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    Online-Ressource
    Online-Ressource
    Ovid Technologies (Wolters Kluwer Health) ; 1986
    In:  Circulation Research Vol. 59, No. 1 ( 1986-07), p. 110-114
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 59, No. 1 ( 1986-07), p. 110-114
    Kurzfassung: Recent evidence indicates that different forms of stress, including hypoxia, can induce specific proteins called heat-shock or stress proteins in various types of mammalian cells. These studies examined whether myocardial ischemia can result in increased levels of proteins with molecular weight and isoelectric point characteristics similar to those described for heat-shock or stress proteins. The left anterior descending coronary artery of the dog heart was completely occluded; normal and ischemic myocardial samples were obtained 6 hours after occlusion; and total cardiac proteins and RNA were prepared. Ribonucleic acid was translated in vitro in a modified rabbit reticulocyte lysate system, and [35S]-methionine-labe lled translational products as well as unlabelled cardiac proteins were separated by two-dimensional gel electrophoresis. Total proteins were visualized by silver staining and in vitro translation products quantified by fluorometry. A translatable mRNA coding for a 71,000 dalton peptide with an isoelectric point of 5.8 was markedly increased in the ischemic myocardium after 6 hours of ischemia. A protein with similar migration characteristics was detected in ischemic myocardium but not in normal myocardium. These results indicate that an mRNA coding for a translational product with similar migration characteristics of heat-shock protein 71 is induced by ischemia in the dog heart.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 1986
    ZDB Id: 1467838-X
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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