Regulation of cardiac and smooth muscle Ca(2+) channels (Ca(V)1.2a,b) by protein kinases

K D Keef1, J R Hume, J Zhong

  • 1Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557, USA. kathy@physio.unr.edu

Insights

This review details how kinases regulate Ca(V)1.2 channels, essential for cardiac and smooth muscle contraction. It highlights recent findings on kinase regulation and specific channel sites involved.

Area of Science:

  • Physiology
  • Molecular Biology
  • Biochemistry

Background:

  • High voltage-activated Ca(2+) channels, specifically Ca(V)1.2 (L-type), are vital for excitation-contraction coupling in cardiac and smooth muscle.
  • These channels are modulated by second messenger pathways to control tissue contractile force.

Purpose of the Study:

  • To review recent advances in understanding the regulation of cardiac Ca(V)1.2a and smooth muscle Ca(V)1.2b channels by various kinases.
  • To discuss kinase-mediated regulation mechanisms and identify key amino acid residues involved.

Main Methods:

  • Literature review focusing on recent research findings.
  • Analysis of studies investigating kinase regulation of Ca(V)1.2 channels.
  • Examination of evidence on protein tyrosine kinase, calmodulin-dependent kinase, and G protein subunit interactions.

Main Results:

  • Multiple kinases, including cGMP-dependent protein kinase, cAMP-dependent protein kinase, and protein kinase C, regulate Ca(V)1.2 channel activity.
  • Recent evidence implicates protein tyrosine kinase and calmodulin-dependent kinase in channel modulation.
  • Specific amino acid residues within the channel are being identified as critical for kinase regulation.

Conclusions:

  • Kinase-dependent regulation is a key mechanism controlling Ca(V)1.2 channel function in muscle tissues.
  • Further research is identifying specific molecular targets and residues involved in this complex regulatory network.

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