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   <subfield code="a">Catecholamines and cardiac growth</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Mahesh Gupta, Madhu Gupta, Smilja Jakovcic, Radovan Zak]</subfield>
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   <subfield code="a">The present knowledge concerning the α- and β-adrenergic systems in the regulation of cardiac growth and gene expression in reviewed. To investigate the mechanism by which CAMP regulates the expression of cardiac genes we have used cultured myocytes derived from fetal rat hearts. We have shown previously that the addition of Br cAMP to the culture medium produced an increase in α-myosin heavy chain (α-MHC) mRNA level, in its rate of transcription as well as in the amount of V1 isomyosin. To characterize the promoter element(s) involved in cAMP responsive regulation of a-MHC expression we performed transient transfection analysis with a series of α-MHC gene promoter-CAT constructs. We have identified a 13 by E-box/M-CAT hybrid motif (EM element) which conferred a basal muscle specific and cAMP inducible expression of the α-MHC gene. Using mobility shift assay we have documented that one of the EM element binding protein is TEF-1. Moreover, by incubating cardiac nuclear extracts with the catalytic subunit of PK-A we have found that factor(s) binding to the EM element is a substrate for CAMP dependent phosphorylation.</subfield>
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   <subfield code="u">Departments of Medicine (Section of Cardiology), Pharmacological and Physiological Sciences and Organismal Biology and Anatomy, The University of Chicago, 60637, IL</subfield>
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