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  • Articles  (224)
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  • 1995-1999  (224)
  • 1996  (224)
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  • Articles  (224)
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  • 2020-2023
  • 2000-2004
  • 1995-1999  (224)
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  • 1
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    Intestinal secretory defects and dwarfism in mice lacking cGMP-dependent protein kinase II (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Cyclic guanosine 3',5'-monophosphate (cGMP)-dependent protein kinases (cGKs) mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was caused by a severe defect in endochondral ossification at the growth plates. These results indicate that cGKII plays a central role in diverse physiological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeifer, A -- Aszodi, A -- Seidler, U -- Ruth, P -- Hofmann, F -- Fassler, R -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2082-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut f-ur Pharmakologie und Toxikologie, Technische Universitat Munchen, Biedersteiner Strasse 29, D-80802 M-unchen, Germany. pfeifer@ipt.med.tu-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953039" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Bacterial Toxins/toxicity ; Body Water/secretion ; *Bone Development ; Crosses, Genetic ; Cyclic GMP/analogs & derivatives/metabolism/pharmacology ; Cyclic GMP-Dependent Protein Kinases/deficiency/genetics/*metabolism ; Diarrhea/physiopathology ; Dwarfism/*enzymology/genetics/pathology ; Enterotoxins/toxicity ; Escherichia coli Proteins ; Female ; Gene Deletion ; Growth Plate/enzymology/pathology ; Intestinal Mucosa/*secretion ; Male ; Mice ; Mice, Inbred C57BL ; Osteogenesis ; Signal Transduction
    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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    Complexities in the treatment of autoimmune disease (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McFarland, H F -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2037-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroimmunology Branch, National Institutes of Health, Bethesda, MD 20892, USA. henrymcf@helix.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Autoimmune Diseases/immunology/*therapy ; CD8-Positive T-Lymphocytes/*immunology ; Callithrix ; Cytokines/*immunology ; Diabetes Mellitus, Type 1/immunology/therapy ; Encephalomyelitis, Autoimmune, Experimental/immunology/therapy ; Humans ; Immune Tolerance ; Immunotherapy/*adverse effects ; Mice ; Myelin Proteins ; Myelin-Associated Glycoprotein/immunology ; Myelin-Oligodendrocyte Glycoprotein ; Ovalbumin/immunology ; Th1 Cells/*immunology ; Th2 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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  • 3
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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
    Publication Date: 1996-12-20
    Description: 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〉
    Keywords: 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
    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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    Reexpression of RAG-1 and RAG-2 genes in activated mature mouse B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Recombination activating genes (RAG-1 and RAG-2), involved in V(D)J rearrangement of immunoglobulin genes, have been thought to be expressed only in immature stages of B-cell development. However, RAG-1 and RAG-2 transcripts were found to be reexpressed in mature mouse B cells after culture with interleukin-4 in association with several different co-stimuli. Reexpression was also detected in draining lymph nodes from immunized mice. RAG-1 and RAG-2 proteins could be detected by immunofluorescence microscopy in the nuclei of B cells cultured in vitro and in the germinal centers of draining lymph nodes. These findings suggest that RAG gene products play a heretofore unsuspected role in mature B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hikida, M -- Mori, M -- Takai, T -- Tomochika, K -- Hamatani, K -- Ohmori, H -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2092-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biotechnology, Faculty of Engineering, Okayama University, Tsushima-Naka, Okayama 700, Japan. hit2224@cc.okayama-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; *Gene Expression ; *Genes, RAG-1 ; Germinal Center/metabolism ; *Homeodomain Proteins ; Immunoglobulin Class Switching ; Interleukin-4/pharmacology ; Interleukins/pharmacology ; Lipopolysaccharides/pharmacology ; Lymph Nodes/metabolism ; *Lymphocyte Activation ; Mice ; Mice, Inbred C3H ; Microscopy, Fluorescence ; Protein Biosynthesis ; Proteins/*genetics
    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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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 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〉
    Keywords: 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
    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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    Ironing out the wrinkles in the prion strain problem (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grady, D -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Creutzfeldt-Jakob Syndrome/metabolism ; Humans ; Mice ; Mice, Transgenic ; Prion Diseases/*etiology/metabolism/transmission ; Prions/*chemistry/genetics ; *Protein Conformation ; *Protein Folding
    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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    Control of EGF receptor signaling by clathrin-mediated endocytosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 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〉
    Keywords: *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
    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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    Genes, junctions, and disease at cell biology meeting (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2008-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8984657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/etiology ; Chromosomes, Human, Pair 21 ; Connexins/genetics/*physiology ; Down Syndrome/*genetics ; Female ; Gap Junctions/*physiology ; Gene Dosage ; Heart Defects, Congenital/etiology ; Humans ; Infertility, Female/etiology ; Mice ; Protein Kinases/*genetics/metabolism ; *Protein-Serine-Threonine Kinases ; *Protein-Tyrosine Kinases
    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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    Evidence for the conformation of the pathologic isoform of the prion protein enciphering and propagating prion diversity (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The fundamental event in prion diseases seems to be a conformational change in cellular prion protein (PrPC) whereby it is converted into the pathologic isoform PrPSc. In fatal familial insomnia (FFI), the protease-resistant fragment of PrPSc after deglycosylation has a size of 19 kilodaltons, whereas that from other inherited and sporadic prion diseases is 21 kilodaltons. Extracts from the brains of FFI patients transmitted disease to transgenic mice expressing a chimeric human-mouse PrP gene about 200 days after inoculation and induced formation of the 19-kilodalton PrPSc fragment, whereas extracts from the brains of familial and sporadic Creutzfeldt-Jakob disease patients produced the 21-kilodalton PrPSc fragment in these mice. The results presented indicate that the conformation of PrPSc functions as a template in directing the formation of nascent PrPSc and suggest a mechanism to explain strains of prions where diversity is encrypted in the conformation of PrPSc.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Telling, G C -- Parchi, P -- DeArmond, S J -- Cortelli, P -- Montagna, P -- Gabizon, R -- Mastrianni, J -- Lugaresi, E -- Gambetti, P -- Prusiner, S B -- NS07219/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2079-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*pathology ; *Brain Chemistry ; Creutzfeldt-Jakob Syndrome/metabolism/pathology ; Humans ; Mice ; Mice, Transgenic ; PrPSc Proteins/analysis/*chemistry ; Prion Diseases/*etiology/metabolism/pathology/transmission ; Prions/*chemistry ; *Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary
    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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    Neoteny in lymphocytes: Rag1 and Rag2 expression in germinal center B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The products of the Rag1 and Rag2 genes drive genomic V(D)J rearrangements that assemble functional immunoglobulin and T cell antigen receptor genes. Expression of the Rag genes has been thought to be limited to developmentally immature lymphocyte populations that in normal adult animals are primarily restricted to the bone marrow and thymus. Abundant RAG1 and RAG2 protein and messenger RNA was detected in the activated B cells that populate murine splenic and Peyer's patch germinal centers. Germinal center B cells thus share fundamental characteristics of immature lymphocytes, raising the possibility that antigen-dependent secondary V(D)J rearrangements modify the peripheral antibody repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, S -- Zheng, B -- Schatz, D G -- Spanopoulou, E -- Kelsoe, G -- AG10207/AG/NIA NIH HHS/ -- AI24335/AI/NIAID NIH HHS/ -- AI32524/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2094-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*metabolism ; DNA Nucleotidyltransferases/metabolism ; *DNA-Binding Proteins ; Female ; *Gene Expression ; Gene Rearrangement ; Genes, Immunoglobulin ; *Genes, RAG-1 ; Germinal Center/*cytology/immunology ; *Homeodomain Proteins ; Immunization ; Immunoglobulin Class Switching ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Polymerase Chain Reaction ; Protein Biosynthesis ; Proteins/*genetics ; VDJ Recombinases
    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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