6
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    Age of Neoproterozoic bilatarian body and trace fossils, White Sea, Russia: implications for metazoan evolution (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: A uranium-lead zircon age for a volcanic ash interstratified with fossil-bearing, shallow marine siliciclastic rocks in the Zimnie Gory section of the White Sea region indicates that a diverse assemblage of body and trace fossils occurred before 555.3 +/- 0.3 million years ago. This age is a minimum for the oldest well-documented triploblastic bilaterian Kimberella. It also makes co-occurring trace fossils the oldest that are reliably dated. This determination of age implies that there is no simple relation between Ediacaran diversity and the carbon isotopic composition of Neoproterozoic seawater.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, M W -- Grazhdankin, D V -- Bowring, S A -- Evans, D A -- Fedonkin, M A -- Kirschvink, J L -- New York, N.Y. -- Science. 2000 May 5;288(5467):841-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Atmospheric and Planetary Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. mwm@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Carbon Isotopes ; *Fossils ; *Geologic Sediments ; *Invertebrates ; Isotopes ; Lead/analysis ; *Paleontology ; Russia ; Seawater ; Silicates ; Uranium ; Zirconium
    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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    More about duikers in ancient Egypt (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flores, D V -- New York, N.Y. -- Science. 2001 Apr 20;292(5516):440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11330295" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antelopes ; Burial ; *Ecosystem ; Egypt ; Paintings
    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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    Semaphorin 3E and plexin-D1 control vascular pattern independently of neuropilins (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-20
    Description: The development of a patterned vasculature is essential for normal organogenesis. We found that signaling by semaphorin 3E (Sema3E) and its receptor plexin-D1 controls endothelial cell positioning and the patterning of the developing vasculature in the mouse. Sema3E is highly expressed in developing somites, where it acts as a repulsive cue for plexin-D1-expressing endothelial cells of adjacent intersomitic vessels. Sema3E-plexin-D1 signaling did not require neuropilins, which were previously presumed to be obligate Sema3 coreceptors. Moreover, genetic ablation of Sema3E or plexin-D1 but not neuropilin-mediated Sema3 signaling disrupted vascular patterning. These findings reveal an unexpected semaphorin signaling pathway and define a mechanism for controlling vascular patterning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Chenghua -- Yoshida, Yutaka -- Livet, Jean -- Reimert, Dorothy V -- Mann, Fanny -- Merte, Janna -- Henderson, Christopher E -- Jessell, Thomas M -- Kolodkin, Alex L -- Ginty, David D -- CA23767-24/CA/NCI NIH HHS/ -- MH59199-06/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):265-8. Epub 2004 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Blood Vessels/*embryology/metabolism ; Body Patterning ; COS Cells ; Cercopithecus aethiops ; Chick Embryo ; Endothelial Cells/cytology/physiology ; Endothelium, Vascular/cytology/embryology ; Glycoproteins/*metabolism ; In Situ Hybridization ; Ligands ; Membrane Glycoproteins/*metabolism ; Membrane Proteins/*metabolism ; Mice ; Morphogenesis ; Mutation ; Nerve Tissue Proteins/*metabolism ; Neuropilin-1/metabolism ; Neuropilin-2/metabolism ; Phenotype ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Somites/*metabolism ; Transfection
    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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    Genetic dissection of complex traits with chromosome substitution strains of mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-20
    Description: Chromosome substitution strains (CSSs) have been proposed as a simple and powerful way to identify quantitative trait loci (QTLs) affecting developmental, physiological, and behavioral processes. Here, we report the construction of a complete CSS panel for a vertebrate species. The CSS panel consists of 22 mouse strains, each of which carries a single chromosome substituted from a donor strain (A/J) onto a common host background (C57BL/6J). A survey of 53 traits revealed evidence for 150 QTLs affecting serum levels of sterols and amino acids, diet-induced obesity, and anxiety. These results demonstrate that CSSs greatly facilitate the detection and identification of genes that control the wide diversity of naturally occurring phenotypic variation in the A/J and C57BL/6J inbred strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singer, Jonathan B -- Hill, Annie E -- Burrage, Lindsay C -- Olszens, Keith R -- Song, Junghan -- Justice, Monica -- O'Brien, William E -- Conti, David V -- Witte, John S -- Lander, Eric S -- Nadeau, Joseph H -- GM07250/GM/NIGMS NIH HHS/ -- HD07518/HD/NICHD NIH HHS/ -- RR12305/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 16;304(5669):445-8. Epub 2004 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15031436" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/blood ; Animals ; Anxiety/genetics ; *Chromosome Mapping ; Chromosomes, Mammalian/*genetics ; Crosses, Genetic ; Diet ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Male ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Microsatellite Repeats ; Obesity/genetics/physiopathology ; Phenotype ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Sterols/blood ; Weight Gain
    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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