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  • 1
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1999-05-21
    Beschreibung: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Structural convergence in the active sites of a family of catalytic antibodies (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1997-02-21
    Beschreibung: The x-ray structures of three esterase-like catalytic antibodies identified by screening for catalytic activity the entire hybridoma repertoire, elicited in response to a phosphonate transition state analog (TSA) hapten, were analyzed. The high resolution structures account for catalysis by transition state stabilization, and in all three antibodies a tyrosine residue participates in the oxyanion hole. Despite significant conformational differences in their combining sites, the three antibodies, which are the most efficient among those elicited, achieve catalysis in essentially the same mode, suggesting that evolution for binding to a single TSA followed by screening for catalysis lead to antibodies with structural convergence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Charbonnier, J B -- Golinelli-Pimpaneau, B -- Gigant, B -- Tawfik, D S -- Chap, R -- Schindler, D G -- Kim, S H -- Green, B S -- Eshhar, Z -- Knossow, M -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1140-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Enzymologie et de Biochimie Structurales, CNRS, 91198 Gif sur Yvette Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027317" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Catalytic/*chemistry/metabolism ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Enzyme-Linked Immunosorbent Assay ; *Evolution, Molecular ; Haptens/chemistry/metabolism ; Hydrogen Bonding ; Immunoglobulin Fab Fragments/chemistry/metabolism ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Organophosphonates/chemistry/metabolism ; *Protein Conformation ; Tyrosine/chemistry
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Role of mutant CFTR in hypersusceptibility of cystic fibrosis patients to lung infections (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-01-05
    Beschreibung: Cystic fibrosis (CF) patients are hypersusceptible to chronic Pseudomonas aeruginosa lung infections. Cultured human airway epithelial cells expressing the delta F508 allele of the cystic fibrosis transmembrane conductance regulator (CFTR) were defective in uptake of P. aeruginosa compared with cells expressing the wild-type allele. Pseudomonas aeruginosa lipopolysaccharide (LPS)-core oligosaccharide was identified as the bacterial ligand for epithelial cell ingestion; exogenous oligosaccharide inhibited bacterial ingestion in a neonatal mouse model, resulting in increased amounts of bacteria in the lungs. CFTR may contribute to a host-defense mechanism that is important for clearance of P. aeruginosa from the respiratory tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677515/" 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/PMC3677515/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pier, G B -- Grout, M -- Zaidi, T S -- Olsen, J C -- Johnson, L G -- Yankaskas, J R -- Goldberg, J B -- AI22806/AI/NIAID NIH HHS/ -- AI35674/AI/NIAID NIH HHS/ -- HL42384/HL/NHLBI NIH HHS/ -- R01 HL058398/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115-5899, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539601" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Newborn ; Cell Line, Transformed ; Cystic Fibrosis/*complications/genetics/microbiology ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics/*physiology ; Disease Susceptibility ; Epithelium/microbiology ; Humans ; Lipopolysaccharides/pharmacology ; Lung/microbiology ; Mice ; Mice, Inbred BALB C ; Pseudomonas Infections/*etiology/microbiology ; Pseudomonas aeruginosa/*physiology ; Respiratory System/*microbiology ; Respiratory Tract Infections/*etiology/microbiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1996-12-20
    Beschreibung: 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〉
    Schlagwort(e): 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-02-03
    Beschreibung: To determine if defects in the atrial natriuretic peptide (ANP) system can cause hypertension, mice were generated with a disruption of the proANP gene. Homozygous mutants had no circulating or atrial ANP, and their blood pressures were elevated by 8 to 23 millimeters of mercury when they were fed standard (0.5 percent sodium chloride) and intermediate (2 percent sodium chloride) salt diets. On standard salt diets, heterozygotes had normal amounts of circulating ANP and normal blood pressures. However, on high (8 percent sodium chloride) salt diets they were hypertensive, with blood pressures elevated by 27 millimeters of mercury. These results demonstrate that genetically reduced production of ANP can lead to salt-sensitive hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉John, S W -- Krege, J H -- Oliver, P M -- Hagaman, J R -- Hodgin, J B -- Pang, S C -- Flynn, T G -- Smithies, O -- GM20069/GM/NIGMS NIH HHS/ -- HL49277/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 3;267(5198):679-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7839143" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Atrial Natriuretic Factor/analysis/blood/*deficiency/*genetics ; *Blood Pressure ; Crosses, Genetic ; Female ; Gene Targeting ; Genotype ; Heart Atria/chemistry/ultrastructure ; Heterozygote ; Homozygote ; Hypertension/genetics/pathology/*physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Protein Precursors/*genetics ; Sodium, Dietary/*administration & dosage
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Prevention of atherosclerosis in apolipoprotein E-deficient mice by bone marrow transplantation (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-02-17
    Beschreibung: Apolipoprotein E (apoE) deficiency causes severe hyperlipidemia and atherosclerosis in humans and in gene-targeted mice. Although the majority of apoE in plasma is of hepatic origin, apoE is synthesized by a variety of cell types, including macrophages. Because macrophages derive from hematopoietic cells, bone marrow transplantation was used to examine the potential of apoE synthesized by bone marrow-derived cells to correct the hyperlipidemia and atherosclerosis caused by apoE deficiency. After transplantation of bone marrow from mice with the normal apoE gene into apoE-deficient mice, apoE was detected in serum and promoted clearance of lipoproteins and normalization of serum cholesterol levels. ApoE-deficient mice given transplants of normal bone marrow showed virtually complete protection from diet-induced atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linton, M F -- Atkinson, J B -- Fazio, S -- DK-26657-15/DK/NIDDK NIH HHS/ -- HL-02925/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 17;267(5200):1034-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-2250.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7863332" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aortic Diseases/prevention & control ; Apolipoproteins E/blood/*deficiency/genetics ; Arteriosclerosis/*prevention & control ; *Bone Marrow Transplantation ; Cholesterol/*blood ; Coronary Artery Disease/prevention & control ; Lipoproteins/*blood ; Lipoproteins, IDL ; Lipoproteins, LDL/blood ; Lipoproteins, VLDL/blood ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1998-11-13
    Beschreibung: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Postnatal sex reversal of the ovaries in mice lacking estrogen receptors alpha and beta (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1999-12-22
    Beschreibung: Mice lacking estrogen receptors alpha and beta were generated to clarify the roles of each receptor in the physiology of estrogen target tissues. Both sexes of alphabeta estrogen receptor knockout (alphabetaERKO) mutants exhibit normal reproductive tract development but are infertile. Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Mullerian inhibiting substance, sulfated glycoprotein-2, and Sox9. Therefore, loss of both receptors leads to an ovarian phenotype that is distinct from that of the individual ERKO mutants, which indicates that both receptors are required for the maintenance of germ and somatic cells in the postnatal ovary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couse, J F -- Hewitt, S C -- Bunch, D O -- Sar, M -- Walker, V R -- Davis, B J -- Korach, K S -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2328-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600740" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anti-Mullerian Hormone ; Cell Differentiation ; Clusterin ; *Disorders of Sex Development ; Estradiol/physiology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Female ; Gene Targeting ; Glycoproteins/analysis ; Growth Inhibitors/analysis ; High Mobility Group Proteins/analysis ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; *Molecular Chaperones ; Ovary/*anatomy & histology/cytology/growth & development/*physiology ; Receptors, Estrogen/genetics/*physiology ; SOX9 Transcription Factor ; Seminiferous Tubules/anatomy & histology/cytology ; Sertoli Cells/cytology ; Signal Transduction ; Testicular Hormones/analysis ; Testis/anatomy & histology/cytology/growth & development/physiology ; Transcription Factors/analysis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Congenital heart disease caused by mutations in the transcription factor NKX2-5 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1998-07-04
    Beschreibung: Mutations in the gene encoding the homeobox transcription factor NKX2-5 were found to cause nonsyndromic, human congenital heart disease. A dominant disease locus associated with cardiac malformations and atrioventricular conduction abnormalities was mapped to chromosome 5q35, where NKX2-5, a Drosophila tinman homolog, is located. Three different NKX2-5 mutations were identified. Two are predicted to impair binding of NKX2-5 to target DNA, resulting in haploinsufficiency, and a third potentially augments target-DNA binding. These data indicate that NKX2-5 is important for regulation of septation during cardiac morphogenesis and for maturation and maintenance of atrioventricular node function throughout life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schott, J J -- Benson, D W -- Basson, C T -- Pease, W -- Silberbach, G M -- Moak, J P -- Maron, B J -- Seidman, C E -- Seidman, J G -- New York, N.Y. -- Science. 1998 Jul 3;281(5373):108-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9651244" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Atrioventricular Node/physiopathology ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; Codon ; Female ; Genes, Dominant ; Genetic Linkage ; Heart Block/*genetics/physiopathology ; Heart Septal Defects, Atrial/*genetics/physiopathology ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Pedigree ; Protein Biosynthesis ; Transcription Factors/*genetics/metabolism ; *Xenopus Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Mediation of neuronal apoptosis by enhancement of outward potassium current (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1997-10-06
    Beschreibung: Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, 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/9311914" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis/drug effects ; Benzopyrans/pharmacology ; Calcium/metabolism ; Cerebral Cortex/cytology ; Cromakalim ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Gadolinium/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/metabolism ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/drug effects/*metabolism ; Pyrroles/pharmacology ; Staurosporine/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Veratridine/pharmacology
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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