We tested the hypothesis that specific isoforms of protein kinase C (PKC) are responsible for modulation of Na+ current (I Na) derived from the human cardiac Na+ channel using activators and inhibitors selective for specific PKCs. Experimental results demonstrated that I Na suppression was mediated by activation of conventional PKCs (cPKCs) and possibly resulted from channel internalization. In the presence of cPKC inhibition, phorbol ester application unexpectedly increased Na+ current, an effect eliminated by inhibition of protein kinase A. These findings demonstrate complex modulation of cardiac I Na by protein kinases and provide further evidence that PKC isoforms have distinct protein targets.
Conventional protein kinase C isoforms and cross‐activation of protein kinase A regulate cardiac Na+ current
Published 2001 in FEBS Letters
ABSTRACT
PUBLICATION RECORD
- Publication year
2001
- Venue
FEBS Letters
- Publication date
2001-04-27
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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