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  • 1
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    Requirement for Tec kinases Rlk and Itk in T cell receptor signaling and immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: T cell receptor (TCR) signaling requires activation of Zap-70 and Src family tyrosine kinases, but requirements for other tyrosine kinases are less clear. Combined deletion in mice of two Tec kinases, Rlk and Itk, caused marked defects in TCR responses including proliferation, cytokine production, and apoptosis in vitro and adaptive immune responses to Toxoplasma gondii in vivo. Molecular events immediately downstream from the TCR were intact in rlk-/-itk-/- cells, but intermediate events including inositol trisphosphate production, calcium mobilization, and mitogen-activated protein kinase activation were impaired, establishing Tec kinases as critical regulators of TCR signaling required for phospholipase C-gamma activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaeffer, E M -- Debnath, J -- Yap, G -- McVicar, D -- Liao, X C -- Littman, D R -- Sher, A -- Varmus, H E -- Lenardo, M J -- Schwartzberg, P L -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Human Genome Research Institute, National Cancer Institute, National Institute for Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CD4-CD8 Ratio ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Diglycerides/metabolism ; Gene Targeting ; Inositol Phosphates/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Isoenzymes/metabolism ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Mice ; Mutation ; Phospholipase C gamma ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; *Signal Transduction ; T-Lymphocytes/*enzymology/*immunology ; Toxoplasmosis, Animal/immunology ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Essential role of growth hormone in ischemia-induced retinal neovascularization (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mice expressing a GH antagonist gene and in normal mice given an inhibitor of GH secretion (MK678). Retinal neovascularization was inhibited in these mice in inverse proportion to serum levels of GH and a downstream effector, insulin-like growth factor-I (IGF-I). Inhibition was reversed with exogenous IGF-I administration. GH inhibition did not diminish hypoxia-stimulated retinal vascular endothelial growth factor (VEGF) or VEGF receptor expression. These data suggest that systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, L E -- Kopchick, J J -- Chen, W -- Knapp, J -- Kinose, F -- Daley, D -- Foley, E -- Smith, R G -- Schaeffer, J M -- EY08670/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology, Harvard Medical School and Children's Hospital, Boston, MA 02115, USA. smith_lo@a1.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelial Growth Factors/genetics/metabolism ; Growth Hormone/agonists/antagonists & inhibitors/blood/pharmacology/*physiology ; Hormone Antagonists/pharmacology ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Ischemia ; Lymphokines/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Peptides, Cyclic/pharmacology ; Recombinant Proteins/pharmacology ; Retinal Neovascularization/*etiology/metabolism/pathology ; Retinal Vessels ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    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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  • 3
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    Rapid identification of subtype-selective agonists of the somatostatin receptor through combinatorial chemistry (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Nonpeptide agonists of each of the five somatostatin receptors were identified in combinatorial libraries constructed on the basis of molecular modeling of known peptide agonists. In vitro experiments using these selective compounds demonstrated the role of the somatostatin subtype-2 receptor in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 receptor as a mediator of insulin secretion from pancreatic beta cells. Both receptors regulated growth hormone release from the rat anterior pituitary gland. The availability of high-affinity, subtype-selective agonists for each of the somatostatin receptors provides a direct approach to defining their physiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohrer, S P -- Birzin, E T -- Mosley, R T -- Berk, S C -- Hutchins, S M -- Shen, D M -- Xiong, Y -- Hayes, E C -- Parmar, R M -- Foor, F -- Mitra, S W -- Degrado, S J -- Shu, M -- Klopp, J M -- Cai, S J -- Blake, A -- Chan, W W -- Pasternak, A -- Yang, L -- Patchett, A A -- Smith, R G -- Chapman, K T -- Schaeffer, J M -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biochemistry and Physiology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA. susanvrohrer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784130" target="_blank"〉PubMed〈/a〉
    Keywords: Amides/metabolism/*pharmacology ; Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Cricetinae ; Drug Design ; Glucagon/secretion ; Growth Hormone/secretion ; Insulin/secretion ; Islets of Langerhans/drug effects/secretion ; Ligands ; Membrane Proteins ; Mice ; Models, Chemical ; Molecular Sequence Data ; Pituitary Gland, Anterior/drug effects/metabolism ; Rats ; Receptors, Somatostatin/*agonists/physiology
    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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