ArticleMolecular and cellular biochemistry
Catecholamines and cardiac growth.
Article in Molecular and cellular biochemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Early postnatal changes in sarcoplasmic reticulum calcium transport function in spontaneously hypertensive rats.Molecular and cellular biochemistryArticle
- Integration of pathways that signal cardiac growth with modulation of myofilament activity.Journal of nuclear cardiology : official publication of the American Society of Nuclear CardiologyReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The present knowledge concerning the alpha- and beta-adrenergic systems in the regulation of cardiac growth and gene expression is 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 alpha-myosin heavy chain (alpha-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 alpha-MHC expression we performed transient transfection analysis with a series of alpha-MHC gene promoter-CAT constructs. We have identified a 13 bp E-box/M-CAT hybrid motif (EM element) which conferred a basal muscle specific and cAMP inducible expression of the alpha-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.