Characterization of β subunit modulation of a rabbit cardiac L‐type Ca2+ channel α1 subunit as expressed in mouse L cells

FEBS Letters

Varadi, Gyula¹  Slish, Donald F.²  Schwartz, Arnold¹  Varadi, Marie¹  Lory, Philippe¹ 

[1] Department of Pharmacology and Cell Biophysics, University of Cincinnati, 231 Bethesda Avenue, Cincinnati, OH 45267-0575, USA;Harvard Medical School, Department of Cellular and Molecular Physiology, 25 Shattuck Street, Boston, MA 02115, USA

关键词: Mouse L cell;    Ca2+ channel expression;    Cardiac α1 subunit;    β Subunit;   

DOI  :  10.1016/0014-5793(93)81156-T

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Functional properties of a rabbit cardiac α₁ Ca²⁺ channel subunit (CARDα₁) were investigated using the patch-clamp technique in mouse L cells, a recipient cell line which is devoid of any Ca²⁺ channel subunits. Cell lines resulting from stable transfection of the CARDα₁ subunit as well as in coexpression with a β subunit (cardα₁β) derived from skeletal muscle (SKMβ) were characterized. The results show that while the CARDα₁-Ca²⁺ channel activity is negligible, the Ba²⁺ current density is dramatically increased in the presence of β subunit (2̃0-fold). CARDα₁- and CARDα₁β-Ba²⁺ currents were both sensitive to the 1,4-dihydropyridine (DHP) agonist, Bay K 8644 (5- to 8-fold increase). Activation kinetics of CARDα₁- and CARDα₁β-Ba²⁺ currents were comparable. The inactivation time-course was faster (3- to 4-fold) for CARDα₁β)-Ba²⁺ currents. We conclude that the main role of the β subunit in heart is to modulate the L-type current density and present several lines of evidence that SKMα₁ and CARDα₁ are differentially regulated by the β subunit.

【 授权许可】

Unknown