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 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.
| Original language | English |
|---|---|
| Pages (from-to) | 496-498 |
| Number of pages | 3 |
| Journal | Journal of Clinical Investigation |
| Volume | 129 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 1 2019 |
Bibliographical note
Publisher Copyright:© 2018 American Society for Clinical Investigation.All right reserved.
Funding
This work is supported by NIH grant HL131782 and grant T32 GM118292 (to BMA).
| Funders | Funder number |
|---|---|
| National Institutes of Health (NIH) | T32 GM118292 |
| National Heart, Lung, and Blood Institute (NHLBI) | R01HL131782 |
ASJC Scopus subject areas
- General Medicine
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