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  • Artikel  (114)
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  • 11
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    Requirement of serine phosphorylation for formation of STAT-promoter complexes (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-03-31
    Beschreibung: Members of the interleukin-6 family of cytokines bind to and activate receptors that contain a common subunit, gp130. This leads to the activation of Stat3 and Stat1, two cytoplasmic signal transducers and activators of transcription (STATs), by tyrosine phosphorylation. Serine phosphorylation of Stat3 was constitutive and was enhanced by signaling through gp130. In cells of lymphoid and neuronal origins, inhibition of serine phosphorylation prevented the formation of complexes of DNA with Stat3-Stat3 but not with Stat3-Stat1 or Stat1-Stat1 dimers. In vitro serine dephosphorylation of Stat3 also inhibited DNA binding of Stat3-Stat3. The requirement of serine phosphorylation for Stat3-Stat3.DNA complex formation was inversely correlated with the affinity of Stat3-Stat3 for the binding site. Thus, serine phosphorylation appears to enhance or to be required for the formation of stable Stat3-Stat3.DNA complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, X -- Blenis, J -- Li, H C -- Schindler, C -- Chen-Kiang, S -- CA46595/CA/NCI NIH HHS/ -- HL 21006/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 31;267(5206):1990-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brookdale Center for Molecular Biology, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701321" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cell Nucleus/metabolism ; Ciliary Neurotrophic Factor ; Cytoplasm/metabolism ; DNA/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Interleukin-6/metabolism/*pharmacology ; Isoquinolines/pharmacology ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/pharmacology ; Phosphorylation ; Piperazines/pharmacology ; *Promoter Regions, Genetic ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Serine/*metabolism ; Signal Transduction ; Threonine/metabolism ; Trans-Activators/*metabolism ; Tumor Cells, Cultured ; Tyrosine/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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  • 12
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    An STS-based map of the human genome (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-12-22
    Beschreibung: A physical map has been constructed of the human genome containing 15,086 sequence-tagged sites (STSs), with an average spacing of 199 kilobases. The project involved assembly of a radiation hybrid map of the human genome containing 6193 loci and incorporated a genetic linkage map of the human genome containing 5264 loci. This information was combined with the results of STS-content screening of 10,850 loci against a yeast artificial chromosome library to produce an integrated map, anchored by the radiation hybrid and genetic maps. The map provides radiation hybrid coverage of 99 percent and physical coverage of 94 percent of the human genome. The map also represents an early step in an international project to generate a transcript map of the human genome, with more than 3235 expressed sequences localized. The STSs in the map provide a scaffold for initiating large-scale sequencing of the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hudson, T J -- Stein, L D -- Gerety, S S -- Ma, J -- Castle, A B -- Silva, J -- Slonim, D K -- Baptista, R -- Kruglyak, L -- Xu, S H -- Hu, X -- Colbert, A M -- Rosenberg, C -- Reeve-Daly, M P -- Rozen, S -- Hui, L -- Wu, X -- Vestergaard, C -- Wilson, K M -- Bae, J S -- Maitra, S -- Ganiatsas, S -- Evans, C A -- DeAngelis, M M -- Ingalls, K A -- Nahf, R W -- Horton, L T Jr -- Anderson, M O -- Collymore, A J -- Ye, W -- Kouyoumjian, V -- Zemsteva, I S -- Tam, J -- Devine, R -- Courtney, D F -- Renaud, M T -- Nguyen, H -- O'Connor, T J -- Fizames, C -- Faure, S -- Gyapay, G -- Dib, C -- Morissette, J -- Orlin, J B -- Birren, B W -- Goodman, N -- Weissenbach, J -- Hawkins, T L -- Foote, S -- Page, D C -- Lander, E S -- HG00017/HG/NHGRI NIH HHS/ -- HG00098/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1995 Dec 22;270(5244):1945-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead-MIT Center for Genome Research, Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8533086" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; *Chromosome Mapping ; Chromosomes, Artificial, Yeast ; Databases, Factual ; Gene Expression ; Genetic Markers ; *Genome, Human ; *Human Genome Project ; Humans ; Hybrid Cells ; Polymerase Chain Reaction ; *Sequence Analysis, DNA ; *Sequence Tagged Sites
    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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  • 13
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    A region of adenylyl cyclase 2 critical for regulation by G protein beta gamma subunits (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-05-26
    Beschreibung: Receptor-mediated activation of heterotrimeric guanine nucleotide-binding proteins (G proteins) results in the dissociation of alpha from beta gamma subunits, thereby allowing both to regulate effectors. Little is known about the regions of effectors required for recognition of G beta gamma. A peptide encoding residues 956 to 982 of adenylyl cyclase 2 specifically blocked G beta gamma stimulation of adenylyl cyclase 2, phospholipase C-beta 3, potassium channels, and beta-adrenergic receptor kinase as well as inhibition of calmodulin-stimulated adenylyl cyclases, but had no effect on interactions between G beta gamma and G alpha o. Substitutions in this peptide identified a functionally important motif, Gln-X-X-Glu-Arg, that is also conserved in regions of potassium channels and beta-adrenergic receptor kinases that participate in G beta gamma interactions. Thus, the region defined by residues 956 to 982 of adenylyl cyclase 2 may contain determinants important for receiving signals from G beta gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- DeVivo, M -- Dingus, J -- Harry, A -- Li, J -- Sui, J -- Carty, D J -- Blank, J L -- Exton, J H -- Stoffel, R H -- CA-44998/CA/NCI NIH HHS/ -- DK-37219/DK/NIDDK NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 May 26;268(5214):1166-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Mount Sinai School of Medicine, City University of New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761832" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/*chemistry/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Enzyme Activation/physiology ; GTP-Binding Proteins/chemistry/*physiology ; Guanosine Triphosphate/physiology ; In Vitro Techniques ; Molecular Sequence Data ; Peptide Fragments/chemical synthesis/chemistry/physiology ; Potassium Channels/physiology ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/physiology ; Structure-Activity Relationship ; 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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  • 14
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    TRAF2-mediated activation of NF-kappa B by TNF receptor 2 and CD40 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-09-08
    Beschreibung: TNF receptor-associated factor (TRAF) proteins are candidate signal transducers that associate with the cytoplasmic domains of members of the tumor necrosis factor (TNF) receptor superfamily. The role of TRAFs in the TNF-R2 and CD40 signal transduction pathways, which result in the activation of transcription factor NF-kappa B, was investigated. Overexpression of TRAF2, but not TRAF1 or TRAF3, was sufficient to induce NF-kappa B activation. A truncated derivative of TRAF2 lacking an amino-terminal RING finger domain was a dominant-negative inhibitor of NF-kappa B activation mediated by TNF-R2 and CD40. Thus, TRAF2 is a common mediator of TNF-R2 and CD40 signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothe, M -- Sarma, V -- Dixit, V M -- Goeddel, D V -- CA64803/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 8;269(5229):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Department, Tularik, Inc., South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7544915" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD/*metabolism ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; Cell Line ; Gene Expression Regulation ; Genes, Reporter ; Mice ; NF-kappa B/*metabolism ; Proteins/*metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; T-Lymphocytes/metabolism ; TNF Receptor-Associated Factor 2 ; 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)
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  • 15
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    Aberrant subcellular localization of BRCA1 in breast cancer (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-11-03
    Beschreibung: The BRCA1 gene product was identified as a 220-kilodalton nuclear phosphoprotein in normal cells, including breast ductal epithelial cells, and in 18 of 20 tumor cell lines derived from tissues other than breast and ovary. In 16 of 17 breast and ovarian cancer lines and 17 of 17 samples of cells obtained from malignant effusions, however, BRCA1 localized mainly in cytoplasm. Absence of BRCA1 or aberrant subcellular location was also observed to a variable extent in histological sections of many breast cancer biopsies. These findings suggest that BRCA1 abnormalities may be involved in the pathogenesis of many breast cancers, sporadic as well as familial.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Y -- Chen, C F -- Riley, D J -- Allred, D C -- Chen, P L -- Von Hoff, D -- Osborne, C K -- Lee, W H -- CA58318/CA/NCI NIH HHS/ -- EY05758/EY/NEI NIH HHS/ -- P50CA58183/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 3;270(5237):789-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine/Institute of Biotechnology, University of Texas Health Science Center at San Antonio 78245, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481765" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; BRCA1 Protein ; Base Sequence ; Breast/*chemistry ; Breast Neoplasms/*chemistry/ultrastructure ; Cell Fractionation ; Cell Line ; Cell Nucleus/chemistry ; Cytoplasm/*chemistry ; Female ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Neoplasm Proteins/*analysis/genetics/metabolism ; Neoplasms/chemistry/ultrastructure ; Ovarian Neoplasms/chemistry/ultrastructure ; Pleural Effusion, Malignant/chemistry/pathology ; Transcription Factors/*analysis/genetics/metabolism ; 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)
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  • 16
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    CFTR as a cAMP-dependent regulator of sodium channels (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-08-11
    Beschreibung: Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3',5'-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Expression of complementary DNAs for rat epithelial Na+ channel (rENaC) alone in Madin Darby canine kidney (MDCK) epithelial cells generated large amiloride-sensitive sodium currents that were stimulated by cAMP, whereas coexpression of human CFTR with rENaC generated smaller basal sodium currents that were inhibited by cAMP. Parallel studies that measured regulation of sodium permeability in fibroblasts showed similar results. In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stutts, M J -- Canessa, C M -- Olsen, J C -- Hamrick, M -- Cohn, J A -- Rossier, B C -- Boucher, R C -- CFF R026/PHS HHS/ -- HL 34322/HL/NHLBI NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 11;269(5225):847-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill 27599-7020, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7543698" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Absorption ; Amiloride/pharmacology ; Animals ; Cell Line ; Cell Membrane Permeability ; Chloride Channels/metabolism ; Cyclic AMP/*metabolism ; Cystic Fibrosis/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA, Complementary ; Dogs ; Humans ; Membrane Proteins/*metabolism ; Mice ; Patch-Clamp Techniques ; Rats ; Sodium/metabolism ; Sodium Channels/*metabolism ; 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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  • 17
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    Glutamate receptor RNA editing in vitro by enzymatic conversion of adenosine to inosine (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-03-10
    Beschreibung: RNA encoding the B subunit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of ionotropic glutamate receptor (GluR-B) undergoes a posttranscriptional modification in which a genomically encoded adenosine is represented as a guanosine in the GluR-B complementary DNA. In vitro editing of GluR-B RNA transcripts with HeLa cell nuclear extracts was found to result from an activity that converts adenosine to inosine in regions of double-stranded RNA by enzymatic base modification. This activity is consistent with that of a double-stranded RNA-specific adenosine deaminase previously described in Xenopus oocytes and widely distributed in mammalian tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rueter, S M -- Burns, C M -- Coode, S A -- Mookherjee, P -- Emeson, R B -- ES00267/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232-6600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7878468" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine/*metabolism ; Animals ; Base Sequence ; Cell Line ; Codon ; Exons ; HeLa Cells ; Humans ; Inosine/*metabolism ; Inosine Monophosphate/metabolism ; Mice ; Molecular Sequence Data ; *RNA Editing ; RNA Precursors/metabolism ; RNA, Double-Stranded/metabolism ; Rats ; Receptors, AMPA/*genetics ; Repetitive Sequences, Nucleic Acid ; 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)
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  • 18
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    Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-11-17
    Beschreibung: A member of the inwardly rectifying potassium channel family was cloned here. The channel, called BIR (Kir6.2), was expressed in large amounts in rat pancreatic islets and glucose-responsive insulin-secreting cell lines. Coexpression with the sulfonylurea receptor SUR reconstituted an inwardly rectifying potassium conductance of 76 picosiemens that was sensitive to adenosine triphosphate (ATP) (IKATP) and was inhibited by sulfonylureas and activated by diazoxide. The data indicate that these pancreatic beta cell potassium channels are a complex composed of at least two subunits--BIR, a member of the inward rectifier potassium channel family, and SUR, a member of the ATP-binding cassette superfamily. Gene mapping data show that these two potassium channel subunit genes are clustered on human chromosome 11 at position 11p15.1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inagaki, N -- Gonoi, T -- Clement, J P 4th -- Namba, N -- Inazawa, J -- Gonzalez, G -- Aguilar-Bryan, L -- Seino, S -- Bryan, J -- DK44311/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1166-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Chiba University School of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502040" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *ATP-Binding Cassette Transporters ; Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Cloning, Molecular ; Cricetinae ; Diazoxide/pharmacology ; Humans ; Islets of Langerhans/metabolism ; KATP Channels ; Mice ; Molecular Sequence Data ; Potassium/*metabolism ; Potassium Channels/*chemistry/genetics/*metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Drug/*chemistry/metabolism ; Rubidium/metabolism ; Sulfonylurea Compounds/pharmacology ; Sulfonylurea Receptors
    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)
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  • 19
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    FGF binding and FGF receptor activation by synthetic heparan-derived di- and trisaccharides (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-04-21
    Beschreibung: Fibroblast growth factors (FGFs) require a polysaccharide cofactor, heparin or heparan sulfate (HS), for receptor binding and activation. To probe the molecular mechanism by which heparin or HS (heparin/HS) activates FGF, small nonsulfated oligosaccharides found within heparin/HS were assayed for activity. These synthetic and isomerically pure compounds can activate the FGF signaling pathway. The crystal structures of complexes between FGF and these heparin/HS oligosaccharides reveal several binding sites on FGF and constrain possible mechanisms by which heparin/HS can activate the FGF receptor. These studies establish a framework for the molecular design of compounds capable of modulating FGF activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ornitz, D M -- Herr, A B -- Nilsson, M -- Westman, J -- Svahn, C M -- Waksman, G -- CA60673/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 21;268(5209):432-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University Medical School, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7536345" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Binding Sites ; Carbohydrate Sequence ; Cell Line ; Crystallization ; Fibroblast Growth Factor 1/chemistry/*metabolism ; Fibroblast Growth Factor 2/*metabolism ; Heparin/metabolism/*pharmacology ; Heparitin Sulfate/chemistry/*pharmacology ; Mitogens/pharmacology ; Molecular Sequence Data ; Oligosaccharides/chemistry/metabolism/*pharmacology ; Receptors, Fibroblast Growth Factor/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
    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)
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  • 20
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    Inhibition of myogenic differentiation in proliferating myoblasts by cyclin D1-dependent kinase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-02-17
    Beschreibung: Although the myogenic regulator MyoD is expressed in proliferating myoblasts, differentiation of these cells is limited to the G0 phase of the cell cycle. Forced expression of cyclin D1, but not cyclins A, B, or E, inhibited the ability of MyoD to transactivate muscle-specific genes and correlated with phosphorylation of MyoD. Transfection of myoblasts with cyclin-dependent kinase (Cdk) inhibitors p21 and p16 augmented muscle-specific gene expression in cells maintained in high concentrations of serum, suggesting that an active cyclin-Cdk complex suppresses MyoD function in proliferating cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skapek, S X -- Rhee, J -- Spicer, D B -- Lassar, A B -- 1F32AR08214-01A1/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 17;267(5200):1022-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7863328" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Carrier Proteins/biosynthesis/physiology ; Cell Cycle ; Cell Differentiation ; Cell Line ; Cyclin D1 ; Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/*metabolism ; Cyclins/biosynthesis/*physiology ; Enzyme Activation ; Mice ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/*antagonists & inhibitors/metabolism ; Oncogene Proteins/*physiology ; Phosphorylation ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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