| First Author | Poomvanicha M | Year | 2017 |
| Journal | J Mol Cell Cardiol | Volume | 111 |
| Pages | 10-16 | PubMed ID | 28778765 |
| Mgi Jnum | J:257165 | Mgi Id | MGI:6102267 |
| Doi | 10.1016/j.yjmcc.2017.07.119 | Citation | Poomvanicha M, et al. (2017) Beta-adrenergic regulation of the heart expressing the Ser1700A/Thr1704A mutated Cav1.2 channel. J Mol Cell Cardiol 111:10-16 |
| abstractText | 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 alpha1c subunit) has been implicated as decisive for the beta-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 alpha1c protein concentration, ICa, and the beta-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. |
