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  • Articles  (128)
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  • American Association for the Advancement of Science (AAAS)  (128)
  • 1995-1999  (67)
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  • 1996  (67)
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  • Articles  (128)
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  • American Association for the Advancement of Science (AAAS)  (128)
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  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; 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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  • 2
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    Toxicology of a PFPE surfactant (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnston, K P -- Randolph, T -- Bright, F -- Howdle, S -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1726.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/drug effects ; Ethers/*toxicity ; Fluorocarbons/*toxicity ; Liver/*drug effects ; Organ Size/drug effects ; Rats ; Surface-Active Agents/*toxicity
    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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    Hippocampal cell death (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cahill, L -- Haigler, H J -- New York, N.Y. -- Science. 1996 May 31;272(5266):1251.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650532" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*pharmacology ; *Aging ; Animals ; Cell Death ; Enkephalin, Methionine/*pharmacology ; Hippocampus/*cytology ; Humans ; Memory ; Pyramidal Cells/cytology/*drug effects/physiology ; Rats
    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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    RAC regulation of actin polymerization and proliferation by a pathway distinct from Jun kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 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〉
    Keywords: 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
    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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    Appetite-suppressing effects of urocortin, a CRF-related neuropeptide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-13
    Description: The neuropeptide corticotropin-releasing factor (CRF) is well known to act on the central nervous system in ways that mimic stress and result in decreases in exploration, increases in sympathetic activity, decreases in parasympathetic outflow, and decreases in appetitive behavior. Urocortin, a neuropeptide related to CRF, binds with high affinity to the CRF2 receptor, is more potent than CRF in suppressing appetite, but is less potent than CRF in producing anxiety-like effects and activation. Doses as low as 10 nanograms injected intracerebroventricularly were effective in decreasing food intake in food-deprived and free-feeding rats. These results suggest that urocortin may be an endogenous CRF-like factor in the brain responsible for the effects of stress on appetite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spina, M -- Merlo-Pich, E -- Chan, R K -- Basso, A M -- Rivier, J -- Vale, W -- Koob, G F -- 1 F05 TW05262/TW/FIC NIH HHS/ -- DK 26741/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Sep 13;273(5281):1561-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropharmacology, Scripps Research Institute, 10666 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/8703220" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite/*drug effects ; Appetite Depressants/administration & dosage/metabolism/*pharmacology ; Behavior, Animal/drug effects ; Blood Pressure/drug effects ; Carrier Proteins/metabolism ; Corticotropin-Releasing Hormone/administration & dosage/metabolism/*pharmacology ; Dose-Response Relationship, Drug ; Eating/drug effects ; Fasting ; Injections, Intraventricular ; Motor Activity/drug effects ; Rats ; Rats, Wistar ; Receptors, Corticotropin-Releasing Hormone/metabolism ; Urocortins ; Urotensins/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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  • 6
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    Stimulation of membrane ruffling and MAP kinase activation by distinct effectors of RAS (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: The RAS guanine nucleotide binding proteins activate multiple signaling events that regulate cell growth and differentiation. In quiescent fibroblasts, ectopic expression of activated H-RAS (H-RASV12, where V12 indicates valine-12) induces membrane ruffling, mitogen-activated protein (MAP) kinase activation, and stimulation of DNA synthesis. A mutant of activated H-RAS, H-RASV12C40 (where C40 indicates cysteine-40), was identified that was defective for MAP kinase activation and stimulation of DNA synthesis, but retained the ability to induce membrane ruffling. Another mutant of activated H-RAS, H-RASV12S35 (where S35 indicates serine-35), which activates MAP kinase, was defective for stimulation of membrane ruffling and induction of DNA synthesis. Expression of both mutants resulted in a stimulation of DNA synthesis that was comparable to that induced by H-RASV12. These results indicate that membrane ruffling and activation of MAP kinase represent distinct RAS effector pathways and that input from both pathways is required for the mitogenic activity of RAS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- White, M A -- Wigler, M H -- Bar-Sagi, D -- CA 55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division ; Cell Line ; Cell Membrane/*ultrastructure ; DNA/biosynthesis ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism ; Microinjections ; Mutation ; Plasmids ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Signal Transduction ; rac GTP-Binding Proteins ; ras Proteins/genetics/*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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  • 7
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    Coupling of the RAS-MAPK pathway to gene activation by RSK2, a growth factor-regulated CREB kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: A signaling pathway has been elucidated whereby growth factors activate the transcription factor cyclic adenosine monophosphate response element-binding protein (CREB), a critical regulator of immediate early gene transcription. Growth factor-stimulated CREB phosphorylation at serine-133 is mediated by the RAS-mitogen-activated protein kinase (MAPK) pathway. MAPK activates CREB kinase, which in turn phosphorylates and activates CREB. Purification, sequencing, and biochemical characterization of CREB kinase revealed that it is identical to a member of the pp90(RSK) family, RSK2. RSK2 was shown to mediate growth factor induction of CREB serine-133 phosphorylation both in vitro and in vivo. These findings identify a cellular function for RSK2 and define a mechanism whereby growth factor signals mediated by RAS and MAPK are transmitted to the nucleus to activate gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xing, J -- Ginty, D D -- Greenberg, M E -- CA43855/CA/NCI NIH HHS/ -- NS34814-01/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):959-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688081" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Epidermal Growth Factor/pharmacology ; *Gene Expression Regulation ; Growth Substances/*pharmacology ; Humans ; Molecular Sequence Data ; Nerve Growth Factors/pharmacology ; PC12 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Rats ; Ribosomal Protein S6 Kinases ; *Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; ras Proteins/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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  • 8
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    G protein-mediated neuronal DNA fragmentation induced by familial Alzheimer's disease-associated mutants of APP (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: Missense mutations in the 695-amino acid form of the amyloid precursor protein (APP695) cosegregate with disease phenotype in families with dominantly inherited Alzheimer's disease. These mutations convert valine at position 642 to isoleucine, phenylalanine, or glycine. Expression of these mutant proteins, but not of normal APP695, was shown to induce nucleosomal DNA fragmentation in neuronal cells. Induction of DNA fragmentation required the cytoplasmic domain of the mutants and appeared to be mediated by heterotrimeric guanosine triphosphate-binding proteins (G proteins).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamatsuji, T -- Matsui, T -- Okamoto, T -- Komatsuzaki, K -- Takeda, S -- Fukumoto, H -- Iwatsubo, T -- Suzuki, N -- Asami-Odaka, A -- Ireland, S -- Kinane, T B -- Giambarella, U -- Nishimoto, I -- New York, N.Y. -- Science. 1996 May 31;272(5266):1349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650548" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/chemistry/genetics/*physiology ; Animals ; Apoptosis ; Base Sequence ; Culture Media, Conditioned ; DNA/*metabolism ; GTP-Binding Proteins/*physiology ; Humans ; Hybrid Cells ; Mice ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Mutation ; Neurons/cytology/*metabolism ; Nucleosomes/*metabolism ; Peptide Fragments/metabolism ; Rats ; Transfection
    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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  • 9
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    Short-term plasticity of a thalamocortical pathway dynamically modulated by behavioral state (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-12
    Description: The neocortex receives information about the environment and the rest of the brain through pathways from the thalamus. These pathways have frequency-dependent properties that can strongly influence their effect on the neocortex. In 1943 Morison and Dempsey described "augmenting responses," a form of short-term plasticity in some thalamocortical pathways that is triggered by 8- to 15-hertz activation. Results from anesthetized rats showed that the augmenting response is initiated by pyramidal cells in layer V. The augmenting response was also observed in awake, unrestrained animals and was found to be dynamically modulated by their behavioral state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castro-Alamancos, M A -- Connors, B W -- MH19118/MH/NIMH NIH HHS/ -- NS25983/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):274-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Brown University, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/*physiology ; Electric Stimulation ; Motor Cortex/physiology ; Neural Pathways ; *Neuronal Plasticity ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Synapses/physiology ; Thalamic Nuclei/*physiology
    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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  • 10
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    Selective activation of NF-kappa B by nerve growth factor through the neurotrophin receptor p75 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) selectively bind to distinct members of the Trk family of tyrosine kinase receptors, but all three bind with similar affinities to the neurotrophin receptor p75 (p75NTR). The biological significance of neurotrophin binding to p75NTR in cells that also express Trk receptors has been difficult to ascertain. In the absence of TrkA, NGF binding to p75NGR activated the transcription factor nuclear factor kappa B (NF-kappa B) in rat Schwann cells. This activation was not observed in Schwann cells isolated from mice that lacked p75NTR. The effect was selective for NGF; NF-kappa B was not activated by BDNF or NT-3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, B D -- Kaltschmidt, C -- Kaltschmidt, B -- Offenhauser, N -- Bohm-Matthaei, R -- Baeuerle, P A -- Barde, Y A -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):542-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiochemistry, Max-Planck Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614802" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/metabolism ; L Cells (Cell Line) ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Nerve Growth Factors/*metabolism/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Neurotrophin 3 ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Schwann Cells/*metabolism ; Signal Transduction/*physiology
    Print ISSN: 0036-8075
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  • 11
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    Structural evidence for functional domains in the rat hippocampus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: The hippocampus has two major outputs: multisynaptic pathways to the cerebral cortex and a massive descending projection directly to the lateral septal part of the basal ganglia. Here it is shown that the descending output is organized in such a way that different hippocampal regions map in an orderly way onto hypothalamic systems mediating the expression of different classes of goal-oriented behavior. This mapping is characterized by a unidirectional hippocampo-lateral septal projection and then by bidirectional lateral septo-hypothalamic projections, all topographically organized. The connectional evidence predicts that information processing in different regions of the hippocampus selectively influences the expression of different classes of behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Risold, P Y -- Swanson, L W -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1484-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neural, Informational, and Behavioral Sciences, University of Southern California, Los Angeles 90089-2520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Behavior, Animal ; *Brain Mapping ; Enkephalins/analysis ; Glutamate Decarboxylase/analysis ; Hippocampus/*anatomy & histology/*physiology ; Hypothalamus/anatomy & histology/physiology ; In Situ Hybridization ; Memory/physiology ; Neural Pathways ; Neuropeptides/analysis ; Pyramidal Cells/cytology/physiology ; Rats ; Septal Nuclei/*anatomy & histology/*physiology ; Somatostatin/analysis ; gamma-Aminobutyric Acid/analysis
    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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  • 12
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    New data help toxicologists home in on assessing risks (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/*etiology ; Carcinogens/*toxicity ; Glutathione/metabolism ; Humans ; Immune System/drug effects ; Methylene Chloride/metabolism/*toxicity ; Mice ; Nitrogen Dioxide/*toxicity ; Rats
    Print ISSN: 0036-8075
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  • 13
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    Diabetes complications: why is glucose potentially toxic? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porte, D Jr -- Schwartz, M W -- New York, N.Y. -- Science. 1996 May 3;272(5262):699-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Department of Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614830" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Diabetes Complications ; Diabetes Mellitus/enzymology ; Diabetes Mellitus, Experimental/complications/enzymology ; Endothelium, Vascular/enzymology ; Enzyme Inhibitors/*pharmacology/toxicity ; Humans ; Hyperglycemia/*complications/enzymology ; Isoenzymes/*antagonists & inhibitors/metabolism ; Kidney/enzymology ; Muscle, Smooth, Vascular/enzymology ; Protein Kinase C/*antagonists & inhibitors/metabolism ; Protein Kinase C beta ; Rats ; Regional Blood Flow/drug effects ; Retina/enzymology ; Retinal Vessels/physiology
    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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  • 14
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    Hippocampal cell death (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landfield, P W -- McEwan, B S -- Sapolsky, R M -- Meaney, M J -- New York, N.Y. -- Science. 1996 May 31;272(5266):1249-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650531" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Count ; Cell Death ; Hippocampus/*cytology ; Humans ; Memory Disorders/etiology ; Neurons/*cytology ; Rats
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  • 15
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    Is hippocampal cell death a myth? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1229-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638100" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Count ; Cell Death ; Hippocampus/*cytology ; Humans ; Memory Disorders/*etiology ; Neurons/*cytology ; Pyramidal Cells/*cytology ; Rats
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  • 16
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    Entorhinal-hippocampal interactions revealed by real-time imaging (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: The entorhinal cortex provides the major cortical input to the hippocampus, and both structures have been implicated in memory processes. The dynamics of neuronal circuits in the entorhinal-hippocampal system were studied in slices by optical imaging with high spatial and temporal resolution. Reverberation of neural activity was detected in the entorhinal cortex and was more prominent when the inhibition due to gamma-aminobutyric acid was slightly suppressed. Neural activity was transferred in a frequency-dependent way from the entorhinal cortex to the hippocampus. The entorhinal neuronal circuit could contribute to memory processes by holding information and selectively gating the entry of information into the hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iijima, T -- Witter, M P -- Ichikawa, M -- Tominaga, T -- Kajiwara, R -- Matsumoto, G -- New York, N.Y. -- Science. 1996 May 24;272(5265):1176-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cellular Neuroscience Section, Electrotechnical Laboratory, Ibaraki, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Electric Stimulation ; Entorhinal Cortex/*physiology ; GABA Antagonists/pharmacology ; Hippocampus/*physiology ; Image Processing, Computer-Assisted ; In Vitro Techniques ; Male ; Memory/*physiology ; Microscopy, Fluorescence ; Neural Pathways ; Rats ; Rats, Wistar ; Synaptic Transmission/drug effects
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  • 17
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    PIN: an associated protein inhibitor of neuronal nitric oxide synthase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: The neurotransmitter functions of nitric oxide are dependent on dynamic regulation of its biosynthetic enzyme, neuronal nitric oxide synthase (nNOS). By means of a yeast two-hybrid screen, a 10-kilodalton protein was identified that physically interacts with and inhibits the activity of nNOS. This inhibitor, designated PIN, appears to be one of the most conserved proteins in nature, showing 92 percent amino acid identity with the nematode and rat homologs. Binding of PIN destabilizes the nNOS dimer, a conformation necessary for activity. These results suggest that PIN may regulate numerous biological processes through its effects on nitric oxide synthase activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaffrey, S R -- Snyder, S H -- DA00074/DA/NIDA NIH HHS/ -- GM-07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864115" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism/pharmacology ; Cell Line ; Cyclic GMP/metabolism ; Dimerization ; *Drosophila Proteins ; Dyneins ; Enzyme Inhibitors/chemistry/*metabolism/pharmacology ; Humans ; Molecular Sequence Data ; Molecular Weight ; Neurons/enzymology ; Nitric Oxide Synthase/*antagonists & inhibitors/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism/pharmacology ; Saccharomyces cerevisiae ; Transfection
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  • 18
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    Direct observation of protein solvation and discrete disorder with experimental crystallographic phases (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-05
    Description: A complete and accurate set of experimental crystallographic phases to a resolution of 1.8 angstroms was obtained for a 230-residue dimeric fragment of rat mannose-binding protein A with the use of multiwavelength anomalous dispersion (MAD) phasing. An accurate image of the crystal structure could thus be obtained without resort to phases calculated from a model. Partially reduced disulfide bonds, local disorder, and differences in the mobility of chemically equivalent molecules are apparent in the experimental electron density map. A solvation layer is visible that includes well-ordered sites of hydration around polar and charged protein atoms, as well as diffuse, partially disordered solvent shells around exposed hydrophobic groups. Because the experimental phases and the resulting electron density map are free from the influence of a model, they provide a stringent test of theoretical models of macromolecular solvation, motion, and conformational heterogeneity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burling, F T -- Weis, W I -- Flaherty, K M -- Brunger, A T -- GM50565/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):72-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*chemistry ; Chemistry, Physical ; Crystallization ; *Crystallography, X-Ray ; Hydrogen Bonding ; Mannose/*metabolism ; *Mannose-Binding Lectin ; Models, Molecular ; Molecular Sequence Data ; Physicochemical Phenomena ; *Protein Conformation ; Rats ; Solvents ; Water
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  • 19
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    Activation of estrogen receptors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joffe, M -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1285-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Synergism ; Estradiol/metabolism ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Humans ; Insecticides/metabolism/*pharmacology ; Polychlorinated Biphenyls/metabolism/*pharmacology ; Rats ; Receptors, Estrogen/drug effects/*metabolism
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  • 20
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    Presynaptic calcium current modulation by a metabotropic glutamate receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-25
    Description: Metabotropic glutamate receptors (mGluRs) regulate transmitter release at mammalian central synapses. However, because of the difficulty of recording from mammalian presynaptic terminals, the mechanism underlying mGluR-mediated presynaptic inhibition is not known. Here, simultaneous recordings from a giant presynaptic terminal, the calyx of Held, and its postsynaptic target in the medial nucleus of the trapezoid body were obtained in rat brainstem slices. Agonists of mGluRs suppressed a high voltage-activated P/Q-type calcium conductance in the presynaptic terminal, thereby inhibiting transmitter release at this glutamatergic synapse. Because several forms of presynaptic modulation and plasticity are mediated by mGluRs, this identification of a target ion channel is a first step toward elucidation of their molecular mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, T -- Forsythe, I D -- Tsujimoto, T -- Barnes-Davies, M -- Onodera, K -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1996 Oct 25;274(5287):594-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Tokyo 113, Japan. ttakahas-tky@umin.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8849448" target="_blank"〉PubMed〈/a〉
    Keywords: Aminobutyrates/pharmacology ; Animals ; Brain Stem ; Cadmium/pharmacology ; Calcium/*metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects/*metabolism ; Excitatory Amino Acid Agonists/pharmacology ; In Vitro Techniques ; Neurotransmitter Agents/metabolism ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channels/drug effects/metabolism ; Presynaptic Terminals/*metabolism ; Rats ; Rats, Wistar ; Receptors, Metabotropic Glutamate/agonists/*metabolism ; Synapses/*metabolism ; *Synaptic Transmission
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  • 21
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    Small-conductance, calcium-activated potassium channels from mammalian brain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: Members of a previously unidentified family of potassium channel subunits were cloned from rat and human brain. The messenger RNAs encoding these subunits were widely expressed in brain with distinct yet overlapping patterns, as well as in several peripheral tissues. Expression of the messenger RNAs in Xenopus oocytes resulted in calcium-activated, voltage-independent potassium channels. The channels that formed from the various subunits displayed differential sensitivity to apamin and tubocurare. The distribution, function, and pharmacology of these channels are consistent with the SK class of small-conductance, calcium-activated potassium channels, which contribute to the afterhyperpolarization in central neurons and other cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohler, M -- Hirschberg, B -- Bond, C T -- Kinzie, J M -- Marrion, N V -- Maylie, J -- Adelman, J P -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1709-14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, L-474, Oregon Health Sciences University, 3181 Southwest Sam Jackson Road, Portland, OR 97201, USA. J. Maylie, Department of Obstetrics and Gyne.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antisense Elements (Genetics) ; Apamin/pharmacology ; *Brain Chemistry ; Calcium/*metabolism/pharmacology ; Cloning, Molecular ; Electric Conductivity ; Female ; Humans ; Membrane Potentials ; Molecular Sequence Data ; Neurons/*physiology ; Oocytes ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channel Blockers ; Potassium Channels/analysis/chemistry/*physiology ; *Potassium Channels, Calcium-Activated ; RNA, Messenger/analysis/genetics ; Rats ; Rats, Sprague-Dawley ; Small-Conductance Calcium-Activated Potassium Channels ; Xenopus
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  • 22
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    Activation of Pyk2 by stress signals and coupling with JNK signaling pathway (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: The c-Jun amino-terminal kinase (JNK) is activated by various heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors, inflammatory cytokines, and stress signals. Yet, upstream mediators that link extracellular signals with the JNK signaling pathway are currently unknown. The tyrosine kinase Pyk2 was activated by tumor necrosis factor alpha, by ultraviolet irradiation, and by changes in osmolarity. Overexpression of Pyk2 led to activation of JNK, and a dominant-negative mutant of Pyk2 interfered with ultraviolet light- or osmotic shock-induced activation of JNK. Pyk2 represents a cell type-specific, stress-sensitive mediator of the JNK signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tokiwa, G -- Dikic, I -- Lev, S -- Schlessinger, J -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):792-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, New York University Medical Center, 550 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Egtazic Acid/pharmacology ; Enzyme Activation ; Focal Adhesion Kinase 2 ; GTP Phosphohydrolases/metabolism ; GTP-Binding Proteins/metabolism ; HL-60 Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *Mitogen-Activated Protein Kinases ; Osmolar Concentration ; PC12 Cells ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Rats ; *Signal Transduction ; Sorbitol/pharmacology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; Ultraviolet Rays
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  • 23
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    Stable expression of mosaic coats of variant surface glycoproteins in Trypanosoma brucei (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: The paradigm of antigenic variation in parasites is the variant surface glycoprotein (VSG) of African trypanosomes. Only one VSG is expressed at any time, except for short periods during switching. The reasons for this pattern of expression and the consequences of expressing more than one VSG are unknown. Trypanosoma brucei was genetically manipulated to generate cell lines that expressed two VSGs simultaneously. These VSGs were produced in equal amounts and were homogeneously distributed on the trypanosome surface. The double-expressor cells had similar population doubling times and were as infective as wild-type cells. Thus, the simultaneous expression of two VSGs is not intrinsically harmful.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Munoz-Jordan, J L -- Davies, K P -- Cross, G A -- AI 21531/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Parasitology, Rockefeller University, New York 10012, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigenic Variation ; Cell Membrane/chemistry ; Gentamicins/pharmacology ; Parasitemia ; Protein Synthesis Inhibitors/pharmacology ; Rats ; Transfection ; Trypanosoma brucei brucei/genetics/growth & ; development/immunology/*metabolism/pathogenicity ; Trypanosomiasis, African/parasitology ; Variant Surface Glycoproteins, Trypanosoma/analysis/*biosynthesis/genetics
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  • 24
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    The cerebellum: movement coordinator or much more? (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):482-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614794" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebellum/*physiology ; Cognition/*physiology ; Humans ; Motor Activity/*physiology ; Movement/physiology ; Perception/physiology ; Psychomotor Performance/physiology ; Rats
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  • 25
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    Researchers nail down leptin receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):913.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/biosynthesis/chemistry/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Diabetes Mellitus/*genetics ; Humans ; Leptin ; Mice ; Mutation ; Obesity/*genetics ; Proteins/genetics ; RNA, Messenger/genetics ; Rats ; *Receptors, Cell Surface ; Receptors, Cytokine/biosynthesis/chemistry/*genetics ; Receptors, Leptin
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  • 26
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    Exposure to methylene chloride (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, W C 3rd -- New York, N.Y. -- Science. 1996 Oct 18;274(5286):327.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8927983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Carcinogens/*toxicity ; Humans ; Methylene Chloride/*toxicity ; Mice ; Neoplasms/*chemically induced ; Rats
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  • 27
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    Role of GTP hydrolysis in fission of caveolae directly from plasma membranes (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: Caveolae are specialized invaginated cell surface microdomains of undefined function. A cell-free system that reconstituted fission of caveolae from lung endothelial plasma membranes was developed. Addition of cytosol and the hydrolysis of guanosine triphosphate (GTP) induced caveolar fission. The budded caveolae were isolated as vesicles rich in caveolin and the sialoglycolipid GM1 but not glycosyl-phosphatidylinositol (GPI)-anchored proteins. These vesicles contained the molecular machinery for endocytosis and transcytosis. In permeabilized endothelial cells, GTP stimulated, whereas GTPgammaS prevented, caveolar budding and endocytosis of the cholera toxin B chain to endosomes. Thus, caveolae may bud to form discrete carrier vesicles that participate in membrane trafficking.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnitzer, J E -- Oh, P -- McIntosh, D P -- HL43278/HL/NHLBI NIH HHS/ -- HL52766/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Beth Israel Hospital, Boston, MA 02215, USA. jschnitz@bih.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824187" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cattle ; Caveolin 1 ; *Caveolins ; Cell Membrane/chemistry/*metabolism/ultrastructure ; Cell-Free System ; Centrifugation, Density Gradient ; Cholera Toxin/metabolism ; Endocytosis ; Endothelium, Vascular/cytology/metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Triphosphate/*metabolism/pharmacology ; Hydrolysis ; Membrane Proteins/analysis/metabolism ; Rats
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  • 28
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    A K+ channel worthy of attention (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-09-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hille, B -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington, Seattle, 98195-7290, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8830412" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Attention/*physiology ; Calcium/*metabolism ; Cloning, Molecular ; Cyclic AMP/metabolism ; Humans ; Norepinephrine/metabolism ; Phosphorylation ; Potassium Channels/metabolism/*physiology ; *Potassium Channels, Calcium-Activated ; Rats ; Small-Conductance Calcium-Activated Potassium Channels
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  • 29
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    A role for brassinosteroids in light-dependent development of Arabidopsis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-19
    Description: Although steroid hormones are important for animal development, the physiological role of plant steroids is unknown. The Arabidopsis DET2 gene encodes a protein that shares significant sequence identity with mammalian steroid 5 alpha-reductases. A mutation of glutamate 204, which is absolutely required for the activity of human steroid reductase, abolishes the in vivo activity of DET2 and leads to defects in light-regulated development that can be ameliorated by application of a plant steroid, brassinolide. Thus, DET2 may encode a reductase in the brassinolide biosynthetic pathway, and brassinosteroids may constitute a distinct class of phytohormones with an important role in light-regulated development of higher plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, J -- Nagpal, P -- Vitart, V -- McMorris, T C -- Chory, J -- New York, N.Y. -- Science. 1996 Apr 19;272(5260):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602526" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Oxo-5-alpha-Steroid 4-Dehydrogenase/chemistry ; Amino Acid Sequence ; Animals ; Arabidopsis/genetics/*growth & development/metabolism ; *Arabidopsis Proteins ; Brassinosteroids ; Cholestanols/*metabolism/pharmacology ; Chromosome Mapping ; *Genes, Plant ; Humans ; Light ; Molecular Sequence Data ; Mutation ; Oxidation-Reduction ; Phenotype ; Plant Growth Regulators/biosynthesis/*metabolism ; Plant Proteins/*genetics ; Rats ; Sequence Alignment ; Signal Transduction ; Steroids, Heterocyclic/*metabolism/pharmacology
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    A receptor in pituitary and hypothalamus that functions in growth hormone release (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: Small synthetic molecules termed growth hormone secretagogues (GHSs) act on the pituitary gland and the hypothalamus to stimulate and amplify pulsatile growth hormone (GH) release. A heterotrimeric GTP-binding protein (G protein)-coupled receptor (GPC-R) of the pituitary and arcuate ventro-medial and infundibular hypothalamus of swine and humans was cloned and was shown to be the target of the GHSs. On the basis of its pharmacological and molecular characterization, this GPC-R defines a neuroendocrine pathway for the control of pulsatile GH release and supports the notion that the GHSs mimic an undiscovered hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howard, A D -- Feighner, S D -- Cully, D F -- Arena, J P -- Liberator, P A -- Rosenblum, C I -- Hamelin, M -- Hreniuk, D L -- Palyha, O C -- Anderson, J -- Paress, P S -- Diaz, C -- Chou, M -- Liu, K K -- McKee, K K -- Pong, S S -- Chaung, L Y -- Elbrecht, A -- Dashkevicz, M -- Heavens, R -- Rigby, M -- Sirinathsinghji, D J -- Dean, D C -- Melillo, D G -- Patchett, A A -- Nargund, R -- Griffin, P R -- DeMartino, J A -- Gupta, S K -- Schaeffer, J M -- Smith, R G -- Van der Ploeg, L H -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688086" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; DNA, Complementary/genetics ; GTP-Binding Proteins/metabolism ; Growth Hormone/*secretion ; Hormones/*metabolism ; Humans ; Hypothalamus, Middle/chemistry ; Indoles/*metabolism/pharmacology ; Macaca mulatta ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Pituitary Gland/chemistry ; RNA, Complementary/genetics ; Rats ; Receptors, Cell Surface/analysis/chemistry/genetics/*metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Ghrelin ; Spiro Compounds/*metabolism/pharmacology ; Swine
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  • 31
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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
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  • 32
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    Methylene chloride (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huff, J -- Bucher, J -- Barrett, J C -- New York, N.Y. -- Science. 1996 May 24;272(5265):1083-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; Carcinogens/*toxicity ; Female ; Humans ; Liver Neoplasms, Experimental/chemically induced ; Lung Neoplasms/chemically induced ; Male ; Methylene Chloride/*toxicity ; Mice ; Mutagens/*toxicity ; Neoplasms/*chemically induced ; Rats
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  • 33
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    Altered reactivity of superoxide dismutase in familial amyotrophic lateral sclerosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: A subset of individuals with familial amyotrophic lateral sclerosis (FALS) possesses dominantly inherited mutations in the gene that encodes copper-zinc superoxide dismutase (CuZnSOD). A4V and G93A, two of the mutant enzymes associated with FALS, were shown to catalyze the oxidation of a model substrate (spin trap 5,5'-dimethyl-1-pyrroline N-oxide) by hydrogen peroxide at a higher rate than that seen with the wild-type enzyme. Catalysis of this reaction by A4V and G93A was more sensitive to inhibition by the copper chelators diethyldithiocarbamate and penicillamine than was catalysis by wild-type CuZnSOD. The same two chelators reversed the apoptosis-inducing effect of mutant enzymes expressed in a neural cell line. These results suggest that oxidative reactions catalyzed by mutant CuZnSOD enzymes initiate the neuropathologic changes in FALS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wiedau-Pazos, M -- Goto, J J -- Rabizadeh, S -- Gralla, E B -- Roe, J A -- Lee, M K -- Valentine, J S -- Bredesen, D E -- AG12282/AG/NIA NIH HHS/ -- DK46828/DK/NIDDK NIH HHS/ -- GM28222/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Los Angeles 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560268" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics ; Animals ; Apoptosis/drug effects ; Binding Sites ; Catalysis ; Cell Line ; Chelating Agents/pharmacology ; Copper/metabolism ; Cyclic N-Oxides/metabolism ; Ditiocarb/pharmacology ; Humans ; Hydrogen Peroxide/metabolism ; Mutation ; Oxidation-Reduction ; Penicillamine/pharmacology ; Rats ; Superoxide Dismutase/genetics/*metabolism
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  • 34
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    Amelioration of vascular dysfunctions in diabetic rats by an oral PKC beta inhibitor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: The vascular complications of diabetes mellitus have been correlated with enhanced activation of protein kinase C (PKC). LY333531, a specific inhibitor of the beta isoform of PKC, was synthesized and was shown to be a competitive reversible inhibitor of PKC beta 1 and beta 2, with a half-maximal inhibitory constant of approximately 5 nM; this value was one-fiftieth of that for other PKC isoenzymes and one-thousandth of that for non-PKC kinases. When administered orally, LY333531 ameliorated the glomerular filtration rate, albumin excretion rate, and retinal circulation in diabetic rats in a dose-responsive manner, in parallel with its inhibition of PKC activities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishii, H -- Jirousek, M R -- Koya, D -- Takagi, C -- Xia, P -- Clermont, A -- Bursell, S E -- Kern, T S -- Ballas, L M -- Heath, W F -- Stramm, L E -- Feener, E P -- King, G L -- DK36836/DK/NIDDK NIH HHS/ -- EY05110-11/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1996 May 3;272(5262):728-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Division, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614835" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Albuminuria/prevention & control ; Animals ; Diabetes Mellitus, Experimental/*complications/enzymology/physiopathology ; Diabetic Angiopathies/enzymology/etiology/*prevention & control ; Diglycerides/metabolism ; Dose-Response Relationship, Drug ; Enzyme Activation ; Enzyme Inhibitors/chemistry/*pharmacology ; Glomerular Filtration Rate/drug effects ; Humans ; Indoles/administration & dosage/chemistry/*pharmacology ; Isoenzymes/*antagonists & inhibitors/metabolism ; Kidney Glomerulus/metabolism ; Male ; Maleimides/administration & dosage/chemistry/*pharmacology ; Muscle, Smooth, Vascular/enzymology ; Phosphorylation/drug effects ; Protein Kinase C/*antagonists & inhibitors/metabolism ; Protein Kinase C beta ; Rats ; Rats, Sprague-Dawley ; Regional Blood Flow/drug effects ; Renal Plasma Flow/drug effects ; Retina/metabolism ; Retinal Vessels/physiopathology ; Substrate Specificity
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    New experiments underscore warnings on maternal drinking (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Braun, S -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):738-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8701322" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Drinking/*adverse effects ; Animals ; Brain/drug effects/*embryology ; Ethanol/administration & dosage/*pharmacology ; Female ; Fetal Alcohol Spectrum Disorders/etiology ; Fetus/drug effects ; Humans ; Leukocyte L1 Antigen Complex ; Long-Term Potentiation/*drug effects ; Membrane Glycoproteins/metabolism ; Neurons/drug effects ; *Pregnancy ; Prenatal Exposure Delayed Effects ; Rats
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  • 36
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    Opposite modulation of cocaine-seeking behavior by D1- and D2-like dopamine receptor agonists (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-15
    Description: Activation of the mesolimbic dopamine system is known to trigger relapse in animal models of cocaine-seeking behavior. We found that this "priming" effect was selectively induced by D2-like, and not by D1-like, dopamine receptor agonists in rats. Moreover, D1-like receptor agonists prevented cocaine-seeking behavior induced by cocaine itself, whereas D2-like receptor agonists enhanced this behavior. These results demonstrate an important dissociation between D1- and D2-like receptor processes in cocaine-seeking behavior and support further evaluation of D1-like receptor agonists as a possible pharmacotherapy for cocaine addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Self, D W -- Barnhart, W J -- Lehman, D A -- Nestler, E J -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1586-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Psychiatry, Department of Psychiatry, Yale University School of Medicine, Connecticut Mental Health Center, New Haven, 06508, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Addictive/*etiology ; Behavior, Animal/drug effects ; Benzazepines/pharmacology ; Caffeine/pharmacology ; *Cocaine/administration & dosage ; Dopamine Agonists/*pharmacology ; Ergolines/pharmacology ; Male ; Motor Activity/drug effects ; Quinpirole ; Rats ; Rats, Sprague-Dawley ; Receptors, Dopamine D1/agonists/*physiology ; Receptors, Dopamine D2/agonists/*physiology ; Recurrence ; Reinforcement (Psychology) ; Substance-Related Disorders/*etiology ; Tetrahydronaphthalenes/pharmacology
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  • 37
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    Bidirectional control of quantal size by synaptic activity in the hippocampus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long-term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size. At a single set of synapses, the increase in quantal size seen with long-term potentiation was completely reversed by depotentiating stimuli. Long-term potentiation and depression are also associated with an increase and decrease, respectively, in the frequency of quantal events, consistent with an all-or-none regulation (up or down) of clusters of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, a change in the release of transmitter, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliet, S H -- Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Electric Stimulation ; Evoked Potentials ; Guinea Pigs ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/*physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Strontium/pharmacology ; Synapses/*physiology ; *Synaptic Transmission
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  • 38
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    Zinc-induced collapse of augmented inhibition by GABA in a temporal lobe epilepsy model (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-01-19
    Description: In the kindling model of temporal lobe epilepsy, several physiological indicators of inhibition by gamma-aminobutyric acid (GABA) in the hippocampal dentate gyrus are consistent with an augmented, rather than a diminished, inhibition. In brain slices obtained from epileptic (kindled) rats, the excitatory drive onto inhibitory interneurons was increased and was paralleled by a reduction in the presynaptic autoinhibition of GABA release. This augmented inhibition was sensitive to zinc most likely after a molecular reorganization of GABAA receptor subunits. Consequently, during seizures, inhibition by GABA may be diminished by the zinc released from aberrantly sprouted mossy fiber terminals of granule cells, which are found in many experimental models of epilepsy and in human temporal lobe epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buhl, E H -- Otis, T S -- Mody, I -- NS 12151/NS/NINDS NIH HHS/ -- NS 30549/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Anatomical Neuropharmacology Unit, Oxford University, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553076" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Chlorides/pharmacology ; Dentate Gyrus/drug effects/*physiology ; Epilepsy, Temporal Lobe/*physiopathology ; Excitatory Amino Acid Antagonists/pharmacology ; GABA-A Receptor Antagonists ; Humans ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; Kindling, Neurologic/*physiology ; Male ; Neural Inhibition/drug effects ; Pyridines/pharmacology ; Rats ; Rats, Wistar ; Receptors, GABA-A/physiology ; Receptors, GABA-B/physiology ; Synaptic Transmission/drug effects ; Zinc/metabolism/*pharmacology ; Zinc Compounds/pharmacology ; gamma-Aminobutyric Acid/*metabolism
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    Hemoglobin reveals new role as blood pressure regulator (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glanz, J -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1670.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/*physiology ; Cysteine/metabolism ; Hemoglobins/chemistry/*metabolism ; *Mercaptoethanol ; Nitric Oxide/blood/*metabolism ; Nitroso Compounds/metabolism ; Rats ; *S-Nitrosothiols ; Vasoconstriction
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  • 40
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    Angiotensin II-forming activity in a reconstructed ancestral chymase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: The current model of serine protease diversity theorizes that the earliest protease molecules were simple digestive enzymes that gained complex regulatory functions and restricted substrate specificities through evolution. Among the chymase group of serine proteases are enzymes that convert angiotensin I to angiotensin II, as well as others that simply degrade angiotensins. An ancestral chymase reconstructed with the use of phylogenetic inference, total gene synthesis, and protein expression had efficient and specific angiotensin II-forming activity (turnover number, about 700 per second). Thus, angiotensin II-forming activity is the more primitive state for chymases, and the loss of such activity occurred later in the evolution of some of these serine proteases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrasekharan, U M -- Sanker, S -- Glynias, M J -- Karnik, S S -- Husain, A -- HL33713/HL/NHLBI NIH HHS/ -- HL44201/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):502-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cardiology, Cleveland Clinic Foundation, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560264" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiotensin I/*metabolism ; Angiotensin II/*metabolism ; Angiotensins/metabolism ; Animals ; Binding Sites ; Chymases ; Evolution, Molecular ; Genes, Synthetic ; Humans ; Molecular Sequence Data ; Rats ; Serine Endopeptidases/chemistry/genetics/*metabolism ; Substrate Specificity
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  • 41
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    Increase in single L-type calcium channels in hippocampal neurons during aging (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-17
    Description: Voltage-activated calcium (Ca2+) influx is increased in mammalian CA1 hippocampal neurons during aging. However, the molecular basis for this elevation is not known. The partially dissociated hippocampal ("zipper") slice preparation was used to analyze single Ca2+ channel activity in CA1 neurons of adult and aged rats. Total L-type Ca2+ channel activity in patches was found to increase with aging, primarily because of an increase in the density of functional channels. Learning in aged animals was inversely correlated with channel density. This increase in functional Ca2+ channels with aging could underlie the vulnerability of neurons to age-associated neurodegenerative conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibault, O -- Landfield, P W -- AG04542/AG/NIA NIH HHS/ -- AG10836/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, College of Medicine, University of Kentucky, Lexington 40536-0084, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638124" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Hippocampus/*cytology/*metabolism ; In Vitro Techniques ; Male ; Maze Learning ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/*metabolism ; Rats ; Rats, Inbred F344
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  • 42
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    The advent of menopause (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knobil, E -- Yen, S S -- New York, N.Y. -- Science. 1996 Oct 4;274(5284):18-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8848714" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Female ; Gonadotropin-Releasing Hormone/secretion ; Humans ; Hypothalamus/*physiology ; Luteinizing Hormone/secretion ; Menopause/*physiology ; Ovary/*physiology ; Rats
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  • 43
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    Hippocampal cell death (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaidel, D W -- Esiri, M M -- New York, N.Y. -- Science. 1996 May 31;272(5266):1249.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650530" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Count ; Cell Death ; Hippocampus/*cytology ; Humans ; *Memory ; Neurons/*cytology ; Rats
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    "Replay" of hippocampal "memories" (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, G P -- Rosenberg, J R -- Hary, D -- Breeze, P -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1216-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966590" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bias (Epidemiology) ; Hippocampus/*physiology ; Memory/*physiology ; Motor Activity ; Rats ; Sleep/*physiology ; Time Factors
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  • 45
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    A receptor for the selective uptake and degradation of proteins by lysosomes (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: Multiple pathways of protein degradation operate within cells. A selective protein import pathway exists for the uptake and degradation of particular cytosolic proteins by lysosomes. Here, the lysosomal membrane glycoprotein LGP96 was identified as a receptor for the selective import and degradation of proteins within lysosomes. Specific substrates of this proteolytic pathway bound to the cytosolic tail of a 96-kilodalton lysosomal membrane protein in two different binding assays. Overexpression of human LGP96 in Chinese hamster ovary cells increased the activity of the selective lysosomal proteolytic pathway in vivo and in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuervo, A M -- Dice, J F -- AG06116/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):501-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662539" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/chemistry/*metabolism ; CHO Cells ; Cricetinae ; Glyceraldehyde-3-Phosphate Dehydrogenases/*metabolism ; HSC70 Heat-Shock Proteins ; *HSP70 Heat-Shock Proteins ; Heat-Shock Proteins/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lysosomal-Associated Membrane Protein 2 ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*metabolism ; Membrane Glycoproteins/chemistry/*metabolism ; Molecular Sequence Data ; Proteins/*metabolism ; Rats ; Ribonuclease, Pancreatic/*metabolism ; Transfection
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  • 46
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    New view of spinal cord injury (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1466.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/drug effects ; Cycloheximide/pharmacology ; Humans ; Nerve Growth Factors/physiology ; Oligodendroglia/*pathology ; Rats ; Spinal Cord/*pathology ; Spinal Cord Injuries/drug therapy/*pathology
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  • 47
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    The cytolytic P2Z receptor for extracellular ATP identified as a P2X receptor (P2X7) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: The P2Z receptor is responsible for adenosine triphosphate (ATP)-dependent lysis of macrophages through the formation of membrane pores permeable to large molecules. Other ATP-gated channels, the P2X receptors, are permeable only to small cations. Here, an ATP receptor, the P2X7 receptor, was cloned from rat brain and exhibited both these properties. This protein is homologous to other P2X receptors but has a unique carboxyl-terminal domain that was required for the lytic actions of ATP. Thus, the P2X7 (or P2Z) receptor is a bifunctional molecule that could function in both fast synaptic transmission and the ATP-mediated lysis of antigen-presenting cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surprenant, A -- Rassendren, F -- Kawashima, E -- North, R A -- Buell, G -- New York, N.Y. -- Science. 1996 May 3;272(5262):735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Glaxo Institute for Molecular Biology, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614837" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cations, Divalent/pharmacology ; Cell Death ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Electric Conductivity ; Humans ; Ion Channels/physiology ; Mice ; Molecular Sequence Data ; Patch-Clamp Techniques ; Rats ; Receptors, Purinergic P2/chemistry/genetics/*physiology ; Receptors, Purinergic P2X7 ; Transfection
    Print ISSN: 0036-8075
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  • 48
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    Regulation of a neuronal form of focal adhesion kinase by anandamide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: Anandamide is an endogenous ligand for central cannabinoid receptors and is released after neuronal depolarization. Anandamide increased protein tyrosine phosphorylation in rat hippocampal slices and neurons in culture. The action of anandamide resulted from the inhibition of adenylyl cyclase and cyclic adenosine 3', 5'-monophosphate-dependent protein kinase. One of the proteins phosphorylated in response to anandamide was an isoform of pp125-focal adhesion kinase (FAK+) expressed preferentially in neurons. Focal adhesion kinase is a tyrosine kinase involved in the interactions between the integrins and actin-based cytoskeleton. Thus, anandamide may exert neurotrophic effects and play a role in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derkinderen, P -- Toutant, M -- Burgaya, F -- Le Bert, M -- Siciliano, J C -- de Franciscis, V -- Gelman, M -- Girault, J A -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1719-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U 114, Chaire de Neuropharmacologie, College de France, 11 place Marcelin Berthelot, 75231 Paris cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781236" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Arachidonic Acid/pharmacology ; Arachidonic Acids/*pharmacology ; Cell Adhesion Molecules/*metabolism ; Cell Line ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Endocannabinoids ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Hippocampus/drug effects/*enzymology ; In Vitro Techniques ; Molecular Sequence Data ; Neuronal Plasticity/drug effects ; Neurons/drug effects/*enzymology ; Phosphorylation ; Phosphotyrosine/metabolism ; Polyunsaturated Alkamides ; Prosencephalon ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/metabolism
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    In vivo gene delivery and stable transduction of nondividing cells by a lentiviral vector (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-04-12
    Description: A retroviral vector system based on the human immunodeficiency virus (HIV) was developed that, in contrast to a murine leukemia virus-based counterpart, transduced heterologous sequences into HeLa cells and rat fibroblasts blocked in the cell cycle, as well as into human primary macrophages. Additionally, the HIV vector could mediate stable in vivo gene transfer into terminally differentiated neurons. The ability of HIV-based viral vectors to deliver genes in vivo into nondividing cells could increase the applicability of retroviral vectors in human gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naldini, L -- Blomer, U -- Gallay, P -- Ory, D -- Mulligan, R -- Gage, F H -- Verma, I M -- Trono, D -- AG08514/AG/NIA NIH HHS/ -- AG10435/AG/NIA NIH HHS/ -- AI37510/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Apr 12;272(5259):263-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8602510" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/cytology/virology ; Cell Division ; Cells, Cultured ; Female ; *Gene Transfer Techniques ; Genetic Therapy ; *Genetic Vectors ; HIV/*genetics/physiology ; HeLa Cells ; Humans ; Macrophages/cytology/virology ; Molecular Sequence Data ; Neurons/cytology/virology ; Plasmids ; Rats ; Transfection ; Virus Integration
    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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  • 50
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    Rat study sheds light on cocaine craving (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C -- New York, N.Y. -- Science. 1996 Mar 15;271(5255):1499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Addictive/*etiology ; *Cocaine ; Dopamine Agonists/*pharmacology ; Rats ; Receptors, Dopamine D1/agonists/*physiology ; Receptors, Dopamine D2/agonists/*physiology ; Substance-Related Disorders/*etiology
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  • 51
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    An RNA polymerase II elongation factor encoded by the human ELL gene (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: The human ELL gene on chromosome 19 undergoes frequent translocations with the trithorax-like MLL gene on chromosome 11 in acute myeloid leukemias. Here, ELL was shown to encode a previously uncharacterized elongation factor that can increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by polymerase at multiple sites along the DNA. Functionally, ELL resembles Elongin (SIII), a transcription elongation factor regulated by the product of the von Hippel-Lindau (VHL) tumor suppressor gene. The discovery of a second elongation factor implicated in oncogenesis provides further support for a close connection between the regulation of transcription elongation and cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shilatifard, A -- Lane, W S -- Jackson, K W -- Conaway, R C -- Conaway, J W -- GM41628/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1873-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City, 73104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596958" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Genes, Tumor Suppressor ; Histone-Lysine N-Methyltransferase ; Humans ; Leukemia/genetics ; Molecular Sequence Data ; Myeloid-Lymphoid Leukemia Protein ; *Neoplasm Proteins ; *Peptide Elongation Factors ; *Proto-Oncogenes ; RNA Polymerase II/*metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Recombinant Proteins/metabolism ; Transcription Factors/chemistry/*genetics/metabolism ; Transcription, Genetic ; Transcriptional Elongation Factors ; Translocation, Genetic ; von Hippel-Lindau Disease/genetics
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  • 52
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    Replay of neuronal firing sequences in rat hippocampus during sleep following spatial experience (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: The correlated activity of rat hippocampal pyramidal cells during sleep reflects the activity of those cells during earlier spatial exploration. Now the patterns of activity during sleep have also been found to reflect the order in which the cells fired during spatial exploration. This relation was reliably stronger for sleep after the behavioral session than before it; thus, the activity during sleep reflects changes produced by experience. This memory for temporal order of neuronal firing could be produced by an interaction between the temporal integration properties of long-term potentiation and the phase shifting of spike activity with respect to the hippocampal theta rhythm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skaggs, W E -- McNaughton, B L -- AG12609/AG/NIA NIH HHS/ -- MH46823/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1870-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arizona Research Laboratories, Division of Neural Systems, Memory and Aging, University of Arizona, Tucson, 85724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596957" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Long-Term Potentiation/*physiology ; Male ; Memory/*physiology ; Motor Activity ; Pyramidal Cells/*physiology ; Rats ; Rats, Inbred F344 ; Sleep/*physiology ; Theta Rhythm ; Time Factors
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  • 53
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    Patch-clamp detection of neurotransmitters in capillary electrophoresis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: Gamma-aminobutyrate acid, L-glutamate, and N-methyl-D-aspartate were separated by capillary electrophoresis and detected by the use of whole-cell and outside-out patch-clamp techniques on freshly dissociated rat olfactory interneurons. These neuroactive compounds could be identified from their electrophoretic migration times, unitary channel conductances, and power spectra that yielded corner frequencies and mean single-channel conductances characteristic for each of the different agonist-receptor interactions. This technique has the sensitivity to observe the opening of a single ion channel for agonists separated by capillary electrophoresis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orwar, O -- Jardemark, K -- Jacobson, I -- Moscho, A -- Fishman, H A -- Scheller, R H -- Zare, R N -- DA 09873-01/DA/NIDA NIH HHS/ -- MH 45423-06/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosensing Techniques ; Electrophoresis, Capillary ; Glutamic Acid/*analysis/isolation & purification ; Interneurons/*chemistry ; Ion Channels/physiology ; N-Methylaspartate/*analysis/isolation & purification ; Olfactory Bulb/cytology ; Patch-Clamp Techniques ; Rats ; Receptors, GABA/physiology ; Receptors, Glutamate/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Sensitivity and Specificity ; gamma-Aminobutyric Acid/*analysis/isolation & purification
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 54
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    Direct measurement of coupling between dendritic spines and shafts (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-03
    Description: Characterization of the diffusional and electrotonic coupling of spines to the dendritic shaft is crucial to understanding neuronal integration and synaptic plasticity. Two-photon photobleaching and photorelease of fluorescein dextran were used to generate concentration gradients between spines and shafts in rat CA1 pyramidal neurons. Diffusional reequilibration was monitored with two-photon fluorescence imaging. The time course of reequilibration was exponential, with time constants in the range of 20 to 100 milliseconds, demonstrating chemical compartmentalization on such time scales. These values imply that electrical spine neck resistances are unlikely to exceed 150 megohms and more likely range from 4 to 50 megohms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svoboda, K -- Tank, D W -- Denk, W -- New York, N.Y. -- Science. 1996 May 3;272(5262):716-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Computation Research Department, Bell Laboratories, Lucent Technologies, Murray Hill, NJ 07974, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendrites/metabolism/*physiology/ultrastructure ; Dextrans/metabolism ; Diffusion ; Electric Conductivity ; Electric Impedance ; Fluoresceins/metabolism ; Fluorescence ; In Vitro Techniques ; Kinetics ; Microscopy/methods ; Models, Neurological ; Neuronal Plasticity ; Pyramidal Cells/metabolism/*physiology/ultrastructure ; Rats
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  • 55
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    Spinal cord regeneration (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, W -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):451.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, New York University Medical Center, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8677439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Fibrin Tissue Adhesive ; Fibroblast Growth Factors/pharmacology ; Hindlimb/physiology ; Locomotion ; *Nerve Regeneration ; Peripheral Nerves/transplantation ; Rats ; Spinal Cord/*physiology ; Spinal Cord Injuries/physiopathology/*surgery ; Tissue Transplantation
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    Immunologic NO synthase: elevation in severe AIDS dementia and induction by HIV-1 gp41 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: Indirect mechanisms are implicated in the pathogenesis of the dementia associated with human immunodeficiency virus-type 1 (HIV-1) infection. Proinflammatory molecules such as tumor necrosis factor alpha and eicosanoids are elevated in the central nervous system of patients with HIV-1-related dementia. Nitric oxide (NO) is a potential mediator of neuronal injury, because cytokines may activate the immunologic (type II) isoform of NO synthase (iNOS). The levels of iNOS in severe HIV-1-associated dementia coincided with increased expression of the HIV-1 coat protein gp41. Furthermore, gp41 induced iNOS in primary cultures of mixed rat neuronal and glial cells and killed neurons through a NO-dependent mechanism. Thus, gp41-induced NO formation may contribute to the severe cognitive dysfunction associated with HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adamson, D C -- Wildemann, B -- Sasaki, M -- Glass, J D -- McArthur, J C -- Christov, V I -- Dawson, T M -- Dawson, V L -- AI35042/AI/NIAID NIH HHS/ -- NS07392/NS/NINDS NIH HHS/ -- NS22643/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1917-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Pathology 2-210, Baltimore, MD 21287, USA. valina.dawson@qmail.bs.jhu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943206" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Dementia Complex/*enzymology/metabolism ; Animals ; Brain/*enzymology/metabolism ; Cell Death ; Cells, Cultured ; Cerebral Cortex/enzymology/metabolism ; Enzyme Induction ; HIV Envelope Protein gp120/metabolism/pharmacology ; HIV Envelope Protein gp41/*metabolism/pharmacology ; *Hiv-1 ; Humans ; Neuroglia/cytology ; Neurons/cytology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/*biosynthesis/genetics ; Polymerase Chain Reaction ; Rats
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    Egr-1-induced endothelial gene expression: a common theme in vascular injury (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: A number of pathophysiologically relevant genes, including platelet-derived growth factor B-chain (PDGF-B), are induced in the vasculature after acute mechanical injury. In rat aorta, the activated expression of these genes was preceded by a marked increase in the amount of the early-growth-response gene product Egr-1 at the endothelial wound edge. Egr-1 interacts with a novel element in the proximal PDGF-B promoter, as well as with consensus elements in the promoters of other genes induced by endothelial injury. This interaction is crucial for injury-induced PDGF-B promoter-dependent expression. Sp1, whose binding site in the PDGF-B promoter overlaps that of Egr-1, occupies this element in unstimulated cells and is displaced by increasing amounts of Egr-1. These findings implicate Egr-1 in the up-regulated expression of PDGF-B and other potent mediators in mechanically injured arterial endothelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khachigian, L M -- Lindner, V -- Williams, A J -- Collins, T -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1427-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Research Division, Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/injuries/metabolism ; Base Sequence ; Binding Sites ; DNA-Binding Proteins/genetics/*metabolism ; Early Growth Response Protein 1 ; Endothelium, Vascular/injuries/*metabolism ; *Gene Expression Regulation ; Genes, Reporter ; Humans ; *Immediate-Early Proteins ; Male ; Molecular Sequence Data ; Platelet-Derived Growth Factor/biosynthesis/*genetics ; *Promoter Regions, Genetic ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/metabolism ; Sp1 Transcription Factor/metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/genetics/*metabolism ; *Zinc Fingers
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    Spinal cord repair in adult paraplegic rats: partial restoration of hind limb function (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: Complete spinal cord gaps in adult rats were bridged with multiple intercostal nerve grafts that redirected specific pathways from white to gray matter. The grafted area was stabilized with fibrin glue containing acidic fibroblast growth factor and by compressive wiring of posterior spinal processes. Hind limb function improved progressively during the first 6 months, as assessed by two scoring systems. The corticospinal tract regenerated through the grafted area to the lumbar enlargement, as did several bulbospinal pathways. These data suggest a possible repair strategy for spinal cord injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, H -- Cao, Y -- Olson, L -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):510-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Female ; Fibrin Tissue Adhesive ; Fibroblast Growth Factor 1/pharmacology ; Hindlimb/*physiology ; Intercostal Nerves/transplantation ; Locomotion ; *Nerve Regeneration ; Neural Pathways/physiology ; Paraplegia/physiopathology/*surgery ; Pyramidal Tracts/physiology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/*physiology ; Spinal Cord Injuries/physiopathology/*surgery ; Tissue Transplantation
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    The role of zinc in selective neuronal death after transient global cerebral ischemia (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: Zinc is present in presynaptic nerve terminals throughout the mammalian central nervous system and likely serves as an endogenous signaling substance. However, excessive exposure to extracellular zinc can damage central neurons. After transient forebrain ischemia in rats, chelatable zinc accumulated specifically in degenerating neurons in the hippocampal hilus and CA1, as well as in the cerebral cortex, thalamus, striatum, and amygdala. This accumulation preceded neurodegeneration, which could be prevented by the intraventricular injection of a zinc chelating agent. The toxic influx of zinc may be a key mechanism underlying selective neuronal death after transient global ischemic insults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Suh, S W -- Gwag, B J -- He, Y Y -- Hsu, C Y -- Choi, D W -- NS30337/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):1013-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638123" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Brain/metabolism/*pathology ; Cell Death ; Chelating Agents/pharmacology ; Dithizone/pharmacology ; Edetic Acid/pharmacology ; Fluorescent Dyes ; Hippocampus/metabolism/pathology ; Ischemic Attack, Transient/*metabolism/*pathology ; Microscopy, Fluorescence ; *Nerve Degeneration ; Neurons/metabolism/*pathology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/metabolism/pathology ; Rats ; Tosyl Compounds ; Zinc/*metabolism
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    A requirement for local protein synthesis in neurotrophin-induced hippocampal synaptic plasticity (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-09-06
    Description: Two neurotrophic factors, brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), are able to produce a long-lasting enhancement of synaptic transmission in the hippocampus. Unlike other forms of plasticity, neurotrophin-induced plasticity exhibited an immediate requirement for protein synthesis. Plasticity in rat hippocampal slices in which the synaptic neuropil was isolated from the principal cell bodies also required early protein synthesis. Thus, the neurotrophins may stimulate the synthesis of proteins in either axonal or dendritic compartments, allowing synapses to exert local control over the complement of proteins expressed at individual synaptic sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, H -- Schuman, E M -- New York, N.Y. -- Science. 1996 Sep 6;273(5280):1402-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703078" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Axons/metabolism ; Brain-Derived Neurotrophic Factor ; Chloramphenicol/pharmacology ; Cycloheximide/pharmacology ; Dendrites/metabolism ; Hippocampus/drug effects/metabolism/*physiology ; In Vitro Techniques ; Male ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/*pharmacology ; *Neuronal Plasticity ; Neurotrophin 3 ; *Protein Biosynthesis ; Protein Synthesis Inhibitors/pharmacology ; Pyramidal Cells/drug effects/metabolism/physiology ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/*drug effects
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    Neuroprotection by aspirin and sodium salicylate through blockade of NF-kappaB activation (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-11-22
    Description: Aspirin (acetylsalicylic acid) is a commonly prescribed drug with a wide pharmacological spectrum. At concentrations compatible with amounts in plasma during chronic anti-inflammatory therapy, acetylsalicylic acid and its metabolite sodium salicylate were found to be protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. The site of action of the drugs appeared to be downstream of glutamate receptors and to involve specific inhibition of glutamate-mediated induction of nuclear factor kappa B. These results may contribute to the emerging theme of anti-inflammatory drugs and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grilli, M -- Pizzi, M -- Memo, M -- Spano, P -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1383-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pharmacology, Department of Biomedical Sciences and Biotechnologies, University of Brescia Medical School, Brescia, I-25123 Italy. mpharm@master.cci.unibs.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Calcium/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology/drug effects/metabolism ; Dentate Gyrus/cytology/drug effects/metabolism ; Glutamic Acid/*pharmacology ; Hippocampus/cytology/*drug effects/metabolism ; In Vitro Techniques ; N-Methylaspartate/pharmacology ; NF-kappa B/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Pyramidal Cells/cytology/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium Salicylate/*pharmacology ; Transcription Factor AP-1/metabolism ; Up-Regulation
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    Reduction of voltage-dependent Mg2+ blockade of NMDA current in mechanically injured neurons (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-12-13
    Description: Activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors is implicated in the pathophysiology of traumatic brain injury. Here, the effects of mechanical injury on the voltage-dependent magnesium (Mg2+) block of NMDA currents in cultured rat cortical neurons were examined. Stretch-induced injury was found to reduce the Mg2+ blockade, resulting in significantly larger ionic currents and increases in intracellular free calcium (Ca2+) concentration after NMDA stimulation of injured neurons. The Mg2+ blockade was partially restored by increased extracellular Mg2+ concentration or by pretreatment with the protein kinase C inhibitor calphostin C. These findings could account for the secondary pathological changes associated with traumatic brain injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, L -- Rzigalinski, B A -- Ellis, E F -- Satin, L S -- HL07537-14/HL/NHLBI NIH HHS/ -- NS 27214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Post Office Box 980524, Richmond, VA 23298-0524, USA. lsatin@gems.vcu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cerebral Cortex/cytology/*metabolism ; Dizocilpine Maleate/pharmacology ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Magnesium/*pharmacology ; Membrane Potentials ; N-Methylaspartate/*pharmacology ; Naphthalenes/pharmacology ; Neurons/cytology/*metabolism ; Patch-Clamp Techniques ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/drug effects/*metabolism
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    Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-16
    Description: Mice harboring mutations in the obese (ob) and diabetes (db) genes display similar phenotypes, and it has been proposed that these genes encode the ligand and receptor, respectively, for a physiologic pathway that regulates body weight. The cloning of ob, and the demonstration that it encodes a secreted protein (leptin) that binds specifically to a receptor (OB-R) in the brain, have validated critical aspects of this hypothesis. Here it is shown by genetic mapping and genomic analysis that mouse db, rat fatty (a homolog of db), and the gene encoding the OB-R are the same gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chua, S C Jr -- Chung, W K -- Wu-Peng, X S -- Zhang, Y -- Liu, S M -- Tartaglia, L -- Leibel, R L -- DK26687/DK/NIDDK NIH HHS/ -- DK47473/DK/NIDDK NIH HHS/ -- HD28047/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 16;271(5251):994-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Human Behavior and Metabolism, Rockefeller University, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8584938" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Southern ; Carrier Proteins/*genetics ; Chromosome Mapping ; Cloning, Molecular ; DNA Mutational Analysis ; Diabetes Mellitus/*genetics ; Genetic Markers ; Leptin ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Molecular Sequence Data ; Obesity/*genetics ; Phenotype ; Polymerase Chain Reaction ; Proteins/genetics ; Rats ; Rats, Inbred Strains ; *Receptors, Cell Surface ; Receptors, Cytokine/*genetics ; Receptors, Leptin
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    Neuronal gene expression in the waking state: a role for the locus coeruleus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: Several transcription factors are expressed at higher levels in the waking than in the sleeping brain. In experiments with rats, the locus coeruleus, a noradrenergic nucleus with diffuse projections, was found to regulate such expression. In brain regions depleted of noradrenergic innervation, amounts of c-Fos and nerve growth factor-induced A after waking were as low as after sleep. Phosphorylation of cyclic adenosine monophosphate response element-binding protein was also reduced. In contrast, electroencephalographic activity was unchanged. The reduced activity of locus coeruleus neurons may explain why the induction of certain transcription factors, with potential effects on plasticity and learning, does not occur during sleep.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cirelli, C -- Pompeiano, M -- Tononi, G -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1211-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Neurosciences Institute, 10640 J. J. Hopkins Drive, San Diego, CA 92121, USA. tononi@nsi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8895474" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/drug effects/physiology ; Animals ; Benzylamines/pharmacology ; Brain/*metabolism ; Cerebral Cortex/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Binding Proteins/genetics ; Early Growth Response Protein 1 ; Electroencephalography ; *Gene Expression Regulation ; *Genes, Immediate-Early ; Genes, fos ; Hippocampus/metabolism ; *Immediate-Early Proteins ; Locus Coeruleus/*physiology ; Neurons/*metabolism ; Norepinephrine/metabolism ; Oxidopamine/pharmacology ; Phosphorylation ; Rats ; Sleep ; Sleep Deprivation ; Sympathectomy, Chemical ; Transcription Factors/genetics ; *Wakefulness
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    Activation of ventrolateral preoptic neurons during sleep (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: The rostral hypothalamus and adjacent basal forebrain participate in the generation of sleep, but the neuronal circuitry involved in this process remains poorly characterized. Immunocytochemistry was used to identify the FOS protein, an immediate-early gene product, in a group of ventrolateral preoptic neurons that is specifically activated during sleep. The retrograde tracer cholera toxin B, in combination with FOS immunocytochemistry, was used to show that sleep-activated ventrolateral preoptic neurons innervate the tuberomammillary nucleus, a posterior hypothalamic cell group thought to participate in the modulation of arousal. This monosynaptic pathway in the hypothalamus may play a key role in determining sleep-wake states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sherin, J E -- Shiromani, P J -- McCarley, R W -- Saper, C B -- MH10709/MH/NIMH NIH HHS/ -- NS22835/NS/NINDS NIH HHS/ -- NS30140/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):216-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Beth Israel Hospital, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Chemistry ; Cholera Toxin ; Circadian Rhythm ; Immunohistochemistry ; Mammillary Bodies/*physiology ; Neural Pathways ; Neurons/chemistry/*physiology ; Preoptic Area/cytology/*physiology ; Proto-Oncogene Proteins c-fos/analysis ; Rats ; Sleep/*physiology
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    Congenital jaundice in rats with a mutation in a multidrug resistance-associated protein gene (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-23
    Description: The human Dubin-Johnson syndrome and its animal model, the TR(-) rat, are characterized by a chronic conjugated hyperbilirubinemia. TR(-) rats are defective in the canalicular multispecific organic anion transporter (cMOAT), which mediates hepatobiliary excretion of numerous organic anions. The complementary DNA for rat cmoat, a homolog of the human multidrug resistance gene (hMRP1), was isolated and shown to be expressed in the canalicular membrane of hepatocytes. In the TR(-) rat, a single-nucleotide deletion in this gene resulted in a reduced messenger RNA level and absence of the protein. It is likely that this mutation accounts for the TR(-) phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paulusma, C C -- Bosma, P J -- Zaman, G J -- Bakker, C T -- Otter, M -- Scheffer, G L -- Scheper, R J -- Borst, P -- Oude Elferink, R P -- New York, N.Y. -- Science. 1996 Feb 23;271(5252):1126-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gastrointestinal and Liver Diseases, Center for Liver and Intestinal Research, Academic Medical Center, Amsterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599091" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/analysis/chemistry/*genetics ; Amino Acid Sequence ; Animals ; Anion Transport Proteins ; Base Sequence ; Carrier Proteins/analysis/chemistry/*genetics ; Cell Membrane/chemistry ; DNA, Complementary/genetics ; Frameshift Mutation ; Humans ; Hyperbilirubinemia, Hereditary/*genetics ; Liver/*chemistry/cytology ; Molecular Sequence Data ; Molecular Weight ; Multidrug Resistance-Associated Proteins ; Phenotype ; Rats ; Rats, Wistar ; Sequence Alignment ; Sequence Deletion
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    Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-12-06
    Description: Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells. The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved. A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity. This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolozin, B -- Iwasaki, K -- Vito, P -- Ganjei, J K -- Lacana, E -- Sunderland, T -- Zhao, B -- Kusiak, J W -- Wasco, W -- D'Adamio, L -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1710-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unit on Alzheimer Biology, Laboratory of Clinical Science, National Institute of Mental Health, Building 10, Room 3D41, 9000 Rockville Pike, Bethesda, MD 20892, USA. ldadamio@atlas.niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939861" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid beta-Peptides/pharmacology ; Amyloid beta-Protein Precursor/metabolism/pharmacology ; Animals ; *Apoptosis ; DNA, Antisense/genetics ; GTP-Binding Protein alpha Subunits, Gi-Go/physiology ; GTP-Binding Protein alpha Subunits, Gs/physiology ; Humans ; Membrane Proteins/*genetics/*physiology ; Mutation ; Nerve Growth Factors/pharmacology ; Neurons/*cytology ; PC12 Cells ; Peptide Fragments/pharmacology ; Pertussis Toxin ; Presenilin-2 ; Rats ; Transfection ; Virulence Factors, Bordetella/pharmacology
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    Identification of the DNA binding site for NGFI-B by genetic selection in yeast (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-31
    Description: An in vivo selection system for isolating targets of DNA binding proteins in yeast was developed and used to identify the DNA binding site for the NGFI-B protein, a member of the steroid-thyroid hormone receptor superfamily. The feasibility of the technique was verified by selecting DNA fragments that contained binding sites for GCN4, a well-characterized yeast transcriptional activator. The DNA binding domain of NGFI-B, expressed as part of a LexA-NGFI-B-GAL4 chimeric activator, was then used to isolate a rat genomic DNA fragment that contained an NGFI-B binding site. The NGFI-B response element (NBRE) is similar to but functionally distinct from elements recognized by the estrogen and thyroid hormone receptors and the hormone receptor-like proteins COUP-TF, CF1, and H-2RIIBP. Cotransfection experiments in mammalian cells demonstrated that NGFI-B can activate transcription from the NBRE with or without its putative ligand binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, T E -- Fahrner, T J -- Johnston, M -- Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1296-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; DNA, Fungal/*metabolism ; DNA-Binding Proteins/genetics/*metabolism/pharmacology ; Fungal Proteins/metabolism ; Molecular Sequence Data ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Plasmids ; *Protein Kinases ; Rats ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Repressor Proteins ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; *Serine Endopeptidases ; Transcription Factors/genetics/*metabolism/pharmacology ; Transcription, Genetic ; Transfection
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    Space may be bad for your health (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1491.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1896859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Models, Biological ; Monitoring, Physiologic ; Motion Sickness/*etiology ; Rats ; Scyphozoa ; *Space Flight ; *Weightlessness
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    Split anergy in a CD8+ T cell: receptor-dependent cytolysis in the absence of interleukin-2 production (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Engagement of the antigen-specific receptor (TCR) of CD4+ T lymphocytes without a second (costimulatory) signal prevents the subsequent production of interleukin-2 (IL-2) by these cells. Because IL-2 is a key immunoregulatory lymphokine and is also produced by a subset of CD8+ T cells that are able to kill target cells, the effect of engaging the TCR of one such clone in the absence of costimulatory signals was examined. The capacity for TCR-dependent IL-2 production was lost, indicating comparable costimulator-dependent signaling requirements for IL-2 production in CD4+ and CD8+ T cells. However, TCR-mediated cytotoxicity was not impaired, implying that costimulation is required for only certain TCR-dependent effector functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otten, G R -- Germain, R N -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigen-Presenting Cells/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Female ; Interleukin-2/biosynthesis/*physiology ; Kinetics ; Lymphocyte Activation ; Mice ; Mice, Inbred Strains ; Ovalbumin/immunology ; Rats ; Receptors, Antigen, T-Cell/*immunology ; Spleen/immunology/radiation effects ; T-Lymphocytes/*immunology
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    Modulation of cardiac sodium channels by cAMP receptors on the myocyte surface (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-13
    Description: The phosphorylation of the cardiac sodium channel by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase A leads to its inactivation. It was shown that extracellular cAMP can also modulate the sodium channel of rat, guinea pig, and frog ventricular myocytes in a rapid (less than 50 milliseconds), reversible, and dose-dependent manner. The decrease in the sodium current was accompanied by a 10- to 15-millivolt shift in the steady-state availability of the sodium channel toward more negative potentials and was inhibited by guanosine-5'-O-(2-thiodiphosphate) or pertussis toxin, suggesting that the extracellular modulation of the sodium channel by cAMP is mediated by a membrane-delimited mechanism that includes a pertussis toxin-sensitive G protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorbera, L A -- Morad, M -- HL16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1286-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1653970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/*pharmacology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Diphosphate/analogs & derivatives/pharmacology ; Guinea Pigs ; Heart/drug effects/*physiology ; Isoproterenol/pharmacology ; Kinetics ; Membrane Potentials/drug effects ; Pertussis Toxin ; Rana pipiens ; Rats ; Receptors, Cyclic AMP/drug effects/*physiology ; Sodium Channels/drug effects/*physiology ; Thionucleotides/pharmacology ; Virulence Factors, Bordetella/pharmacology
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    Cloning and expression of a cocaine-sensitive rat dopamine transporter (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-25
    Description: The action of dopamine and other monoamine neurotransmitters at synapses is terminated predominantly by high-affinity reuptake into presynaptic terminals by specific sodium-dependent neurotransmitter transport proteins. A complementary DNA encoding a rat dopamine transporter has been isolated that exhibits high sequence similarity with the previously cloned norepinephrine and gamma-aminobutyric acid transporters. Transient expression of the complementary DNA in HeLa cells confirms the cocaine sensitivity of this transporter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kilty, J E -- Lorang, D -- Amara, S G -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cloning, Molecular ; Cocaine/*pharmacology ; Dopamine/*metabolism ; Dopamine Plasma Membrane Transport Proteins ; Gene Expression ; HeLa Cells ; Humans ; Kinetics ; *Membrane Glycoproteins ; *Membrane Transport Proteins ; Molecular Sequence Data ; *Nerve Tissue Proteins ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Rats ; Sequence Homology, Nucleic Acid ; Transfection
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    Exchange of conduction pathways between two related K+ channels (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-02-22
    Description: The structure of the ion conduction pathway or pore of voltage-gated ion channels is unknown, although the linker between the membrane spanning segments S5 and S6 has been suggested to form part of the pore in potassium channels. To test whether this region controls potassium channel conduction, a 21-amino acid segment of the S5-S6 linker was transplanted from the voltage-activated potassium channel NGK2 to another potassium channel DRK1, which has very different pore properties. In the resulting chimeric channel, the single channel conductance and blockade by external and internal tetraethylammonium (TEA) ion were characteristic of the donor NGK2 channel. Thus, this 21-amino acid segment controls the essential biophysical properties of the pore and may form the conduction pathway of these potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartmann, H A -- Kirsch, G E -- Drewe, J A -- Taglialatela, M -- Joho, R H -- Brown, A M -- NS08805/NS/NINDS NIH HHS/ -- NS23877/NS/NINDS NIH HHS/ -- NS28407/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 22;251(4996):942-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2000495" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/physiology ; Chimera ; Cloning, Molecular ; Female ; Ion Channel Gating ; Membrane Potentials ; Molecular Sequence Data ; Oligonucleotide Probes ; Oocytes/physiology ; Polymerase Chain Reaction ; Potassium Channels/drug effects/genetics/*physiology ; Rats ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Xenopus
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    Engineers open a dialogue with neurons (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, I -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):34.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Engineering ; Electric Stimulation ; Electrodes, Implanted ; *Neurons ; Rats
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    Protein kinase activity closely associated with a reconstituted calcium-activated potassium channel (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-02
    Description: Modulation of the activity of potassium and other ion channels is an essential feature of nervous system function. The open probability of a large conductance Ca(2+)-activated K+ channel from rat brain, incorporated into planar lipid bilayers, is increased by the addition of adenosine triphosphate (ATP) to the cytoplasmic side of the channel. This modulation takes place without the addition of protein kinase, requires Mg2+, and is mimicked by an ATP analog that serves as a substrate for protein kinases but not by a nonhydrolyzable ATP analog. Addition of protein phosphatase 1 reverses the modulation by MgATP. Thus, there may be an endogenous protein kinase activity firmly associated with this K+ channel. Some ion channels may exist in a complex that contains regulatory protein kinases and phosphatases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, S K -- Reinhart, P H -- Martin, B L -- Brautigan, D -- Levitan, I B -- DK31374/DK/NIDDK NIH HHS/ -- NS17910/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 2;253(5019):560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Department of Biochemistry, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857986" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Brain/*physiology ; Calcium/*pharmacology ; Kinetics ; Lipid Bilayers ; Potassium Channels/drug effects/metabolism/*physiology ; Protein Kinases/*metabolism ; Rats
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    Crystal structure of defensin HNP-3, an amphiphilic dimer: mechanisms of membrane permeabilization (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-22
    Description: Defensins (molecular weight 3500 to 4000) act in the mammalian immune response by permeabilizing the plasma membranes of a broad spectrum of target organisms, including bacteria, fungi, and enveloped viruses. The high-resolution crystal structure of defensin HNP-3 (1.9 angstrom resolution, R factor 0.19) reveals a dimeric beta sheet that has an architecture very different from other lytic peptides. The dimeric assembly suggests mechanisms by which defensins might bind to and permeabilize the lipid bilayer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, C P -- Yee, J -- Selsted, M E -- Eisenberg, D -- New York, N.Y. -- Science. 1991 Mar 22;251(5000):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eisenberg, Molecular Biology Institute, Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006422" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blood Proteins/chemistry/*ultrastructure ; Cell Membrane Permeability ; Crystallography ; Defensins ; Guinea Pigs ; Humans ; Macromolecular Substances ; Membrane Proteins/chemistry/ultrastructure ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Protein Conformation ; Rabbits ; Rats ; Structure-Activity Relationship ; X-Ray Diffraction ; *alpha-Defensins
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    Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-11
    Description: It is generally accepted that glutamate serves as the neurotransmitter at most excitatory synapses in the mammalian central nervous system (CNS). Synaptic release of glutamate may trigger a fast and a slow excitatory postsynaptic current (EPSC). The slow EPSC is mediated by N-methyl-D-aspartate (NMDA) receptor channels, whereas the fast EPSC is mediated by non-NMDA receptor channels. The nootropic agent aniracetam selectively and reversibly slows the desensitization kinetics of non-NMDA channels and lengthens their single-channel open times. Antiracetam also modulates the kinetics of the fast EPSC in a manner that mirrors its action on the kinetics of the non-NMDA channels. These results support the hypothesis that the properties of the non-NMDA glutamate channels rather than the rate of neurotransmitter clearance are the primary determinants of the kinetics of the fast EPSC in the mammalian CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, C M -- Shi, Q Y -- Katchman, A -- Lynch, G -- NS28158/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):288-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Pennsylvania, Philadelphia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1681589" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Glutamates/*physiology ; Glutamic Acid ; Kinetics ; Pyrrolidinones/*pharmacology ; Rats ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, Neurotransmitter/drug effects ; Synapses/*drug effects
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    Requirement of nuclear prolactin for interleukin-2--stimulated proliferation of T lymphocytes (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-05
    Description: Prolactin (PRL) is necessary for the proliferation of cloned T lymphocytes in response to interleukin-2 (IL-2). Translocation of PRL into the nucleus occurs during IL-2--stimulated mitogenesis. Therefore, the function of intranuclear PRL in T cell proliferation was tested. Eukaryotic expression vectors were prepared to express wild-type PRL [PRL(WT)], PRL that lacks the signal sequence for translocation into the endoplasmic reticulum [PRL(ER-)], and chimeric PRL in which the signal peptide was replaced with the sequence that directs the nuclear translocation of the SV40 large T antigen [PRL(NT+)]. Expression of these constructs in a T cell line (Nb2) responsive to PRL and IL-2 resulted in localization of PRL in the extracellular milieu, cytoplasm, or nucleus, respectively. Stimulation with IL-2 alone resulted in a five- to tenfold increase in the incorporation of [3H]thymidine by cells expressing PRL(NT+) or PRL(WT) as compared to PRL(ER-) or the parental Nb2 cells. Only the PRL(NT+) clone proliferated continuously with IL-2 stimulation in the presence of antiserum to PRL. These results demonstrate that nuclear PRL is necessary for IL-2--stimulated proliferation and suggest that a peptide hormone can function in the nucleus without binding to its cell surface receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clevenger, C V -- Altmann, S W -- Prystowsky, M B -- GM-13901/GM/NIGMS NIH HHS/ -- GM-36962/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):77-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063207" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport, Active ; Cell Cycle/drug effects ; Cell Nucleus/metabolism ; Drug Synergism ; Genetic Vectors ; In Vitro Techniques ; Interleukin-2/pharmacology ; Lymphocyte Activation/*drug effects ; Molecular Sequence Data ; Prolactin/pharmacokinetics/*pharmacology ; Rats ; Transfection
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    Control of alternative splicing by the differential binding of U1 small nuclear ribonucleoprotein particle (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-01
    Description: Cellular factors controlling alternative splicing of precursor messenger RNA are largely unknown, even though this process plays a central role in specifying the diversity of proteins in the eukaryotic cell. For the identification of such factors, a segment of the rat preprotachykinin gene was used in which differential expression of neuropeptides gamma and K is dependent on alternative splicing of the fourth exon (E4). Sequence variants of the three-exon segment, (E3-E4-E5) were created, resulting in a sensitive assay for factors mediating the splicing switch between E4-skipping and E4-inclusion. A dinucleotide mutation in the 5' splice site of E4 that increase base-pairing of this site to U1 small nuclear RNA resulted in uniform selection of E4, whereas a control mutation that destroyed base-pairing resulted in uniform E4-skipping. Affinity selection of spliceosomes formed on these functionally distinct substrates revealed that the extreme difference in splicing was mediated by differential binding of the U1 small nuclear ribonucleoprotein particle (snRNP) to the 5' splice site of E4. These data show that, apart from its established role in selecting 5' splice sites, U1 snRNP plays a fundamental role in 3' exon selection and provides insight into possible mechanisms of alternative splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, H C -- Nasim, F H -- Grabowski, P J -- GM-39695/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 1;251(4997):1045-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1825520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Mutational Analysis ; Exons ; Hydrogen Bonding ; Macromolecular Substances ; Molecular Sequence Data ; Protein Precursors/*genetics ; *RNA Splicing ; RNA, Messenger/*metabolism ; RNA, Small Nuclear/*physiology ; Rats ; Ribonucleoproteins/chemistry/*physiology ; Ribonucleoproteins, Small Nuclear ; Structure-Activity Relationship ; Tachykinins/*genetics
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    Maintenance of normoglycemia in diabetic mice by subcutaneous xenografts of encapsulated islets (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-12-20
    Description: The goal of islet transplantation in human diabetes is to maintain the islet grafts in the recipients without the use of immunosuppression. One approach is to encapsulate the donor islets in permselective membranes. Hollow fibers fabricated from an acrylic copolymer were used to encapsulate small numbers of rat islets that were immobilized in an alginate hydrogel for transplantation in diabetic mice. The fibers were biocompatible, prevented rejection, and maintained normoglycemia when transplanted intraperitoneally; hyperglycemia returned when the fibers were removed at 60 days. Normoglycemia was also maintained by subcutaneous implants that had an appropriately constructed outer surface on the fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacy, P E -- Hegre, O D -- Gerasimidi-Vazeou, A -- Gentile, F T -- Dionne, K E -- DK01226/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763328" target="_blank"〉PubMed〈/a〉
    Keywords: *Acrylic Resins ; Animals ; Animals, Newborn ; Blood Glucose/*metabolism ; Diabetes Mellitus, Experimental/blood/*surgery ; In Vitro Techniques ; Insulin/secretion ; Islets of Langerhans/*secretion ; Islets of Langerhans Transplantation/*physiology ; Male ; Membranes, Artificial ; Mice ; Mice, Inbred C57BL ; *Polyvinyl Chloride ; Rats ; Rats, Inbred WF ; Time Factors ; Transplantation, Heterologous
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    Identification of Ets- and notch-related subunits in GA binding protein (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-08-16
    Description: Recombinant cDNA clones that encode two distinct subunits of the transcription factor GA binding protein (GABP) have been isolated. The predicted amino acid sequence of one subunit, GABP alpha, exhibits similarity to the sequence of the product of the ets-1 protooncogene in a region known to encompass the Ets DNA binding domain. The sequence of the second subunit, GABP beta, contains four 33-amino acid repeats located close to the NH2-terminus of the subunit. The sequences of these repeats are similar to repeats in several transmembrane proteins, including Notch from Drosophila melanogaster and Glp-1 and Lin-12 from Caenorhabditis elegans. Avid, sequence-specific binding to DNA required the presence of both polypeptides, revealing a conceptual convergence of nuclear transforming proteins and membrane-anchored proteins implicated in developmentally regulated signal transduction processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaMarco, K -- Thompson, C C -- Byers, B P -- Walton, E M -- McKnight, S L -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):789-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876836" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cloning, Molecular ; DNA-Binding Proteins/*chemistry/genetics ; GA-Binding Protein Transcription Factor ; Gene Expression ; Molecular Sequence Data ; Nuclear Proteins/chemistry/genetics ; Peptides/chemistry ; Proto-Oncogene Protein c-ets-1 ; Proto-Oncogene Proteins/chemistry ; Proto-Oncogene Proteins c-ets ; RNA, Messenger/genetics ; Rats ; Recombinant Proteins ; Transcription Factors/*chemistry/genetics
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    More pieces in the dioxin puzzle (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):377.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/*toxicity ; Dioxins/*toxicity ; Dose-Response Relationship, Drug ; Models, Theoretical ; Rats ; Receptors, Aryl Hydrocarbon ; Receptors, Drug/metabolism ; Risk
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    Convergence of Ets- and notch-related structural motifs in a heteromeric DNA binding complex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: Analysis of the heteromeric DNA binding protein GABP has revealed the interaction of two distinct peptide sequence motifs normally associated with proteins located in different cellular compartments. The alpha subunit of GABP contains an 85-amino acid segment related to the Ets family of DNA binding proteins. The ETS domain of GABP alpha facilitates weak binding to DNA and, together with an adjacent segment of 37 amino acids, mediates stable interaction with GABP beta. The beta subunit of GABP contains four imperfect repeats of a sequence present in several transmembrane proteins including the product of the Notch gene of Drosophila melanogaster. These amino-terminal repeats of GABP beta mediate stable interaction with GABP alpha and, when complexed with GABP alpha, directly contact DNA. These observations provide evidence for a distinct biochemical role for the 33-amino acid repeats, and suggest that they may serve as a module for the generation of specific dimerization interfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, C C -- Brown, T A -- McKnight, S L -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):762-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cross-Linking Reagents ; DNA/metabolism ; DNA-Binding Proteins/*chemistry/metabolism ; GA-Binding Protein Transcription Factor ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Multigene Family ; Nuclear Proteins/*chemistry/metabolism ; Oligonucleotides/chemistry ; Proto-Oncogene Proteins/chemistry ; Proto-Oncogene Proteins c-ets ; Rats ; Recombinant Proteins ; Structure-Activity Relationship ; Transcription Factors/*chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    Stimulation of protein tyrosine phosphorylation by NMDA receptor activation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-23
    Description: The N-methyl-D-aspartate (NMDA) receptor, a subtype of glutamate receptors, plays a key role in synaptic plasticity in the nervous system. After NMDA receptor activation, calcium entry into the postsynaptic neuron is a critical initial event. However, the subsequent mechanisms by which the NMDA receptor signal is processed are incompletely understood. Stimulation of cultured rat hippocampal cells with glutamate resulted in the rapid and transient tyrosine phosphorylation of a 39-kilodalton protein (p39). Tyrosine phosphorylation of p39 was triggered by the NMDA receptor and required an influx of Ca2+ from the extracellular medium. Because p39 was found to be highly related or identical to the microtubule-associated protein 2 kinase, the NMDA receptor signal may be processed by a sequential activation of protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bading, H -- Greenberg, M E -- CA 43855/CA/NCI NIH HHS/ -- NS 28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 23;253(5022):912-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1715095" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases ; Cells, Cultured ; Glutamates/pharmacology ; Glutamic Acid ; Hippocampus/drug effects/metabolism ; Immunoblotting ; Kinetics ; Phosphoproteins/*metabolism ; Phosphorylation ; Phosphotyrosine ; Protein Kinases/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Tyrosine/*analogs & derivatives/metabolism
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  • 85
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    New vector delivers genes to lung cells (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):374.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2017677" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics ; Animals ; Emphysema/therapy ; Genetic Therapy ; *Genetic Vectors ; Humans ; *Lung ; Rats ; *Transfection ; alpha 1-Antitrypsin/genetics
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  • 86
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    EPA moves to reassess the risk of dioxin (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 May 17;252(5008):911.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2035022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests ; *Carcinogens ; Dioxins/*toxicity ; Humans ; National Institute for Occupational Safety and Health (U.S.) ; Neoplasms, Experimental/chemically induced ; Rats ; Risk Factors ; United States ; *United States Environmental Protection Agency
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  • 87
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    Inhibition of morphine tolerance and dependence by the NMDA receptor antagonist MK-801 (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-04
    Description: The N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor is an important mediator of several forms of neural and behavioral plasticity. The present studies examined whether NMDA receptors might be involved in the development of opiate tolerance and dependence, two examples of behavioral plasticity. The noncompetitive NMDA receptor antagonist MK-801 attenuated the development of tolerance to the analgesic effect of morphine without affecting acute morphine analgesia. In addition, MK-801 attenuated the development of morphine dependence as assessed by naloxone-precipitated withdrawal. These results suggest that NMDA receptors may be important in the development of opiate tolerance and dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trujillo, K A -- Akil, H -- DA02265/DA/NIDA NIH HHS/ -- DA05336/DA/NIDA NIH HHS/ -- MH422251/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):85-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mental Health Research Institute, University of Michigan, Ann Arbor 48109-0720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1824728" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Behavior, Animal/drug effects ; Dizocilpine Maleate/*pharmacology ; Drug Tolerance ; Male ; *Morphine ; Naloxone/pharmacology ; Pain Measurement ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; *Substance-Related Disorders
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  • 88
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    The brain as "sexual organ" (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1991 Aug 30;253(5023):957-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1887226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*anatomy & histology/physiology ; Corpus Callosum/anatomy & histology/physiology ; Female ; Humans ; Hypothalamus/*anatomy & histology/physiology ; Male ; Rats ; *Sex Characteristics
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  • 89
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    Clusters of coupled neuroblasts in embryonic neocortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: The neocortex of the brain develops from a simple germinal layer into a complex multilayer structure. To investigate cellular interactions during early neocortical development, whole-cell patch clamp recordings were made from neuroblasts in the ventricular zone of fetal rats. During early corticogenesis, neuroblasts are physiologically coupled by gap junctions into clusters of 15 to 90 cells. The coupled cells form columns within the ventricular zone and, by virtue of their membership in clusters, have low apparent membrane resistances and generate large responses to the inhibitory neurotransmitter gamma-aminobutyric acid. As neuronal migration out of the ventricular zone progresses, the number of cells within the clusters decreases. These clusters allow direct cell to cell interaction at the earliest stages of corticogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo Turco, J J -- Kriegstein, A R -- NS07280/NS/NINDS NIH HHS/ -- NS12151/NS/NINDS NIH HHS/ -- NS21223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/cytology/embryology/*physiology ; Electric Conductivity ; Electrophysiology/methods ; Embryo, Mammalian ; Evoked Potentials/drug effects ; In Vitro Techniques ; Membrane Potentials/drug effects ; Neurons/cytology/drug effects/*physiology ; Rats ; Receptors, GABA-A/physiology ; gamma-Aminobutyric Acid/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Transmission between pairs of hippocampal slice neurons: quantal levels, oscillations, and LTP (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: Long-term potentiation (LTP) of synaptic transmission after coincident pre- and postsynaptic activity is considered a cellular model of changes underlying learning and memory. In intact tissue, LTP has been observed only between populations of neurons, making analysis of mechanisms difficult. Transmission between individual pre- and postsynaptic hippocampal cells was studied, suggesting quantal amplitude distributions with little variability in quantal size. LTP between such pairs is manifested by large, persistent, and synapse-specific potentiation with a shift in amplitude distribution that suggests presynaptic changes. Oscillations in amplitude of transmission, apparently of presynaptic origin, are common and can be triggered by LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malinow, R -- New York, N.Y. -- Science. 1991 May 3;252(5006):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Conductivity ; Electrophysiology ; Hippocampus/*cytology ; Kinetics ; Membrane Potentials ; Neurons/*physiology ; Rats ; Statistics as Topic ; Synapses/*physiology ; Synaptic Transmission/*physiology
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  • 91
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    Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-15
    Description: In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, M M -- Foskett, J K -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1014-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Chlorides/physiology ; Cytosol/physiology ; In Vitro Techniques ; Male ; Ouabain/pharmacology ; Parotid Gland/*physiology ; Periodicity ; Potassium/physiology ; Rats ; Rats, Inbred Strains ; Sodium/*physiology ; Water-Electrolyte Balance
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  • 92
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    Effect of light chain V region duplication on IgG oligomerization and in vivo efficacy (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: A human immunoglobulin G1 (IgG1) antibody oligomer was isolated from a transfected myeloma cell line that produced a monoclonal antibody to group B streptococci. Compared to the IgG1 monomer, the oligomer was significantly more effective at protecting neonatal rats from infection in vivo. The oligomer was also shown to cross the placenta and to be stable in neonatal rats. Immunochemical analysis and complementary DNA sequencing showed that the transfected cell line produced two distinct kappa light chains: a normal light chain (Ln) with a molecular mass of 25 kilodaltons and a 37-kilodalton species (L37), the domain composition of which was variable-variable-constant (V-V-C). Cotransfection of vectors encoding the heavy chain and L37 resulted in production of oligomeric IgG.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shuford, W -- Raff, H V -- Finley, J W -- Esselstyn, J -- Harris, L J -- New York, N.Y. -- Science. 1991 May 3;252(5006):724-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immune Sciences, Bristol-Myers Squibb Pharmaceutical Research Institute-Seattle, WA 98121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1902593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies, Bacterial/biosynthesis/immunology/pharmacokinetics ; Antibodies, Monoclonal/biosynthesis/immunology/pharmacokinetics ; Cell Line ; Female ; Humans ; Immunization, Passive ; Immunoglobulin G/*biosynthesis/genetics/immunology ; Immunoglobulin M/genetics ; Immunoglobulin Variable Region/*biosynthesis/genetics/immunology ; Immunoglobulin kappa-Chains/*biosynthesis/genetics/immunology ; Macromolecular Substances ; Maternal-Fetal Exchange ; Multiple Myeloma ; Pregnancy ; Rats ; Streptococcal Infections/prevention & control ; Streptococcus agalactiae/immunology ; Transfection
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  • 93
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    OPC-21268, an orally effective, nonpeptide vasopressin V1 receptor antagonist (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-04-26
    Description: An orally effective, nonpeptide, vasopressin V1 receptor antagonist, OPC-21268, has been identified. This compound selectively antagonized binding to the V1 subtype of the vasopressin receptor in a competitive manner. In vivo, the compound acted as a specific antagonist of arginine vasopressin (AVP)-induced vasoconstriction. After oral administration in conscious rats, the compound also antagonized pressor responses to AVP. OPC-21268 can be used to study the physiological role of AVP and may be therapeutically useful in the treatment of hypertension and congestive heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamura, Y -- Ogawa, H -- Chihara, T -- Kondo, K -- Onogawa, T -- Nakamura, S -- Mori, T -- Tominaga, M -- Yabuuchi, Y -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Second Tokushima Institute of New Drug Research, Otsuka Pharmaceutical Co., Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850553" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/antagonists & inhibitors/metabolism/*pharmacology ; Binding, Competitive ; Blood Pressure/*drug effects ; Cell Membrane/metabolism ; Kidney/metabolism ; Kinetics ; Liver/metabolism ; Norepinephrine/pharmacology ; Piperidines/administration & dosage/*pharmacology ; Quinolones/administration & dosage/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Vasopressin ; Time Factors
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  • 94
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    The anion paradox in sodium taste reception: resolution by voltage-clamp studies (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-01
    Description: Sodium salts are potent taste stimuli, but their effectiveness is markedly dependent on the anion, with chloride yielding the greatest response. The cellular mechanisms that mediate this phenomenon are not known. This "anion paradox" has been resolved by considering the field potential that is generated by restricted electrodiffusion of the anion through paracellular shunts between taste-bud cells. Neural responses to sodium chloride, sodium acetate, and sodium gluconate were studied while the field potential was voltage-clamped. Clamping at electronegative values eliminated the anion effect, whereas clamping at electropositive potentials exaggerated it. Thus, field potentials across the lingual epithelium modulate taste reception, indicating that the functional unit of taste reception includes the taste cell and its paracellular microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Q -- Heck, G L -- DeSimone, J A -- DC00122/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):724-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Virginia Commonwealth University, Richmond 23298-0551.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anions ; Chemoreceptor Cells/physiology ; Epithelium/physiology ; Evoked Potentials ; Female ; Models, Biological ; Mouth Mucosa/innervation/*physiology ; Neurons/physiology ; Rats ; Rats, Inbred Strains ; *Sodium ; *Sodium Chloride ; Taste/*physiology ; Tongue/*innervation
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  • 95
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    Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-15
    Description: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Nilbert, M C -- Vogelstein, B -- Bryan, T M -- Levy, D B -- Smith, K J -- Preisinger, A C -- Hamilton, S R -- Hedge, P -- Markham, A -- 6M 07184/PHS HHS/ -- CA 06973/CA/NCI NIH HHS/ -- CA 09243/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848370" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; *Chromosomes, Human, Pair 5 ; Colorectal Neoplasms/*genetics ; Exons ; GTP-Binding Proteins/metabolism ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Proteins/*genetics/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; *Tumor Suppressor Proteins
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  • 96
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    Characterization of a cofactor that regulates dimerization of a mammalian homeodomain protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Dimerization among transcription factors has become a recurrent theme in the regulation of eukaryotic gene expression. Hepatocyte nuclear factor-1 alpha (HNF-1 alpha) is a homeodomain-containing protein that functions as a dimer. A dimerization cofactor of HNF-1 alpha (DCoH) was identified that displayed a restricted tissue distribution and did not bind to DNA, but, rather, selectively stabilized HNF-1 alpha dimers. The formation of a stable tetrameric DCoH-HNF-1 alpha complex, which required the dimerization domain of HNF-1 alpha, did not change the DNA binding characteristics of HNF-1 alpha, but enhanced its transcriptional activity. However, DCoH did not confer transcriptional activation to the GAL4 DNA binding domain. These results indicate that DCoH regulates formation of transcriptionally active tetrameric complexes and may contribute to the developmental specificity of the complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendel, D B -- Khavari, P A -- Conley, P B -- Graves, M K -- Hansen, L P -- Admon, A -- Crabtree, G R -- CA 09302/CA/NCI NIH HHS/ -- HD 07201/HD/NICHD NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1762-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763325" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/physiology ; Chromosome Deletion ; DNA-Binding Proteins/*metabolism ; Gene Library ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Humans ; *Hydro-Lyases ; Liver/physiology ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Protein Biosynthesis ; RNA, Messenger/genetics ; Rabbits ; Rats ; Reticulocytes/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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  • 97
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    Cloning of a serotonin transporter affected by antidepressants (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: A complementary DNA clone for a serotonin (5HT) transporter has been isolated from rat basophilic leukemia cells. The complementary DNA sequence predicts a 653-amino acid protein with 12 to 13 putative transmembrane domains. The 5HT transporter has significant homology to the gamma-aminobutyric acid, dopamine, and norepinephrine transporters. Uptake by CV-1 cells expressing the transporter complementary DNA resembles 5HT uptake by platelets and brain synaptosomes; it is sensitive to antidepressants, amphetamine derivatives, and cocaine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, B J -- Mezey, E -- Brownstein, M J -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):579-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948036" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antidepressive Agents/*pharmacology ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cell Line ; Cloning, Molecular ; Kinetics ; Leukemia, Basophilic, Acute ; Molecular Sequence Data ; Oligonucleotide Probes ; Rats ; Serotonin/*metabolism ; Transfection
    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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  • 98
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    Hypotensive activity of fibroblast growth factor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: Acidic and basic fibroblast growth factors (FGFs) are members of a family of proteins that are broad-spectrum mitogens, have diverse hormone-like activities, and function in tumorigenesis. FGF's ability to raise the concentration of intracellular calcium ion suggests that FGF could induce the synthesis of endothelium-derived relaxing factor (EDRF) and consequently vasodilation. Systemic administration of FGF decreased arterial blood pressure. This effect was mediated by EDRF and by adenosine triphosphate-sensitive potassium ion channels. The hypotensive effect of FGF was segregated from its mitogenic activity by protein engineering. These results extend the range of FGF autocrine activities and potential therapeutic applications, emphasize the role of endothelium as an arterial blood pressure--regulating organ, and provide insight on the structural basis of FGF functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuevas, P -- Carceller, F -- Ortega, S -- Zazo, M -- Nieto, I -- Gimenez-Gallego, G -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1208-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital Universitario Ramon y Cajal, Carretera de Colmenar, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/*drug effects ; Dose-Response Relationship, Drug ; Fibroblast Growth Factors/chemistry/*pharmacology ; Glyburide/pharmacology ; Nitric Oxide/physiology ; Potassium Channels/drug effects ; Rabbits ; Rats ; Structure-Activity Relationship ; Time 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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  • 99
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    Functional modulation of brain sodium channels by protein kinase C phosphorylation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: Voltage-gated sodium channels, which are responsible for the generation of action potentials in the brain, are phosphorylated by protein kinase C (PKC) in purified form. Activation of PKC decreases peak sodium current up to 80 percent and slows its inactivation for sodium channels in rat brain neurons and for rat brain type IIA sodium channel alpha subunits heterologously expressed in Chinese hamster ovary cells. These effects are specific for PKC because they can be blocked by specific peptide inhibitors of PKC and can be reproduced by direct application of PKC to the cytoplasmic surface of sodium channels in excised inside-out membrane patches. Modulation of brain sodium channels by PKC is likely to have important effects on signal transduction and synaptic transmission in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Numann, R -- Catterall, W A -- Scheuer, T -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology ; CHO Cells ; Cloning, Molecular ; Cricetinae ; Diglycerides/pharmacology ; In Vitro Techniques ; Neurons/physiology ; Phosphoproteins/physiology ; Phosphorylation ; Protein Kinase C/*physiology ; Protein Kinases/physiology ; Rats ; Sodium/*physiology ; Sodium Channels/*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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  • 100
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    NMDA antagonist neurotoxicity: mechanism and prevention (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-06
    Description: Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, including phencyclidine (PCP) and ketamine, protect against brain damage in neurological disorders such as stroke. However, these agents have psychotomimetic properties in humans and morphologically damage neurons in the cerebral cortex of rats. It is now shown that the morphological damage can be prevented by certain anticholinergic drugs or by diazepam and barbiturates, which act at the gamma-aminobutyric acid (GABA) receptor-channel complex and are known to suppress the psychotomimetic symptoms caused by ketamine. Thus, it may be possible to prevent the unwanted side effects of NMDA antagonists, thereby enhancing their utility as neuroprotective drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Labruyere, J -- Wang, G -- Wozniak, D F -- Price, M T -- Sesma, M A -- AG 05681/AG/NIA NIH HHS/ -- DA 53568/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1835799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barbiturates/pharmacology ; Chick Embryo ; Dizocilpine Maleate/*antagonists & inhibitors ; Neurotoxins/*antagonists & inhibitors ; Parasympatholytics/pharmacology ; Pilocarpine/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*drug effects ; Scopolamine Hydrobromide/pharmacology ; Vacuoles/ultrastructure
    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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