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  • 1
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Chloride conductance expressed by delta F508 and other mutant CFTRs in Xenopus oocytes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR) is associated with expression of a chloride conductance that is defective in cystic fibrosis (CF). Xenopus oocytes injected with RNA coding for CFTR that contained mutations in the first nucleotide binding fold (NBF1) expressed chloride currents in response to raising adenosine 3',5'-monophosphate (cAMP) with forskolin and 3-isobutyl-1-methylxanthine (IBMX). The mutant CFTRs were less sensitive than wild-type CFTR to this activating stimulus, and the reduction in sensitivity correlated with the severity of cystic fibrosis in patients carrying the corresponding mutations. This demonstration provides the basis for detailed analyses of NBF1 function and suggests potential pharmacologic treatments for cystic fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drumm, M L -- Wilkinson, D J -- Smit, L S -- Worrell, R T -- Strong, T V -- Frizzell, R A -- Dawson, D C -- Collins, F S -- DK29786/DK/NIDDK NIH HHS/ -- DK39690/DK/NIDDK NIH HHS/ -- DK42718/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1797-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Michigan, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1722350" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Chloride Channels ; Chlorides/*metabolism ; Cystic Fibrosis/genetics/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Genetic Variation ; Genotype ; Humans ; Ion Channels/physiology ; Membrane Potentials/drug effects ; Membrane Proteins/drug effects/genetics/*physiology ; Microinjections ; *Mutation ; Oocytes/drug effects/*physiology ; RNA/administration & dosage/genetics ; Transcription, Genetic ; Xenopus
    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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    Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, T M -- Arriza, J L -- Jaworsky, D E -- Borisy, F F -- Attramadal, H -- Lefkowitz, R J -- Ronnett, G V -- NS 01578-01/NS/NINDS NIH HHS/ -- NS-02131/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8381559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*metabolism ; *Arrestins ; Cells, Cultured ; Cyclic AMP/metabolism ; *Cyclic AMP-Dependent Protein Kinases ; Cytosol/metabolism ; Dendrites/physiology ; Eye Proteins/*metabolism ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Proteins/*metabolism ; Isoenzymes/metabolism ; Male ; Mechanoreceptors/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Bulb/*physiology ; Protein Kinases/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; *Smell ; Testis/physiology ; Turbinates/*physiology ; beta-Adrenergic Receptor Kinases
    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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  • 4
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    Endothelial NOS and the blockade of LTP by NOS inhibitors in mice lacking neuronal NOS (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: Long-term potentiation (LTP) is a persistent increase in synaptic strength implicated in certain forms of learning and memory. In the CA1 region of the hippocampus, LTP is thought to involve the release of one or more retrograde messengers from the postsynaptic cell that act on the presynaptic terminal to enhance transmitter release. One candidate retrograde messenger is the membrane-permeant gas nitric oxide (NO), which in the brain is released after activation of the neuronal-specific NO synthase isoform (nNOS). To assess the importance of NO in hippocampal synaptic plasticity, LTP was examined in mice where the gene encoding nNOS was disrupted by gene targeting. In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal except for a slight reduction in comparison to that in wild-type mice and was blocked by NOS inhibitors, just as it was in wild-type mice. Immunocytochemical studies indicate that in the nNOS- mice as in wild-type mice, the endothelial form of NOS (eNOS) is expressed in CA1 neurons. These findings suggest that eNOS, rather than nNOS, generates NO within the postsynaptic cell during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Dell, T J -- Huang, P L -- Dawson, T M -- Dinerman, J L -- Snyder, S H -- Kandel, E R -- Fishman, M C -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- MH-45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):542-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518615" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/genetics/*metabolism ; Animals ; Arginine/*analogs & derivatives/pharmacology ; Electric Stimulation ; Endothelium/enzymology ; Hippocampus/drug effects/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Mice ; Mutation ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine ; Pyramidal Cells/drug effects/enzymology/*physiology ; Synaptic Transmission/drug effects
    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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  • 5
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    Retinoids selective for retinoid X receptor response pathways (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: Retinoids have a broad spectrum of biological activities and are useful therapeutic agents. Their physiological activities are mediated by two types of receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs). RARs, as well as several related receptors, require heterodimerization with RXRs for effective DNA binding and function. However, in the presence of 9-cis-retinoic acid, a ligand for both RARs and RXRs, RXRs can also form homodimers. A series of retinoids is reported that selectively activates RXR homodimers but does not affect RAR-RXR heterodimers and thus demonstrates that both retinoid response pathways can be independently activated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lehmann, J M -- Jong, L -- Fanjul, A -- Cameron, J F -- Lu, X P -- Haefner, P -- Dawson, M I -- Pfahl, M -- CA50676/CA/NCI NIH HHS/ -- P01 CA51993/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1944-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center, La Jolla Cancer Research Foundation, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1335166" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Kinetics ; Macromolecular Substances ; Molecular Structure ; Receptors, Cell Surface/drug effects/genetics/*metabolism ; *Receptors, Retinoic Acid ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Retinoids/chemistry/*metabolism/pharmacology ; Structure-Activity Relationship ; *Transcription Factors ; Transcription, Genetic ; Transfection ; Tretinoin/metabolism/pharmacology
    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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