Commentary 10.1172/JCI125958

The L-type calcium channel current modulation mechanism: the plot thickens and fogs

Brooke M. Ahern and Jonathan Satin

Department of Physiology, University of Kentucky College of Medicine, Lexington, Kentucky, USA.

Address correspondence to: Jonathan Satin, Department of Physiology, University of Kentucky College of Medicine, 800 Rose Street, Lexington, Kentucky 40536-0298, USA. Phone: 859.323.5356. Email: jsatin1@uky.edu.

Find articles by Ahern, B. in: JCI | PubMed | Google Scholar

Department of Physiology, University of Kentucky College of Medicine, Lexington, Kentucky, USA.

Address correspondence to: Jonathan Satin, Department of Physiology, University of Kentucky College of Medicine, 800 Rose Street, Lexington, Kentucky 40536-0298, USA. Phone: 859.323.5356. Email: jsatin1@uky.edu.

Find articles by Satin, J. in: JCI | PubMed | Google Scholar |

First published January 7, 2019 - More info

Published in Volume 129, Issue 2 on February 1, 2019
J Clin Invest. 2019;129(2):496–498. https://doi.org/10.1172/JCI125958.
Copyright © 2019, American Society for Clinical Investigation
First published January 7, 2019 - Version history

Stressful situations provoke the fight-or-flight response, incurring rapid elevation of cardiac output via activation of protein kinase A (PKA). In this issue of the JCI, Yang et al. focus on the L-type calcium channel complex (LTCC), and their findings require reexamination of dogmatic principles. LTCC phosphorylation sites identified and studied to date are dispensable for PKA modulation of LTCC; however, a CaVβ2-CaV1.2 calcium channel interaction is now shown to be required. Yang et al. suggest a new hypothesis that LTCC modulation involves rearrangement of auxiliary proteins within the LTCC. However, we still do not know the targets of PKA that mediate LTCC modulation.

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