Commentary 10.1172/JCI125958
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
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.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.