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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-09-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, P -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1466-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Sir William Dunn School of Pathology, Oxford OX2 3RE, UK. peter.cook@path.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750117" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Nucleus/*metabolism ; *DNA Replication ; *Genome ; Genome, Human ; Humans ; Models, Biological ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1999-06-12
    Beschreibung: Models for replication and transcription often display polymerases that track like locomotives along their DNA templates. However, recent evidence supports an alternative model in which DNA and RNA polymerases are immobilized by attachment to larger structures, where they reel in their templates and extrude newly made nucleic acids. These polymerases do not act independently; they are concentrated in discrete "factories," where they work together on many different templates. Evidence for models involving tracking and immobile polymerases is reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, P R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1790-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. Peter.Cook@Path.OX.AC.UK〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364545" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *DNA Replication ; DNA-Directed DNA Polymerase/*metabolism ; DNA-Directed RNA Polymerases/*metabolism ; Humans ; Models, Genetic ; Replication Origin ; Templates, Genetic ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1998-01-10
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook-Deegan, R M -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):560-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381158" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Specimen Banks ; *Cloning, Molecular ; Insulin/*genetics ; *Patents as Topic ; Rats
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-02-21
    Beschreibung: Phototransduction in Drosophila occurs through the ubiquitous phosphoinositide-mediated signal transduction system. Major unresolved questions in this pathway are the identity and role of the internal calcium stores in light excitation and the mechanism underlying regulation of Ca2+ release from internal stores. Treatment of Drosophila photoreceptors with ryanodine and caffeine disrupted the current induced by light, whereas subsequent application of calcium-calmodulin (Ca-CaM) rescued the inactivated photoresponse. In calcium-deprived wild-type Drosophila and in calmodulin-deficient transgenic flies, the current induced by light was disrupted by a specific inhibitor of Ca-CaM. Furthermore, inhibition of Ca-CaM revealed light-induced release of calcium from intracellular stores. It appears that functional ryanodine-sensitive stores are essential for the photoresponse. Moreover, calcium release from these stores appears to be a component of Drosophila phototransduction, and Ca-CaM regulates this process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnon, A -- Cook, B -- Montell, C -- Selinger, Z -- Minke, B -- EY03529/EY/NEI NIH HHS/ -- EY10852/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1119-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and the Kuhne Minerva Center for Studies of Visual Transduction, Hebrew University, Jerusalem 91120, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027311" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Genetically Modified ; Caffeine/pharmacology ; Calcium/*metabolism ; Calcium-Transporting ATPases/antagonists & inhibitors ; Calmodulin/*metabolism ; Drosophila/genetics/metabolism ; Enzyme Inhibitors/pharmacology ; In Vitro Techniques ; *Light ; Patch-Clamp Techniques ; Photoreceptor Cells, Invertebrate/drug effects/*metabolism ; Ryanodine/pharmacology ; *Signal Transduction/drug effects ; Thapsigargin/pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 1995-09-15
    Beschreibung: Macrophage inflammatory protein-1 alpha (MIP-1 alpha) is a chemokine that has pro-inflammatory and stem cell inhibitory activities in vitro. Its biologic role in vivo was examined in mice in which the gene encoding MIP-1 alpha had been disrupted. Homozygous MIP-1 alpha mutant (-/-) mice were resistant to Coxsackievirus-induced myocarditis seen in infected wild-type (+/+) mice. Influenza virus-infected -/- mice had reduced pneumonitis and delayed clearance of the virus compared with infected +/+ mice. The -/- mice had no overt hematopoietic abnormalities. These results demonstrate that MIP-1 alpha is an important mediator of virus-induced inflammation in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, D N -- Beck, M A -- Coffman, T M -- Kirby, S L -- Sheridan, J F -- Pragnell, I B -- Smithies, O -- GM20069/GM/NIGMS NIH HHS/ -- HL37001/HL/NHLBI NIH HHS/ -- R29HL46195/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 15;269(5230):1583-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599-7525, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7667639" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Viral/blood ; B-Lymphocytes/immunology ; Base Sequence ; Chemokine CCL4 ; Coxsackievirus Infections/*immunology/virology ; Cytokines/genetics/*physiology ; *Enterovirus B, Human/growth & development/immunology ; Gene Targeting ; Hematopoiesis ; *Influenza A virus/growth & development/immunology ; Lymphocyte Activation ; Macrophage Inflammatory Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Monokines/genetics/*physiology ; Myocarditis/*immunology/virology ; Neutralization Tests ; Orthomyxoviridae Infections/*immunology/virology ; Stem Cells ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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