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 Ca V β 2 -Ca V 1.2 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.
|Number of pages||3|
|Journal||Journal of Clinical Investigation|
|State||Published - Feb 1 2019|
Bibliographical noteFunding Information:
This work is supported by NIH grant HL131782 and grant T32 GM118292 (to BMA).
© 2018 American Society for Clinical Investigation.All right reserved.
ASJC Scopus subject areas
- Medicine (all)