ArticleChannels (Austin, Tex.)
AKAP79 modulation of L-type channels involves disruption of intramolecular interactions in the CaV1.2 subunit.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Pathogenicity of de novo CACNA1D CaEuropean journal of human genetics : EJHG · 2024Article
- Compartmentalized cAMP signalling and control of cardiac rhythm.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Rapid Turnover of the Cardiac L-Type CaiScience · 2018Article
- Molecular mimicking of C-terminal phosphorylation tunes the surface dynamics of CaThe Journal of biological chemistry · 2018Article
- A systems biology analysis of brain microvascular endothelial cell lipotoxicity.BMC systems biology · 2014Article
- C-terminal modulatory domain controls coupling of voltage-sensing to pore opening in Cav1.3 L-type Ca(2+) channels.Biophysical journal · 2014Article
- L-type CaWiley interdisciplinary reviews. Membrane transport and signaling · 2014Article
- What can naturally occurring mutations tell us about Ca(v)1.x channel function?Biochimica et biophysica acta · 2013Review
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- L-type Ca2+ channel function during Timothy syndrome.Trends in cardiovascular medicine · 2012Review
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Authors and funding
9 authors.
Funding
Abstract
L-type voltage gated calcium channels (VGCCs) interact with a variety of proteins that modulate both their function and localization. A-Kinase Anchoring Proteins (AKAPs) facilitate L-type calcium channel phosphorylation through β adrenergic stimulation. Our previous work indicated a role of neuronal AKAP79/150 in the membrane targeting of Ca(V)1.2 L-type calcium channels, which involved a proline rich domain (PRD) in the intracellular II-III loop of the channel.(1) Here, we show that mutation of proline 857 to alanine (P857A) into the PRD does not disrupt the AKAP79-induced increase in Ca(v)1.2 membrane expression. Furthermore, deletion of two other PRDs into the carboxy terminal domain of Ca(V)1.2 did not alter the targeting role of AKAP79. In contrast, the distal carboxy terminus region of the channel directly interacts with AKAP79. This protein-protein interaction competes with a direct association of the channel II-III linker on the carboxy terminal tail and modulates membrane targeting of Ca(V)1.2. Thus, our results suggest that the effects of AKAP79 occur through relief of an autoinhibitory mechanism mediated by intramolecular interactions of Ca(v)1.2 intracellular regions.
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