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  • United States  (292)
  • Rats  (97)
  • American Association for the Advancement of Science (AAAS)  (386)
  • American Chemical Society
  • Cambridge University Press
  • 2000-2004  (386)
  • 1940-1944
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  • American Association for the Advancement of Science (AAAS)  (386)
  • American Chemical Society
  • Cambridge University Press
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Year
  • 1
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    Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-01-06
    Description: Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S T -- Benson, B G -- Bramson, H N -- Chapman, D E -- Dickerson, S H -- Dold, K M -- Eberwein, D J -- Edelstein, M -- Frye, S V -- Gampe Jr, R T -- Griffin, R J -- Harris, P A -- Hassell, A M -- Holmes, W D -- Hunter, R N -- Knick, V B -- Lackey, K -- Lovejoy, B -- Luzzio, M J -- Murray, D -- Parker, P -- Rocque, W J -- Shewchuk, L -- Veal, J M -- Walker, D H -- Kuyper, L F -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Glaxo Wellcome Research and Development, Research Triangle Park, NC 27709, USA. std41085@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141566" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*chemically induced/*prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents/*toxicity ; Antineoplastic Combined Chemotherapy Protocols/toxicity ; Apoptosis/drug effects ; *CDC2-CDC28 Kinases ; Cell Cycle/drug effects ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclophosphamide/toxicity ; Cytoprotection/drug effects ; DNA/biosynthesis ; Doxorubicin/toxicity ; Drug Design ; Enzyme Inhibitors/chemical synthesis/chemistry/*pharmacology ; Epithelium/drug effects ; Etoposide/toxicity ; Hair Follicle/cytology/*drug effects ; Humans ; Indoles/chemical synthesis/chemistry/*pharmacology ; Mice ; Mice, SCID ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Rats ; Retinoblastoma Protein/metabolism ; Scalp/transplantation ; Sulfonamides/chemical synthesis/chemistry/*pharmacology ; Transplantation, Heterologous
    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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    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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  • 3
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    Contribution of increasing CO2 and climate to carbon storage by ecosystems in the United States (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: The effects of increasing carbon dioxide (CO2) and climate on net carbon storage in terrestrial ecosystems of the conterminous United States for the period 1895-1993 were modeled with new, detailed historical climate information. For the period 1980-1993, results from an ensemble of three models agree within 25%, simulating a land carbon sink from CO2 and climate effects of 0.08 gigaton of carbon per year. The best estimates of the total sink from inventory data are about three times larger, suggesting that processes such as regrowth on abandoned agricultural land or in forests harvested before 1980 have effects as large as or larger than the direct effects of CO2 and climate. The modeled sink varies by about 100% from year to year as a result of climate variability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schimel, D -- Melillo, J -- Tian, H -- McGuire, A D -- Kicklighter, D -- Kittel, T -- Rosenbloom, N -- Running, S -- Thornton, P -- Ojima, D -- Parton, W -- Kelly, R -- Sykes, M -- Neilson, R -- Rizzo, B -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2004-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Biogeochemistry, Postfach 10 01 64, D-07701 Jena, Germany. dschimel@bgc-jena.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720324" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Atmosphere ; Carbon/*metabolism ; Carbon Dioxide/*metabolism ; *Climate ; Computer Simulation ; *Ecosystem ; Geography ; Trees ; 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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  • 4
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    Inactivation of TNF signaling by rationally designed dominant-negative TNF variants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steed, Paul M -- Tansey, Malu G -- Zalevsky, Jonathan -- Zhukovsky, Eugene A -- Desjarlais, John R -- Szymkowski, David E -- Abbott, Christina -- Carmichael, David -- Chan, Cheryl -- Cherry, Lisa -- Cheung, Peter -- Chirino, Arthur J -- Chung, Hyo H -- Doberstein, Stephen K -- Eivazi, Araz -- Filikov, Anton V -- Gao, Sarah X -- Hubert, Rene S -- Hwang, Marian -- Hyun, Linus -- Kashi, Sandhya -- Kim, Alice -- Kim, Esther -- Kung, James -- Martinez, Sabrina P -- Muchhal, Umesh S -- Nguyen, Duc-Hanh T -- O'Brien, Christopher -- O'Keefe, Donald -- Singer, Karen -- Vafa, Omid -- Vielmetter, Jost -- Yoder, Sean C -- Dahiyat, Bassil I -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Xencor, 111 West Lemon Avenue, Monrovia, CA 91016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512626" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antigens, CD/metabolism ; Apoptosis ; Arthritis, Experimental/drug therapy ; Biopolymers ; Caspases/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Computer Simulation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Galactosamine/pharmacology ; HeLa Cells ; Humans ; Liver/drug effects ; NF-kappa B/metabolism ; Point Mutation ; *Protein Engineering ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/*antagonists & ; inhibitors/genetics/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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  • 5
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    The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-27
    Description: Multiple sclerosis is a demyelinating disease, characterized by inflammation in the brain and spinal cord, possibly due to autoimmunity. Large-scale sequencing of cDNA libraries, derived from plaques dissected from brains of patients with multiple sclerosis (MS), indicated an abundance of transcripts for osteopontin (OPN). Microarray analysis of spinal cords from rats paralyzed by experimental autoimmune encephalomyelitis (EAE), a model of MS, also revealed increased OPN transcripts. Osteopontin-deficient mice were resistant to progressive EAE and had frequent remissions, and myelin-reactive T cells in OPN-/- mice produced more interleukin 10 and less interferon-gamma than in OPN+/+ mice. Osteopontin thus appears to regulate T helper cell-1 (TH1)-mediated demyelinating disease, and it may offer a potential target in blocking development of progressive MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chabas, D -- Baranzini, S E -- Mitchell, D -- Bernard, C C -- Rittling, S R -- Denhardt, D T -- Sobel, R A -- Lock, C -- Karpuj, M -- Pedotti, R -- Heller, R -- Oksenberg, J R -- Steinman, L -- New York, N.Y. -- Science. 2001 Nov 23;294(5547):1731-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, B002, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11721059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Encephalomyelitis, Autoimmune, ; Experimental/genetics/immunology/metabolism/pathology ; Expressed Sequence Tags ; Gene Deletion ; *Gene Expression Profiling ; Gene Library ; Humans ; Inflammation/genetics/immunology/metabolism/pathology ; Interferon-gamma/genetics/metabolism ; Interleukin-10/genetics/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Multiple Sclerosis/*genetics/immunology/*metabolism/pathology ; Oligonucleotide Array Sequence Analysis ; Osteopontin ; RNA, Messenger/genetics/metabolism ; Rats ; Sialoglycoproteins/deficiency/genetics/*metabolism ; Spinal Cord/metabolism ; Th1 Cells/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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  • 6
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    Identification of ubiquitin ligases required for skeletal muscle atrophy (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-27
    Description: Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 (MuRF1), and a gene we designate Muscle Atrophy F-box (MAFbx), the latter being a member of the SCF family of E3 ubiquitin ligases. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodine, S C -- Latres, E -- Baumhueter, S -- Lai, V K -- Nunez, L -- Clarke, B A -- Poueymirou, W T -- Panaro, F J -- Na, E -- Dharmarajan, K -- Pan, Z Q -- Valenzuela, D M -- DeChiara, T M -- Stitt, T N -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 2001 Nov 23;294(5547):1704-8. Epub 2001 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY, 10591-6707, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Creatine Kinase/genetics ; Creatine Kinase, MM Form ; *DNA-Binding Proteins ; Gene Deletion ; *Gene Expression Profiling ; Hindlimb Suspension ; Humans ; Immobilization ; Isoenzymes/genetics ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Muscle Denervation ; Muscle Proteins/genetics ; Muscle, Skeletal/growth & development/*metabolism/pathology/physiopathology ; Muscular Atrophy/*genetics/pathology/physiopathology ; MyoD Protein/genetics ; Myogenic Regulatory Factor 5 ; Myogenin/genetics ; Peptide Synthases/chemistry/deficiency/genetics/*metabolism ; Phenotype ; Protein Binding ; RNA, Messenger/analysis/genetics ; Rats ; Rats, Sprague-Dawley ; SKP Cullin F-Box Protein Ligases ; *Trans-Activators ; Up-Regulation
    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 on science and politics (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bass, Gary D -- Blumenthal, Paul D -- Corfman, Phil -- Darney, Philip D -- Gonsalves, Gregg -- Levin, Arthur A -- Trussell, James -- Shields, Wayne C -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610277" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; *Advisory Committees ; Federal Government ; Humans ; *Politics ; *Public Health ; *Science ; 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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  • 8
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    Ecology. Ecosystem-based fishery management (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pikitch, E K -- Santora, C -- Babcock, E A -- Bakun, A -- Bonfil, R -- Conover, D O -- Dayton, P -- Doukakis, P -- Fluharty, D -- Heneman, B -- Houde, E D -- Link, J -- Livingston, P A -- Mangel, M -- McAllister, M K -- Pope, J -- Sainsbury, K J -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):346-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pew Institute for Ocean Science, Rosenstiel School of Marine and Atmospheric Science (RSMAS), University of Miami, New York, NY 10022, USA. epikitch@rsmas.miami.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15256658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources ; *Ecosystem ; Environment ; *Fisheries ; *Fishes ; 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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  • 9
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    Public health. A sound rationale needed for phase III HIV-1 vaccine trials (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burton, Dennis R -- Desrosiers, Ronald C -- Doms, Robert W -- Feinberg, Mark B -- Gallo, Robert C -- Hahn, Beatrice -- Hoxie, James A -- Hunter, Eric -- Korber, Bette -- Landay, Alan -- Lederman, Michael M -- Lieberman, Judy -- McCune, Joseph M -- Moore, John P -- Nathanson, Neal -- Picker, Louis -- Richman, Douglas -- Rinaldo, Charles -- Stevenson, Mario -- Watkins, David I -- Wolinsky, Steven M -- Zack, Jerome A -- New York, N.Y. -- Science. 2004 Jan 16;303(5656):316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scripps Research Institute, La Jolla, California, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14726576" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; *Clinical Trials, Phase III as Topic/economics ; Costs and Cost Analysis ; HIV Envelope Protein gp120/*immunology ; HIV Infections/*immunology/prevention & control/therapy ; HIV-1/*immunology ; Humans ; Immunization Schedule ; Immunization, Secondary ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Thailand ; United States ; Vaccines, Synthetic/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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  • 10
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    Varshavsky's contributions (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baumeister, Wolfgang -- Bachmair, Andreas -- Chau, Vincent -- Cohen, Robert -- Coffino, Phil -- Demartino, George -- Deshaies, Raymond -- Dohmen, Juergen -- Emr, Scott -- Finley, Daniel -- Hampton, Randy -- Hill, Christopher -- Hochstrasser, Mark -- Huber, Robert -- Jackson, Peter -- Jentsch, Stefan -- Johnson, Erica -- Kwon, Yong Tae -- Pagano, Michele -- Pickart, Cecile -- Rechsteiner, Martin -- Scheffner, Martin -- Sommer, Thomas -- Tansey, William -- Tyers, Mike -- Vierstra, Richard -- Weissman, Allan -- Wilkinson, Keith D -- Wolf, Dieter -- New York, N.Y. -- Science. 2004 Nov 19;306(5700):1290-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550643" target="_blank"〉PubMed〈/a〉
    Keywords: History, 20th Century ; History, 21st Century ; Nobel Prize ; Proteasome Endopeptidase Complex/*metabolism ; Proteins/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/genetics/*metabolism ; 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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