ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • Mice  (52)
  • 550 - Earth sciences
  • Models, Molecular
  • Superfluidity and superconductivity
  • 2010-2014
  • 1995-1999  (114)
  • 1995  (114)
Sammlung
Schlagwörter
Verlag/Herausgeber
Erscheinungszeitraum
  • 2010-2014
  • 1995-1999  (114)
Jahr
  • 1
    facet.materialart.
    Unbekannt
    Activation of a G protein complex by aggregation of beta-1,4-galactosyltransferase on the surface of sperm (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-09-22
    Beschreibung: Fertilization is initiated by the species-specific binding of sperm to the extracellular coat of the egg. One sperm receptor for the mouse egg is beta-1,4-galactosyltransferase (GalTase), which binds O-linked oligosaccharides on the egg coat glycoprotein ZP3. ZP3 binding induces acrosomal exocytosis through the activation of a pertussis toxin-sensitive heterotrimeric guanine nucleotide-binding protein (G protein). The cytoplasmic domain of sperm surface GalTase bound to and activated a heterotrimeric G protein complex that contained the Gi alpha subunit. Aggregation of GalTase by multivalent ligands elicited G protein activation. Sperm from transgenic mice that overexpressed GalTase had higher rates of G protein activation than did wild-type sperm, which rendered transgenic sperm hypersensitive to their ZP3 ligand. Thus, the cytoplasmic domain of cell surface GalTase appears to enable it to function as a signal-transducing receptor for extracellular oligosaccharide ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, X -- Dubois, D H -- Miller, D J -- Shur, B D -- R01 HD22590/HD/NICHD NIH HHS/ -- R01 HD23479/HD/NICHD NIH HHS/ -- T32 HD07324/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Sep 22;269(5231):1718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569899" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acrosome/physiology ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Animals ; Cell Membrane/enzymology/metabolism ; Egg Proteins/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Ligands ; Male ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; N-Acetyllactosamine Synthase/*metabolism ; Peptide Fragments/metabolism ; Pertussis Toxin ; *Receptors, Cell Surface ; Signal Transduction ; Spermatozoa/enzymology/*metabolism ; Virulence Factors, Bordetella/pharmacology ; Zona Pellucida/*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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 2
    facet.materialart.
    Unbekannt
    Impaired energy homeostasis in C/EBP alpha knockout mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-08-25
    Beschreibung: Mice homozygous for the targeted deletion of the c/ebp alpha gene, which expresses the CCAAT/enhancer-binding protein alpha (C/EBP alpha), did not store hepatic glycogen and died from hypoglycemia within 8 hours after birth. In these mutant mice, the amounts of glycogen synthase messenger RNA were 50 to 70 percent of normal and the transcriptional induction of the genes for two gluconeogenic enzymes, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, was delayed. The hepatocytes and adipocytes of the mutant mice failed to accumulate lipid and the expression of the gene for uncoupling protein, the defining marker of brown adipose tissue, was reduced. This study demonstrates that C/EBP alpha is critical for the establishment and maintenance of energy homeostasis in neonates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, N D -- Finegold, M J -- Bradley, A -- Ou, C N -- Abdelsayed, S V -- Wilde, M D -- Taylor, L R -- Wilson, D R -- Darlington, G J -- DK 45285/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 25;269(5227):1108-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652557" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipose Tissue/metabolism ; Adipose Tissue, Brown/metabolism ; Animals ; Animals, Newborn ; Blood Glucose/metabolism ; CCAAT-Enhancer-Binding Proteins ; Carrier Proteins/genetics ; DNA-Binding Proteins/genetics/*physiology ; *Energy Metabolism ; Female ; Gene Expression Regulation ; Glucose-6-Phosphatase/genetics ; Glycogen Synthase/genetics/metabolism ; Homeostasis ; Humans ; Ion Channels ; Lipid Metabolism ; Liver/metabolism ; Liver Glycogen/metabolism ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Mitochondrial Proteins ; Nuclear Proteins/genetics/*physiology ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; RNA, Messenger/metabolism ; Serum Albumin/genetics
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 3
    facet.materialart.
    Unbekannt
    Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-05-05
    Beschreibung: The aryl hydrocarbon (Ah) receptor (AHR) mediates many carcinogenic and teratogenic effects of environmentally toxic chemicals such as dioxin. An AHR-deficient (Ahr-/-) mouse line was constructed by homologous recombination in embryonic stem cells. Almost half of the mice died shortly after birth, whereas survivors reached maturity and were fertile. The Ahr-/- mice showed decreased accumulation of lymphocytes in the spleen and lymph nodes, but not in the thymus. The livers of Ahr-/- mice were reduced in size by 50 percent and showed bile duct fibrosis Ahr-/- mice were also nonresponsive with regard to dioxin-mediated induction of genes encoding enzymes that catalyze the metabolism of foreign compounds. Thus, the AHR plays an important role in the development of the liver and the immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez-Salguero, P -- Pineau, T -- Hilbert, D M -- McPhail, T -- Lee, S S -- Kimura, S -- Nebert, D W -- Rudikoff, S -- Ward, J M -- Gonzalez, F J -- P30 ES06096/ES/NIEHS NIH HHS/ -- R01 ES06811/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1995 May 5;268(5211):722-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7732381" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Female ; Gene Expression Regulation/physiology ; Immunity/*physiology ; Liver/*physiology ; Liver Cirrhosis, Experimental/genetics/pathology ; Lymphoid Tissue/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Aryl Hydrocarbon/genetics/*physiology
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 4
    facet.materialart.
    Unbekannt
    Involvement of CRAF1, a relative of TRAF, in CD40 signaling (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-03-10
    Beschreibung: CD40 is a receptor on the surface of B lymphocytes, the activation of which leads to B cell survival, growth, and differentiation. A yeast two-hybrid screen identified a gene, CRAF1, encoding a protein that interacts directly with the CD40 cytoplasmic tail through a region of similarity to the tumor necrosis factor-alpha (TNF-alpha) receptor-associated factors. Overexpression of a truncated CRAF1 gene inhibited CD40-mediated up-regulation of CD23. A region of CRAF1 was similar to the TNF-alpha receptor-associated factors TRAF1 and TRAF2 and so defined a shared TRAF-C domain that was necessary and sufficient for CD40 binding and homodimerization. The CRAF1 sequence also predicted a long amphipathic helix, a pattern of five zinc fingers, and a zinc ring finger. It is likely that other members of the TNF receptor superfamily use CRAF-related proteins in their signal transduction processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, G -- Cleary, A M -- Ye, Z S -- Hong, D I -- Lederman, S -- Baltimore, D -- 5-T32-GM07367/GM/NIGMS NIH HHS/ -- A122346/PHS HHS/ -- R01-CA55713/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1494-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7533327" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Antigens, CD/*metabolism ; Antigens, CD40 ; Antigens, Differentiation, B-Lymphocyte/*metabolism ; Humans ; Mice ; Molecular Sequence Data ; Protein Structure, Secondary ; Proteins/chemistry/genetics/*physiology ; Receptors, IgE/metabolism ; Sequence Homology, Amino Acid ; *Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; TNF Receptor-Associated Factor 3 ; Up-Regulation ; Zinc Fingers
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 5
    facet.materialart.
    Unbekannt
    Simultaneous identification of bacterial virulence genes by negative selection (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-07-21
    Beschreibung: An insertional mutagenesis system that uses transposons carrying unique DNA sequence tags was developed for the isolation of bacterial virulence genes. The tags from a mixed population of bacterial mutants representing the inoculum and bacteria recovered from infected hosts were detected by amplification, radiolabeling, and hybridization analysis. When applied to a murine model of typhoid fever caused by Salmonella typhimurium, mutants with attenuated virulence were revealed by use of tags that were present in the inoculum but not in bacteria recovered from infected mice. This approach resulted in the identification of new virulence genes, some of which are related to, but functionally distinct from, the inv/spa family of S. typhimurium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensel, M -- Shea, J E -- Gleeson, C -- Jones, M D -- Dalton, E -- Holden, D W -- New York, N.Y. -- Science. 1995 Jul 21;269(5222):400-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases and Bacteriology, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618105" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; *DNA Transposable Elements ; *Genes, Bacterial ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; *Mutagenesis, Insertional ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Salmonella Infections, Animal/*microbiology ; Salmonella typhimurium/genetics/*pathogenicity ; Sequence Tagged Sites ; Virulence/genetics
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 6
    facet.materialart.
    Unbekannt
    E5531, a pure endotoxin antagonist of high potency (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-04-07
    Beschreibung: Shock due to Gram-negative bacterial sepsis is a consequence of acute inflammatory response to lipopolysaccharide (LPS) or endotoxin released from bacteria. LPS is a major constituent of the outer membrane of Gram-negative bacteria, and its terminal disaccharide phospholipid (lipid A) portion contains the key structural features responsible for toxic activity. Based on the proposed structure of nontoxic Rhodobacter capsulatus lipid A, a fully stabilized endotoxin antagonist E5531 has been synthesized. In vitro, E5531 demonstrated potent antagonism of LPS-mediated cellular activation in a variety of systems. In vivo, E5531 protected mice from LPS-induced lethality and, in cooperation with an antibiotic, protected mice from a lethal infection of viable Escherichia coli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christ, W J -- Asano, O -- Robidoux, A L -- Perez, M -- Wang, Y -- Dubuc, G R -- Gavin, W E -- Hawkins, L D -- McGuinness, P D -- Mullarkey, M A -- New York, N.Y. -- Science. 1995 Apr 7;268(5207):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Elsai Research Institute, Andover, MA 01810-2441, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701344" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; BCG Vaccine/immunology ; Cytokines/secretion ; Drug Design ; Endotoxins/*antagonists & inhibitors ; Escherichia coli Infections/immunology ; Gram-Negative Bacteria/immunology ; Humans ; In Vitro Techniques ; Lipid A/*analogs & derivatives/chemical synthesis/chemistry/pharmacology ; Lipopolysaccharides/antagonists & inhibitors ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Moxalactam/pharmacology ; Nitric Oxide/metabolism ; Rhodobacter capsulatus/immunology ; Tumor Necrosis Factor-alpha/secretion
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 7
    facet.materialart.
    Unbekannt
    Correlation of terminal cell cycle arrest of skeletal muscle with induction of p21 by MyoD (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-02-17
    Beschreibung: Skeletal muscle differentiation entails the coordination of muscle-specific gene expression and terminal withdrawal from the cell cycle. This cell cycle arrest in the G0 phase requires the retinoblastoma tumor suppressor protein (Rb). The function of Rb is negatively regulated by cyclin-dependent kinases (Cdks), which are controlled by Cdk inhibitors. Expression of MyoD, a skeletal muscle-specific transcriptional regulator, activated the expression of the Cdk inhibitor p21 during differentiation of murine myocytes and in nonmyogenic cells. MyoD-mediated induction of p21 did not require the tumor suppressor protein p53 and correlated with cell cycle withdrawal. Thus, MyoD may induce terminal cell cycle arrest during skeletal muscle differentiation by increasing the expression of p21.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halevy, O -- Novitch, B G -- Spicer, D B -- Skapek, S X -- Rhee, J -- Hannon, G J -- Beach, D -- Lassar, A B -- F32ARO8214-01A1/AR/NIAMS NIH HHS/ -- N01-HD-6-2915/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 17;267(5200):1018-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7863327" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Carrier Proteins ; *Cell Cycle ; *Cell Cycle Proteins ; *Cell Differentiation ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinases/*antagonists & inhibitors ; Cyclins/*biosynthesis/genetics ; *DNA-Binding Proteins ; E2F Transcription Factors ; G0 Phase ; Humans ; Mice ; Microtubule-Associated Proteins/biosynthesis/genetics ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/*physiology ; RNA, Messenger/genetics/metabolism ; Retinoblastoma Protein/physiology ; Retinoblastoma-Binding Protein 1 ; Transcription Factor DP1 ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology ; *Tumor Suppressor 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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 8
    facet.materialart.
    Unbekannt
    Solution structure of a bovine immunodeficiency virus Tat-TAR peptide-RNA complex (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-11-17
    Beschreibung: The Tat protein of bovine immunodeficiency virus (BIV) binds to its target RNA, TAR, and activates transcription. A 14-amino acid arginine-rich peptide corresponding to the RNA-binding domain of BIV Tat binds specifically to BIV TAR, and biochemical and in vivo experiments have identified the amino acids and nucleotides required for binding. The solution structure of the RNA-peptide complex has now been determined by nuclear magnetic resonance spectroscopy. TAR forms a virtually continuous A-form helix with two unstacked bulged nucleotides. The peptide adopts a beta-turn conformation and sits in the major groove of the RNA. Specific contacts are apparent between critical amino acids in the peptide and bases and phosphates in the RNA. The structure is consistent with all biochemical data and demonstrates ways in which proteins can recognize the major groove of RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puglisi, J D -- Chen, L -- Blanchard, S -- Frankel, A D -- AI08591/AI/NIAID NIH HHS/ -- AI29135/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1200-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Santa Cruz 95064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502045" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Base Composition ; Base Sequence ; Gene Products, tat/*chemistry/metabolism ; Hydrogen Bonding ; Immunodeficiency Virus, Bovine/*chemistry ; Magnetic Resonance Spectroscopy ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; Protein Conformation ; Protein Structure, Secondary ; RNA, Viral/*chemistry/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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 9
    facet.materialart.
    Unbekannt
    Early-onset epilepsy and postnatal lethality associated with an editing-deficient GluR-B allele in mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-12-08
    Beschreibung: The arginine residue at position 586 of the GluR-B subunit renders heteromeric alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-sensitive glutamate receptor channels impermeable to calcium. The codon for this arginine is introduced at the precursor messenger RNA (pre-mRNA) stage by site-selective adenosine editing of a glutamine codon. Heterozygous mice engineered by gene targeting to harbor an editing-incompetent GluR-B allele synthesized unedited GluR-B subunits and, in principal neurons and interneurons, expressed AMPA receptors with increased calcium permeability. These mice developed seizures and died by 3 weeks of age, showing that GluR-B pre-mRNA editing is essential for brain function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brusa, R -- Zimmermann, F -- Koh, D S -- Feldmeyer, D -- Gass, P -- Seeburg, P H -- Sprengel, R -- New York, N.Y. -- Science. 1995 Dec 8;270(5242):1677-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502080" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Base Sequence ; Calcium/metabolism ; Epilepsy/*genetics/pathology ; Gene Targeting ; Glutamic Acid/metabolism ; Heterozygote ; Hippocampus/pathology ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Degeneration ; Neurons/*metabolism ; Polymerase Chain Reaction ; Purkinje Cells/metabolism ; Pyramidal Cells/metabolism ; *RNA Editing ; RNA Precursors/genetics/metabolism ; Receptors, AMPA/chemistry/*genetics/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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 10
    facet.materialart.
    Unbekannt
    Potentiated necrosis of cultured cortical neurons by neurotrophins (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-04-28
    Beschreibung: The effects of neurotrophins on several forms of neuronal degeneration in murine cortical cell cultures were examined. Consistent with other studies, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 all attenuated the apoptotic death induced by serum deprivation or exposure to the calcium channel antagonist nimodipine. Unexpectedly, however, 24-hour pretreatment with these same neurotrophins markedly potentiated the necrotic death induced by exposure to oxygen-glucose deprivation or N-methyl-D-aspartate. Thus, certain neurotrophins may have opposing effects on different types of death in the same neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Gwag, B J -- Lobner, D -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/7725105" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis/drug effects ; Brain-Derived Neurotrophic Factor ; Calcium/metabolism ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; Dizocilpine Maleate/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Necrosis ; Nerve Degeneration/*drug effects ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/pharmacology ; Neurons/*cytology/drug effects/pathology ; Neurotrophin 3 ; Quinoxalines/pharmacology ; Receptors, AMPA/antagonists & inhibitors
    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
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...