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  • Artikel  (108)
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  • 1
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    Association of Src tyrosine kinase with a human potassium channel mediated by SH3 domain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-20
    Beschreibung: The human Kv1.5 potassium channel (hKv1.5) contains proline-rich sequences identical to those that bind to Src homology 3 (SH3) domains. Direct association of the Src tyrosine kinase with cloned hKv1.5 and native hKv1.5 in human myocardium was observed. This interaction was mediated by the proline-rich motif of hKv1.5 and the SH3 domain of Src. Furthermore, hKv1.5 was tyrosine phosphorylated, and the channel current was suppressed, in cells coexpressing v-Src. These results provide direct biochemical evidence for a signaling complex composed of a potassium channel and a protein tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, T C -- Fadool, D A -- Ren, R -- Levitan, I B -- F32 NS009952/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Volen Center for Complex Systems, Brandeis University, Waltham, MA 02254, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953041" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Cell Line ; Cloning, Molecular ; Humans ; Kv1.5 Potassium Channel ; Molecular Sequence Data ; Myocardium/chemistry ; Oncogene Protein pp60(v-src)/metabolism ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Potassium Channels/chemistry/*metabolism ; *Potassium Channels, Voltage-Gated ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; src Homology Domains/*physiology ; src-Family Kinases/chemistry/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-20
    Beschreibung: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Control of EGF receptor signaling by clathrin-mediated endocytosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-20
    Beschreibung: Epidermal growth factor receptor (EGFR) signaling was analyzed in mammalian cells conditionally defective for receptor-mediated endocytosis. EGF-dependent cell proliferation was enhanced in endocytosis-defective cells. However, early EGF-dependent signaling events were not uniformly up-regulated. A subset of signal transducers required the normal endocytic trafficking of EGFR for full activation. Thus, endocytic trafficking of activated EGFR plays a critical role not only in attenuating EGFR signaling but also in establishing and controlling specific signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vieira, A V -- Lamaze, C -- Schmid, S L -- CA58689/CA/NCI NIH HHS/ -- CA69099/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. slschmid@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953040" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Adaptor Proteins, Signal Transducing ; *Adaptor Proteins, Vesicular Transport ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Division/drug effects ; Cell Membrane/metabolism ; Clathrin/*physiology ; Coated Pits, Cell-Membrane/physiology ; Dynamins ; *Endocytosis ; Enzyme Activation ; Epidermal Growth Factor/metabolism/pharmacology ; GTP Phosphohydrolases/physiology ; HeLa Cells ; Humans ; Isoenzymes/metabolism ; Phosphatidylinositol 3-Kinases ; Phospholipase C gamma ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Phosphotyrosine/metabolism ; Proteins/metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Shc Signaling Adaptor Proteins ; *Signal Transduction ; Type C Phospholipases/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Enhancement of class II-restricted T cell responses by costimulatory NK receptors for class I MHC proteins (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-20
    Beschreibung: An important feature of the human immune system is the ability of T cells to respond to small quantities of antigen. Class II major histocompatibility complex (MHC)-restricted T cells that expressed a costimulatory natural killer (NK) cell receptor for class I MHC proteins were cloned. In the presence of low doses of superantigen, the proliferative response of these T cell clones was three- to ninefold greater when the T cells were costimulated by way of the NK receptor. Thus, the action of costimulatory NK receptors on T cells may play a significant role in initiating and sustaining immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandelboim, O -- Davis, D M -- Reyburn, H T -- Vales-Gomez, M -- Sheu, E G -- Pazmany, L -- Strominger, J L -- CA 47554/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2097-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA. jlstrom@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953044" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): B-Lymphocytes/immunology ; Cell Line ; Clone Cells ; HLA Antigens/immunology ; HLA-C Antigens/immunology ; HLA-G Antigens ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/*immunology ; Humans ; *Lymphocyte Activation ; Receptors, Immunologic/*immunology ; Superantigens/immunology ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    NF-AT-Driven interleukin-4 transcription potentiated by NIP45 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-13
    Beschreibung: The induction of cytokine gene transcription is mediated in part by the nuclear factor of activated T cells (NF-AT). Factors involved in the mechanisms of NF-AT-mediated transcription are not well understood. A nuclear factor that interacted with the Rel homology domain (RHD) of NF-ATp was identified with the use of a two-hybrid interaction trap. Designated NIP45 (NF-AT interacting protein), it has minimal similarity to any known genes. Transcripts encoding this factor were enriched in lymphoid tissues and testes. NIP45 synergized with NF-ATp and the proto-oncogene c-Maf to activate the interleukin-4 (IL-4) cytokine promoter; transient overexpression of NIP45 with NF-ATp and c-maf in B lymphoma cells induced measurable endogenous IL-4 protein production. The identification of NIP45 advances our understanding of gene activation of cytokines, critical mediators of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hodge, M R -- Chun, H J -- Rengarajan, J -- Alt, A -- Lieberson, R -- Glimcher, L H -- AI37833/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1903-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943202" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cloning, Molecular ; DNA-Binding Proteins/*metabolism ; Genes, Reporter ; Humans ; Interleukin-4/*genetics ; *Intracellular Signaling Peptides and Proteins ; Male ; Molecular Sequence Data ; NFATC Transcription Factors ; Nuclear Proteins/chemistry/genetics/*metabolism ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Spleen/metabolism ; Testis/metabolism ; Thymus Gland/metabolism ; Transcription Factors/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Molecular mimicry of human cytokine and cytokine response pathway genes by KSHV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-06
    Beschreibung: Four virus proteins similar to two human macrophage inflammatory protein (MIP) chemokines, interleukin-6 (IL-6), and interferon regulatory factor (IRF) are encoded by the Kaposi's sarcoma-associated herpesvirus (KSHV) genome. vIL-6 was functional in B9 proliferation assays and primarily expressed in KSHV-infected hematopoietic cells rather than KS lesions. HIV-1 transmission studies showed that vMIP-I is similar to human MIP chemokines in its ability to inhibit replication of HIV-1 strains dependent on the CCR5 co-receptor. These viral genes may form part of the response to host defenses contributing to virus-induced neoplasia and may have relevance to KSHV and HIV-I interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, P S -- Boshoff, C -- Weiss, R A -- Chang, Y -- CA67391/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1739-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939871" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Cell Division ; Cell Line ; Chemokine CCL4 ; Gene Expression ; Genes, Viral ; HIV-1/physiology ; Herpesvirus 4, Human/physiology ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Interleukin-6/chemistry/genetics ; Lymph Nodes/virology ; Lymphoma, B-Cell/virology ; Macrophage Inflammatory Proteins/chemistry/genetics ; Mice ; *Molecular Mimicry ; Molecular Sequence Data ; Receptors, CCR5 ; Receptors, Cytokine/metabolism ; Receptors, HIV/metabolism ; Sarcoma, Kaposi/virology ; Sequence Alignment ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured ; Viral Nonstructural Proteins/chemistry/*genetics/physiology ; Virus Replication
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Survival of cholinergic forebrain neurons in developing p75NGFR-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-06
    Beschreibung: The functions of the low-affinity p75 nerve growth factor receptor (p75(NGFR)) in the central nervous system were explored in vivo. In normal mice, approximately 25 percent of the cholinergic basal forebrain neurons did not express TrkA and died between postnatal day 6 and 15. This loss did not occur in p75(NGFR)-deficient mice or in normal mice systemically injected with a p75(NGFR)-inhibiting peptide. Control, but not p75(NGFR)-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75(NGFR) mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75(NGFR) can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van der Zee, C E -- Ross, G M -- Riopelle, R J -- Hagg, T -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1729-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Tupper Building, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. thagg@is.dal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939868" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; Cell Survival ; Choline O-Acetyltransferase/metabolism ; DNA Fragmentation ; Interneurons/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neostriatum/cytology ; Neurons/*cytology/enzymology ; Oligopeptides/pharmacology ; Parasympathetic Nervous System/*cytology ; Phosphorylation ; Prosencephalon/*cytology ; Proto-Oncogene Proteins/metabolism ; Purkinje Cells/cytology ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/deficiency/metabolism/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-11-29
    Beschreibung: Transporter-facilitated uptake of serotonin (5-hydroxytryptamine or 5-HT) has been implicated in anxiety in humans and animal models and is the site of action of widely used uptake-inhibiting antidepressant and antianxiety drugs. Human 5-HT transporter (5-HTT) gene transcription is modulated by a common polymorphism in its upstream regulatory region. The short variant of the polymorphism reduces the transcriptional efficiency of the 5-HTT gene promoter, resulting in decreased 5-HTT expression and 5-HT uptake in lymphoblasts. Association studies in two independent samples totaling 505 individuals revealed that the 5-HTT polymorphism accounts for 3 to 4 percent of total variation and 7 to 9 percent of inherited variance in anxiety-related personality traits in individuals as well as sibships.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lesch, K P -- Bengel, D -- Heils, A -- Sabol, S Z -- Greenberg, B D -- Petri, S -- Benjamin, J -- Muller, C R -- Hamer, D H -- Murphy, D L -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1527-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Wurzburg, Fuchsleinstrasse 15, 97080 Wurzburg, Germany. kplesch@rzbox.uni-wuerzburg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8929413" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Alleles ; Anxiety Disorders/*genetics ; Carrier Proteins/*genetics ; Cell Line ; Female ; Genetic Markers ; Genotype ; Humans ; Male ; Membrane Glycoproteins/*genetics ; *Membrane Transport Proteins ; Middle Aged ; *Nerve Tissue Proteins ; Neurotic Disorders/*genetics ; Nuclear Family ; Personality Tests ; Phenotype ; *Polymorphism, Genetic ; *Promoter Regions, Genetic ; Serotonin/*metabolism ; Serotonin Plasma Membrane Transport Proteins ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Sequence similarity between the 73-kilodalton protein of mammalian CPSF and a subunit of yeast polyadenylation factor I (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-11-29
    Beschreibung: The 3' ends of most eukaryotic messenger RNAs are generated by endonucleolytic cleavage and polyadenylation. In mammals, the cleavage and polyadenylation specificity factor (CPSF) plays a central role in both steps of the processing reaction. Here, the cloning of the 73-kilodalton subunit of CPSF is reported. Sequence analyses revealed that a yeast protein (Ysh1) was highly similar to the 73-kD polypeptide. Ysh1 constitutes a new subunit of polyadenylation factor I (PFI), which has a role in yeast pre-mRNA 3'-end formation. This finding was unexpected because in contrast to CPSF, PFI is only required for the polyadenylation reaction. These results contribute to the understanding of how 3'-end processing factors may have evolved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jenny, A -- Minvielle-Sebastia, L -- Preker, P J -- Keller, W -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1514-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Biozentrum, University of Basel, CH-4056 Basel, Switzerland. Keller2@ubaclu.unibas.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8929409" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; Evolution, Molecular ; Fungal Proteins/*chemistry/genetics/metabolism ; Humans ; Molecular Sequence Data ; Molecular Weight ; Poly A/metabolism ; Polynucleotide Adenylyltransferase/metabolism ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; RNA, Fungal/metabolism ; RNA, Messenger/metabolism ; RNA-Binding Proteins/*chemistry/genetics/metabolism ; Sequence Homology, Amino Acid ; mRNA Cleavage and Polyadenylation Factors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    RAC regulation of actin polymerization and proliferation by a pathway distinct from Jun kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-11-22
    Beschreibung: The RAC guanine nucleotide binding proteins regulate multiple biological activities, including actin polymerization, activation of the Jun kinase (JNK) cascade, and cell proliferation. RAC effector loop mutants were identified that separate the ability of RAC to interact with different downstream effectors. One mutant of activated human RAC protein, RACV12H40 (with valine and histidine substituted at position 12 and 40, respectively), was defective in binding to PAK3, a Ste20-related p21-activated kinase (PAK), but bound to POR1, a RAC-binding protein. This mutant failed to stimulate PAK and JNK activity but still induced membrane ruffling and mediated transformation. A second mutant, RACV12L37 (with leucine substituted at position 37), which bound PAK but not POR1, induced JNK activation but was defective in inducing membrane ruffling and transformation. These results indicate that the effects of RAC on the JNK cascade and on actin polymerization and cell proliferation are mediated by distinct effector pathways that diverge at the level of RAC itself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- McDonough, M -- Bar-Sagi, D -- Van Aelst, L -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1374-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910277" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Actins/*metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; *Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism/*physiology ; Humans ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Mutagenesis ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Transfection ; p21-Activated Kinases ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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