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  • Articles  (175)
  • Phosphorylation  (175)
  • 2000-2004  (81)
  • 1995-1999  (94)
  • Biology  (175)
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  • Articles  (175)
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  • 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
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  • 2
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    Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Tau proteins aggregate as cytoplasmic inclusions in a number of neurodegenerative diseases, including Alzheimer's disease and hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Over 10 exonic and intronic mutations in the tau gene have been identified in about 20 FTDP-17 families. Analyses of soluble and insoluble tau proteins from brains of FTDP-17 patients indicated that different pathogenic mutations differentially altered distinct biochemical properties and stoichiometry of brain tau isoforms. Functional assays of recombinant tau proteins with different FTDP-17 missense mutations implicated all but one of these mutations in disease pathogenesis by reducing the ability of tau to bind microtubules and promote microtubule assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, M -- Zhukareva, V -- Vogelsberg-Ragaglia, V -- Wszolek, Z -- Reed, L -- Miller, B I -- Geschwind, D H -- Bird, T D -- McKeel, D -- Goate, A -- Morris, J C -- Wilhelmsen, K C -- Schellenberg, G D -- Trojanowski, J Q -- Lee, V M -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1914-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836646" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Brain/*metabolism ; Cerebellum/metabolism ; Chromosomes, Human, Pair 17 ; Dementia/*genetics/metabolism ; Frontal Lobe/metabolism ; Humans ; Microtubules/*metabolism ; Mutation ; Mutation, Missense ; Parkinson Disease, Secondary/*genetics/metabolism ; Phosphorylation ; Protein Isoforms/chemistry/genetics/metabolism ; Recombinant Proteins/metabolism ; Solubility ; Syndrome ; tau Proteins/chemistry/*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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  • 3
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    Oscillations in NF-kappaB signaling control the dynamics of gene expression (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: Signaling by the transcription factor nuclear factor kappa B (NF-kappaB) involves its release from inhibitor kappa B (IkappaB) in the cytosol, followed by translocation into the nucleus. NF-kappaB regulation of IkappaBalpha transcription represents a delayed negative feedback loop that drives oscillations in NF-kappaB translocation. Single-cell time-lapse imaging and computational modeling of NF-kappaB (RelA) localization showed asynchronous oscillations following cell stimulation that decreased in frequency with increased IkappaBalpha transcription. Transcription of target genes depended on oscillation persistence, involving cycles of RelA phosphorylation and dephosphorylation. The functional consequences of NF-kappaB signaling may thus depend on number, period, and amplitude of oscillations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, D E -- Ihekwaba, A E C -- Elliott, M -- Johnson, J R -- Gibney, C A -- Foreman, B E -- Nelson, G -- See, V -- Horton, C A -- Spiller, D G -- Edwards, S W -- McDowell, H P -- Unitt, J F -- Sullivan, E -- Grimley, R -- Benson, N -- Broomhead, D -- Kell, D B -- White, M R H -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):704-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Imaging, School of Biological Sciences, Bioscience Research Building, Crown Street, Liverpool, L69 7ZB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499023" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Computer Simulation ; Cytoplasm/metabolism ; Etoposide/pharmacology ; Feedback, Physiological ; *Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Proteins/genetics/metabolism ; Models, Biological ; NF-kappa B/*metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/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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    DARPP-32: regulator of the efficacy of dopaminergic neurotransmission (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Dopaminergic neurons exert a major modulatory effect on the forebrain. Dopamine and adenosine 3',5'-monophosphate-regulated phosphoprotein (32 kilodaltons) (DARPP-32), which is enriched in all neurons that receive a dopaminergic input, is converted in response to dopamine into a potent protein phosphatase inhibitor. Mice generated to contain a targeted disruption of the DARPP-32 gene showed profound deficits in their molecular, electrophysiological, and behavioral responses to dopamine, drugs of abuse, and antipsychotic medication. The results show that DARPP-32 plays a central role in regulating the efficacy of dopaminergic neurotransmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fienberg, A A -- Hiroi, N -- Mermelstein, P G -- Song, W -- Snyder, G L -- Nishi, A -- Cheramy, A -- O'Callaghan, J P -- Miller, D B -- Cole, D G -- Corbett, R -- Haile, C N -- Cooper, D C -- Onn, S P -- Grace, A A -- Ouimet, C C -- White, F J -- Hyman, S E -- Surmeier, D J -- Girault, J -- Nestler, E J -- Greengard, P -- DA 08227/DA/NIDA NIH HHS/ -- DA10044/DA/NIDA NIH HHS/ -- F31 DA005794/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):838-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694658" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamines/pharmacology ; Animals ; Behavior, Animal/drug effects ; Calcium/metabolism ; Cocaine/pharmacology ; Corpus Striatum/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dopamine/pharmacology/*physiology ; Dopamine Agents/pharmacology ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Female ; Gene Expression Regulation ; Gene Targeting ; Genes, fos ; Glutamic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics/*metabolism ; Neurons/*metabolism ; Phosphoprotein Phosphatases/metabolism ; *Phosphoproteins ; Phosphorylation ; Raclopride ; Receptors, Dopamine D1/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Salicylamides/pharmacology ; Sodium-Potassium-Exchanging ATPase/metabolism ; *Synaptic Transmission ; gamma-Aminobutyric Acid/metabolism
    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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  • 5
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    Role of Raf in vascular protection from distinct apoptotic stimuli (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: Raf kinases have been linked to endothelial cell survival. Here, we show that basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) differentially activate Raf, resulting in protection from distinct pathways of apoptosis in human endothelial cells and chick embryo vasculature. bFGF activated Raf-1 via p21-activated protein kinase-1 (PAK-1) phosphorylation of serines 338 and 339, resulting in Raf-1 mitochondrial translocation and endothelial cell protection from the intrinsic pathway of apoptosis, independent of the mitogen-activated protein kinase kinase-1 (MEK1). In contrast, VEGF activated Raf-1 via Src kinase, leading to phosphorylation of tyrosines 340 and 341 and MEK1-dependent protection from extrinsic-mediated apoptosis. These findings implicate Raf-1 as a pivotal regulator of endothelial cell survival during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alavi, Alireza -- Hood, John D -- Frausto, Ricardo -- Stupack, Dwayne G -- Cheresh, David A -- CA45726/CA/NCI NIH HHS/ -- CA50286/CA/NCI NIH HHS/ -- CA75924/CA/NCI NIH HHS/ -- P01 CA78045/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, 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/12843393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/*cytology/drug effects ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Flavonoids/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/pharmacology ; Lymphokines/pharmacology ; MAP Kinase Kinase 1 ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neovascularization, Pathologic ; *Neovascularization, Physiologic/drug effects ; Phosphorylation ; Point Mutation ; Protein Transport ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins B-raf ; Proto-Oncogene Proteins c-raf/chemistry/genetics/*metabolism ; Signal Transduction ; Umbilical Veins ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; p21-Activated Kinases ; src-Family Kinases/antagonists & inhibitors/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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    Two-state allosteric behavior in a single-domain signaling protein (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-27
    Description: Protein actions are usually discussed in terms of static structures, but function requires motion. We find a strong correlation between phosphorylation-driven activation of the signaling protein NtrC and microsecond time-scale backbone dynamics. Using nuclear magnetic resonance relaxation, we characterized the motions of NtrC in three functional states: unphosphorylated (inactive), phosphorylated (active), and a partially active mutant. These dynamics are indicative of exchange between inactive and active conformations. Both states are populated in unphosphorylated NtrC, and phosphorylation shifts the equilibrium toward the active species. These results support a dynamic population shift between two preexisting conformations as the underlying mechanism of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Volkman, B F -- Lipson, D -- Wemmer, D E -- Kern, D -- GM62117/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Mar 23;291(5512):2429-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Magnetic Resonance Facility at Madison (NMRFAM), Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11264542" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; *Bacterial Proteins ; Binding Sites ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Models, Molecular ; Motion ; Mutation ; Nuclear Magnetic Resonance, Biomolecular ; PII Nitrogen Regulatory Proteins ; Phosphorylation ; *Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Signal Transduction ; Time ; *Trans-Activators ; *Transcription Factors
    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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  • 7
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    Discovery of a small molecule insulin mimetic with antidiabetic activity in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Insulin elicits a spectrum of biological responses by binding to its cell surface receptor. In a screen for small molecules that activate the human insulin receptor tyrosine kinase, a nonpeptidyl fungal metabolite (L-783,281) was identified that acted as an insulin mimetic in several biochemical and cellular assays. The compound was selective for insulin receptor versus insulin-like growth factor I (IGFI) receptor and other receptor tyrosine kinases. Oral administration of L-783,281 to two mouse models of diabetes resulted in significant lowering in blood glucose levels. These results demonstrate the feasibility of discovering novel insulin receptor activators that may lead to new therapies for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, B -- Salituro, G -- Szalkowski, D -- Li, Z -- Zhang, Y -- Royo, I -- Vilella, D -- Diez, M T -- Pelaez, F -- Ruby, C -- Kendall, R L -- Mao, X -- Griffin, P -- Calaycay, J -- Zierath, J R -- Heck, J V -- Smith, R G -- Moller, D E -- New York, N.Y. -- Science. 1999 May 7;284(5416):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Endocrinology, Merck Research Laboratories, R80W250, Post Office Box 2000, Rahway, NJ 07065, USA. bei_zhang@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320380" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Ascomycota/*metabolism ; Binding Sites ; Blood Glucose/metabolism ; CHO Cells ; Cricetinae ; Diabetes Mellitus, Type 2/*drug therapy ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Enzyme Activation ; Glucose Tolerance Test ; Hyperglycemia/drug therapy ; Hypoglycemic Agents/chemistry/metabolism/*pharmacology/therapeutic use ; Indoles/chemistry/metabolism/*pharmacology/therapeutic use ; Insulin/blood/metabolism/*pharmacology ; Insulin Receptor Substrate Proteins ; Mice ; Mice, Mutant Strains ; Mice, Obese ; Molecular Mimicry ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Conformation/drug effects ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/chemistry/*metabolism ; Signal Transduction
    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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  • 8
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    Regulation of MAPK function by direct interaction with the mating-specific Galpha in yeast (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-25
    Description: The mating response of the budding yeast Saccharomyces cerevisiae is mediated by a prototypical heterotrimeric GTP-binding protein (G protein) and mitogen-activated protein kinase (MAPK) cascade. Although signal transmission by such pathways has been modeled in detail, postreceptor down-regulation is less well understood. The pheromone-responsive G protein alpha subunit (Galpha) of yeast down-regulates the mating signal, but its targets are unknown. We have found that Galpha binds directly to the mating-specific MAPK in yeast cells responding to pheromone. This interaction contributes both to modulation of the mating signal and to the chemotropic response, and it demonstrates direct communication between the top and bottom of a Galpha-MAPK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metodiev, Metodi V -- Matheos, Dina -- Rose, Mark D -- Stone, David E -- New York, N.Y. -- Science. 2002 May 24;296(5572):1483-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Laboratory for Molecular Biology, University of Illinois at Chicago, 900 South Ashland Avenue (M/C 567), Chicago, IL 60607, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12029138" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Down-Regulation ; *GTP-Binding Protein alpha Subunits ; GTP-Binding Protein alpha Subunits, Gq-G11 ; *GTP-Binding Protein beta Subunits ; Guanosine Diphosphate/metabolism ; Heterotrimeric GTP-Binding Proteins/chemistry/genetics/*metabolism ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/*metabolism ; Molecular Sequence Data ; Mutation ; Pheromones/pharmacology ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/*metabolism/physiology ; Saccharomyces cerevisiae Proteins/*metabolism
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  • 9
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    Regulation of lineage commitment distinct from positive selection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Developing alphabeta T cells diverge into the CD4 and CD8 lineages as they mature in the thymus. It is unclear whether lineage commitment is mechanistically distinct from the process that selects for the survival of T cells with useful T cell receptor (TCR) specificities (positive selection). In HD mice, which lack mature CD4+ T cells, major histocompatibility complex (MHC) class II-restricted T cells are redirected to the CD8 lineage independent of MHC class I expression. However, neither TCR-mediated signaling nor positive selection is impaired. Thus, the HD mutation provides genetic evidence that lineage commitment may be mechanistically distinct from positive selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keefe, R -- Dave, V -- Allman, D -- Wiest, D -- Kappes, D J -- AI34472/AI/NIAID NIH HHS/ -- CA06927/CA/NCI NIH HHS/ -- CA74620/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1149-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*cytology/immunology ; CD8-Positive T-Lymphocytes/*cytology/immunology ; Cell Differentiation ; *Cell Lineage ; Crosses, Genetic ; Female ; Hematopoietic Stem Cells/cytology/immunology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Phenotype ; Phosphorylation ; Radiation Chimera ; Receptors, Antigen, T-Cell, alpha-beta/*metabolism ; Signal Transduction ; T-Lymphocyte Subsets/*cytology/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    PDGFRA activating mutations in gastrointestinal stromal tumors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity. Here we show that approximately 35% (14 of 40) of GISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor alpha (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinrich, Michael C -- Corless, Christopher L -- Duensing, Anette -- McGreevey, Laura -- Chen, Chang-Jie -- Joseph, Nora -- Singer, Samuel -- Griffith, Diana J -- Haley, Andrea -- Town, Ajia -- Demetri, George D -- Fletcher, Christopher D M -- Fletcher, Jonathan A -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):708-10. Epub 2003 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Department of Pathology, Oregon Health & Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA. heinrich@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Chromosome Aberrations ; Cricetinae ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Exons ; Gastrointestinal Neoplasms/*genetics/metabolism ; Humans ; Karyotyping ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Oncogenes ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-kit/*genetics/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/*genetics/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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