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Brooke M. Ahern, Jonathan Satin
Citation Information: J Clin Invest. 2019;129(2):496-498. https://doi.org/10.1172/JCI125958.
Brooke M. Ahern, Jonathan Satin
Published February 1, 2019; First published January 7, 2019
Citation Information: J Clin Invest. 2019;129(2):496-498. https://doi.org/10.1172/JCI125958.
Abstract
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 CaVĪ²2-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.
Authors
Brooke M. Ahern, Jonathan Satin
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Copyright © 2020 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)
Copyright © 2020 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)