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  • Rats  (229)
  • American Association for the Advancement of Science (AAAS)  (229)
  • American Institute of Physics
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  • 2010-2014  (34)
  • 1980-1984  (195)
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  • 1
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    Cardiac myosin activation: a potential therapeutic approach for systolic heart failure (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-19
    Description: Decreased cardiac contractility is a central feature of systolic heart failure. Existing drugs increase cardiac contractility indirectly through signaling cascades but are limited by their mechanism-related adverse effects. To avoid these limitations, we previously developed omecamtiv mecarbil, a small-molecule, direct activator of cardiac myosin. Here, we show that it binds to the myosin catalytic domain and operates by an allosteric mechanism to increase the transition rate of myosin into the strongly actin-bound force-generating state. Paradoxically, it inhibits adenosine 5'-triphosphate turnover in the absence of actin, which suggests that it stabilizes an actin-bound conformation of myosin. In animal models, omecamtiv mecarbil increases cardiac function by increasing the duration of ejection without changing the rates of contraction. Cardiac myosin activation may provide a new therapeutic approach for systolic heart failure.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090309/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malik, Fady I -- Hartman, James J -- Elias, Kathleen A -- Morgan, Bradley P -- Rodriguez, Hector -- Brejc, Katjusa -- Anderson, Robert L -- Sueoka, Sandra H -- Lee, Kenneth H -- Finer, Jeffrey T -- Sakowicz, Roman -- Baliga, Ramesh -- Cox, David R -- Garard, Marc -- Godinez, Guillermo -- Kawas, Raja -- Kraynack, Erica -- Lenzi, David -- Lu, Pu Ping -- Muci, Alexander -- Niu, Congrong -- Qian, Xiangping -- Pierce, Daniel W -- Pokrovskii, Maria -- Suehiro, Ion -- Sylvester, Sheila -- Tochimoto, Todd -- Valdez, Corey -- Wang, Wenyue -- Katori, Tatsuo -- Kass, David A -- Shen, You-Tang -- Vatner, Stephen F -- Morgans, David J -- 1-R43-HL-66647-1/HL/NHLBI NIH HHS/ -- R01 HL106511/HL/NHLBI NIH HHS/ -- R43 HL066647/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 18;331(6023):1439-43. doi: 10.1126/science.1200113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Preclinical Research and Development, Cytokinetics, Inc., South San Francisco, CA 94080, USA. fmalik@cytokinetics.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415352" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Actins/metabolism ; Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Adrenergic beta-Agonists/pharmacology ; Allosteric Regulation ; Animals ; Binding Sites ; Calcium/metabolism ; Cardiac Myosins/chemistry/*metabolism ; Cardiac Output/drug effects ; Dogs ; Female ; Heart Failure, Systolic/*drug therapy/physiopathology ; Isoproterenol/pharmacology ; Male ; Myocardial Contraction/*drug effects ; Myocytes, Cardiac/*drug effects/physiology ; Phosphates/metabolism ; Protein Binding ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Rats ; Rats, Sprague-Dawley ; Urea/*analogs & derivatives/chemistry/metabolism/pharmacology ; Ventricular Function, Left/drug effects
    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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    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/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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  • 3
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    Pregnenolone can protect the brain from cannabis intoxication (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-05
    Description: Pregnenolone is considered the inactive precursor of all steroid hormones, and its potential functional effects have been largely uninvestigated. The administration of the main active principle of Cannabis sativa (marijuana), Delta(9)-tetrahydrocannabinol (THC), substantially increases the synthesis of pregnenolone in the brain via activation of the type-1 cannabinoid (CB1) receptor. Pregnenolone then, acting as a signaling-specific inhibitor of the CB1 receptor, reduces several effects of THC. This negative feedback mediated by pregnenolone reveals a previously unknown paracrine/autocrine loop protecting the brain from CB1 receptor overactivation that could open an unforeseen approach for the treatment of cannabis intoxication and addiction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057431/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057431/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vallee, Monique -- Vitiello, Sergio -- Bellocchio, Luigi -- Hebert-Chatelain, Etienne -- Monlezun, Stephanie -- Martin-Garcia, Elena -- Kasanetz, Fernando -- Baillie, Gemma L -- Panin, Francesca -- Cathala, Adeline -- Roullot-Lacarriere, Valerie -- Fabre, Sandy -- Hurst, Dow P -- Lynch, Diane L -- Shore, Derek M -- Deroche-Gamonet, Veronique -- Spampinato, Umberto -- Revest, Jean-Michel -- Maldonado, Rafael -- Reggio, Patricia H -- Ross, Ruth A -- Marsicano, Giovanni -- Piazza, Pier Vincenzo -- 260515/European Research Council/International -- DA-003934/DA/NIDA NIH HHS/ -- DA-03672/DA/NIDA NIH HHS/ -- DA-09789/DA/NIDA NIH HHS/ -- K05 DA021358/DA/NIDA NIH HHS/ -- R01 DA003934/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):94-8. doi: 10.1126/science.1243985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Neurocentre Magendie, Physiopathologie de la Plasticite Neuronale, U862, F-33000 Bordeaux, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24385629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*drug effects/metabolism ; Cannabinoid Receptor Antagonists/administration & dosage ; Cannabis/*toxicity ; Dronabinol/*toxicity ; Male ; Marijuana Abuse/drug therapy ; Mice ; Mice, Inbred C57BL ; Pregnenolone/*administration & dosage/*metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptor, Cannabinoid, CB1/*agonists/*antagonists & inhibitors
    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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    Identification and rescue of alpha-synuclein toxicity in Parkinson patient-derived neurons (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-26
    Description: The induced pluripotent stem (iPS) cell field holds promise for in vitro disease modeling. However, identifying innate cellular pathologies, particularly for age-related neurodegenerative diseases, has been challenging. Here, we exploited mutation correction of iPS cells and conserved proteotoxic mechanisms from yeast to humans to discover and reverse phenotypic responses to alpha-synuclein (alphasyn), a key protein involved in Parkinson's disease (PD). We generated cortical neurons from iPS cells of patients harboring alphasyn mutations, who are at high risk of developing PD dementia. Genetic modifiers from unbiased screens in a yeast model of alphasyn toxicity led to identification of early pathogenic phenotypes in patient neurons. These included nitrosative stress, accumulation of endoplasmic reticulum (ER)-associated degradation substrates, and ER stress. A small molecule identified in a yeast screen (NAB2), and the ubiquitin ligase Nedd4 it affects, reversed pathologic phenotypes in these neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022187/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Chee Yeun -- Khurana, Vikram -- Auluck, Pavan K -- Tardiff, Daniel F -- Mazzulli, Joseph R -- Soldner, Frank -- Baru, Valeriya -- Lou, Yali -- Freyzon, Yelena -- Cho, Sukhee -- Mungenast, Alison E -- Muffat, Julien -- Mitalipova, Maisam -- Pluth, Michael D -- Jui, Nathan T -- Schule, Birgitt -- Lippard, Stephen J -- Tsai, Li-Huei -- Krainc, Dimitri -- Buchwald, Stephen L -- Jaenisch, Rudolf -- Lindquist, Susan -- 5 R01CA084198/CA/NCI NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- P50 AG005134/AG/NIA NIH HHS/ -- R01 CA084198/CA/NCI NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):983-7. doi: 10.1126/science.1245296. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Endoplasmic Reticulum Stress/drug effects ; Female ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Mutation ; Neurogenesis ; Neurons/*drug effects/metabolism/pathology ; Parkinson Disease/genetics/*metabolism ; Rats ; alpha-Synuclein/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Epidermal growth factor immunoreactive material in the central nervous system: location and development (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-08
    Description: Epidermal growth factor (EGF) is a potent mitogen with hormonal activity in the gastrointestinal tract. Material cross-reacting with EGF was detected in the central nervous system of the developing and adult albino rat by the indirect immunofluorescence technique. High concentrations of EGF-cross-reacting material were identified in forebrain and midbrain structures of pallidal areas of the brain. These include the globus pallidus, ventral pallidum, entopeduncular nucleus, substantia nigra pars reticulata, and the islands of Calleja . Thus, EGF may represent another gut-brain peptide with potential neurotransmitter-neuromodulator functions in pallidal structures of the extrapyramidal motor systems of the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fallon, J H -- Seroogy, K B -- Loughlin, S E -- Morrison, R S -- Bradshaw, R A -- Knaver, D J -- Cunningham, D D -- GM31609/GM/NIGMS NIH HHS/ -- NS16017/NS/NINDS NIH HHS/ -- NS19964/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1107-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6144184" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/growth & development/*physiology ; Epidermal Growth Factor/*physiology ; Fluorescent Antibody Technique ; Globus Pallidus/physiology ; Mitogens/physiology ; Neurotransmitter Agents/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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  • 6
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    Hypoxic coordinate regulation of mitochondrial enzymes in mammalian cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, B J -- Robin, E D -- Tapper, D P -- Wong, R J -- Clayton, D A -- 5 R01 HL23701-14/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):707-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320368" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Anaerobiosis ; Animals ; Anoxia/physiopathology ; Citrate (si)-Synthase/genetics/*metabolism ; DNA, Mitochondrial/*genetics ; Electron Transport Complex IV/genetics/*metabolism ; Macrophages/*enzymology ; Mice ; Mitochondria/*enzymology ; Mitochondria, Muscle/*enzymology ; Oxidoreductases/genetics/*metabolism ; Oxo-Acid-Lyases/*metabolism ; 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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  • 7
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    Sustained intracerebroventricular infusion of brain fuels reduces body weight and food intake in rats (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: Long-term infusion of glucose, beta-hydroxybutyrate, and glycerol into the third ventricle of the rat brain caused a stabilization of body weight at a lower than normal level. Among the glucose- and glycerol-treated animals this weight loss was caused in part by temporary hypophagia. Among the animals treated with beta-hydroxybutyrate the weight loss was unaccompanied by a reduction in food intake. The results are consistent with the view that the systems controlling food intake and body weight are sensitive to the availability of brain fuels. They are not consistent however, with the view that these control systems monitor calories independently of their source.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, J D -- Wirtshafter, D -- Asin, K E -- Brief, D -- AM 26030/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):81-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7193909" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxybutyric Acid ; Animals ; *Appetite Regulation/drug effects ; *Body Weight/drug effects ; Brain/drug effects/*physiology ; Circadian Rhythm ; Drinking/drug effects ; *Eating/drug effects ; Glucose/*pharmacology ; Glycerol/*pharmacology ; Hydroxybutyrates/administration & dosage/*pharmacology ; Hypothalamus/drug effects ; Injections, Intraventricular ; Male ; 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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  • 8
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    Hyperglycemia of diabetic rats decreased by a glucagon receptor antagonist (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-02-26
    Description: The glucagon analog [l-N alpha-trinitrophenylhistidine, 12-homoarginine]-glucagon (THG) was examined for its ability to lower blood glucose concentrations in rats made diabetic with streptozotocin. In vitro, THG is a potent antagonist of glucagon activation of the hepatic adenylate cyclase assay system. Intravenous bolus injections of THG caused rapid decreases (20 to 35 percent) of short duration in blood glucose. Continuous infusion of low concentrations of the inhibitor led to larger sustained decreases in blood glucose (30 to 65 percent). These studies demonstrate that a glucagon receptor antagonist can substantially reduce blood glucose levels in diabetic animals without addition of exogenous insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, D G -- Goebel, C U -- Hruby, V J -- Bregman, M D -- Trivedi, D -- AM21085/AM/NIADDK NIH HHS/ -- AM25318/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1982 Feb 26;215(4536):1115-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6278587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Experimental/*drug therapy ; Glucagon/*analogs & derivatives/*antagonists & inhibitors/therapeutic use ; Hyperglycemia/*drug therapy ; Male ; Rats ; Receptors, Cell Surface/*drug effects ; Receptors, Glucagon ; Structure-Activity Relationship
    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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    Progesterone administration in vivo stimulates release of luteinizing hormone-releasing hormone in vitro (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-05-30
    Description: The release of luteinizing hormone-releasing hormone (LHRH) from tissue from the mediobasal hypothalamic-anterior hypothalamic-preoptic area of prepuberal female rats was measured in a perfusion system. Measurements were also made of the concentrations of LHRH in these tissue fragments and of luteinizing hormone in serum obtained when the rats were killed. Four groups of immature rats were studied: intact, ovariectomized, ovariectomized and implanted with estradiol-containing capsules, and ovariectomized rats primed with estradiol and injected with progesterone. The release of LHRH from the tissue of ovariectomized animals was significantly less than that of intact females and was not modified when the ovariectomized rats received estradiol. However, there was a four- to fivefold increase in LHRH release from tissue of ovariectomized rats primed with estradiol when they were killed 6 hours after they received an injection of progesterone. The concentrations of LHRH in tissue and of luteinizing hormone in serum varied among groups and with the time of day that the animals were killed. The interactions among luteinizing hormone, gonadal steroids, and the photoperiod seem to set the appropriate conditions for neural processes triggering a complete and normal release of luteinizing hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramirez, V D -- Dluzen, D -- Lin, D -- New York, N.Y. -- Science. 1980 May 30;208(4447):1037-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6990489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Castration ; Circadian Rhythm ; Estradiol/pharmacology ; Female ; Gonadotropin-Releasing Hormone/*metabolism ; Hypothalamus/*metabolism ; Hypothalamus, Anterior/metabolism ; Light ; Luteinizing Hormone/blood ; Preoptic Area/metabolism ; Progesterone/*pharmacology ; Rats
    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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    Mechanism of voltage gating in potassium channels (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: The mechanism of ion channel voltage gating-how channels open and close in response to voltage changes-has been debated since Hodgkin and Huxley's seminal discovery that the crux of nerve conduction is ion flow across cellular membranes. Using all-atom molecular dynamics simulations, we show how a voltage-gated potassium channel (KV) switches between activated and deactivated states. On deactivation, pore hydrophobic collapse rapidly halts ion flow. Subsequent voltage-sensing domain (VSD) relaxation, including inward, 15-angstrom S4-helix motion, completes the transition. On activation, outward S4 motion tightens the VSD-pore linker, perturbing linker-S6-helix packing. Fluctuations allow water, then potassium ions, to reenter the pore; linker-S6 repacking stabilizes the open pore. We propose a mechanistic model for the sodium/potassium/calcium voltage-gated ion channel superfamily that reconciles apparently conflicting experimental data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jensen, Morten O -- Jogini, Vishwanath -- Borhani, David W -- Leffler, Abba E -- Dror, Ron O -- Shaw, David E -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):229-33. doi: 10.1126/science.1216533.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉D E Shaw Research, New York, NY 10036, USA. morten.jensen@DEShawResearch.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Hydrophobic and Hydrophilic Interactions ; *Ion Channel Gating ; Kv1.2 Potassium Channel/*chemistry/*metabolism ; Membrane Potentials ; Models, Biological ; Models, Molecular ; Molecular Dynamics Simulation ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Shab Potassium Channels/*chemistry/*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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