Proteomics

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Molecular basis of b-adrenergic regulation of cardiac calcium current


ABSTRACT: Increased cardiac contractility during fight-or-flight response is caused by b-adrenergic augmentation of CaV1.2 channels. It is assumed that this iconic regulation involves phosphorylation of CaV1.2 a1/b-subunits. In transgenic murine hearts expressing fully PKA phosphorylation-deficient mutant a1C/b, this regulation persists, however, suggesting involvement of extra-channel factors. We here show that PKA up-regulates cardiac CaV1.2 channels by phosphorylating the small G-protein Rad, relieving constitutive inhibition of CaV1.2. Peroxidase-catalyzed labeling in mice hearts expressing ascorbate peroxidase conjugated-a1C or b2b with multiplexed quantitative proteomics allowed tracking of thousands of proteins in proximity of CaV1.2.

INSTRUMENT(S): Orbitrap Fusion Lumos

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TISSUE(S): Heart, Cardiac Muscle Cell

DISEASE(S): Cardiovascular System Disease,Cervix Carcinoma

SUBMITTER: Marian Kalocsay  

LAB HEAD: Marian Kalocsay

PROVIDER: PXD014499 | Pride | 2019-11-19

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
307125.mzXML Mzxml
307126.mzXML Mzxml
307779.mzXML Mzxml
307780.mzXML Mzxml
307781.mzXML Mzxml
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Publications


Increased cardiac contractility during the fight-or-flight response is caused by β-adrenergic augmentation of Ca<sub>V</sub>1.2 voltage-gated calcium channels<sup>1-4</sup>. However, this augmentation persists in transgenic murine hearts expressing mutant Ca<sub>V</sub>1.2 α<sub>1C</sub> and β subunits that can no longer be phosphorylated by protein kinase A-an essential downstream mediator of β-adrenergic signalling-suggesting that non-channel factors are also required. Here we identify the mec  ...[more]

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