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Beta-adrenergic regulation of the heart expressing the Ser1700A/Thr1704A mutated Cav1.2 channel

Poomvanicha M, Matthes J, Domes K, Patrucco E, Angermeier E, Laugwitz KL, Schneider T, Hofmann F (2017)

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Publication Type: Journal article

Publication year: 2017

Journal

Book Volume: 111

Pages Range: 10-16

DOI: 10.1016/j.yjmcc.2017.07.119

Abstract

Beta-adrenergic stimulation of the heart increases ICa. PKA dependent phosphorylation of several amino acids (among them Ser 1700 and Thr 1704 in the carboxy-terminus of the Cav1.2 α1c subunit) has been implicated as decisive for the β-adrenergic up-regulation of cardiac ICa. Mutation of Ser 1700 and Thr 1704 to alanine results in the Cav1.2PKA_P2^−/− mice. Cav1.2PKA_P2^−/− mice display reduced cardiac L-type current. Fractional shortening and ejection fraction in the intact animal and ICa in isolated cardiomyocytes (CM) are stimulated by isoproterenol. Cardiac specific expression of the mutated Cav1.2PKA_P2^−/− gene reduces Cav1.2 α1c protein concentration, ICa, and the β-adrenergic stimulation of L-type ICa in CMs. Single channels were not detected on the CM surface of the cCav1.2PKA_P2^−/− hearts. This outcome supports the notion that S1700/1704 is essential for expression of the Cav1.2 channel and that isoproterenol stimulates ICa in Cav1.2PKA_P2^−/− CMs.

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How to cite

APA:

Poomvanicha, M., Matthes, J., Domes, K., Patrucco, E., Angermeier, E., Laugwitz, K.-L.,... Hofmann, F. (2017). Beta-adrenergic regulation of the heart expressing the Ser1700A/Thr1704A mutated Cav1.2 channel. Journal of Molecular and Cellular Cardiology, 111, 10-16. https://doi.org/10.1016/j.yjmcc.2017.07.119

MLA:

Poomvanicha, Montatip, et al. "Beta-adrenergic regulation of the heart expressing the Ser1700A/Thr1704A mutated Cav1.2 channel." Journal of Molecular and Cellular Cardiology 111 (2017): 10-16.

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