Characterization of beta subunit modulation of a rabbit cardiac L-type Ca2+ channel alpha 1 subunit as expressed in mouse L cells.
Characterization of beta subunit modulation of a rabbit cardiac L-type Ca2+ channel alpha 1 subunit as expressed in mouse L cells.
复制标题
小鼠 L 细胞中表达的兔心脏 L 型 Ca2 通道 α 1 亚基的 β 亚基调节的表征。
DOI：
10.1016/0014-5793(93)81156-t
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发表时间：
1993
期刊：
影响因子：
3.5
通讯作者：
Schwartz,A
中科院分区：
文献类型：
--
作者：
Lory,P;Varadi,G;Slish,DF;Varadi,M;Schwartz,A
采用膜片钳技术在小鼠L细胞中研究了兔心脏α 1Ca 2+通道亚基（CARDα1）的功能特性，L细胞是一种缺乏任何Ca 2+通道亚基的受体细胞系。对稳定转染CARDα 1亚基以及与骨骼肌来源的β亚基（CARDα1β）共表达的细胞系进行了表征。结果表明，虽然CARDα1-Ca 2+通道活性可忽略不计，但在β亚基存在下，Ba 2+电流密度显著增加（2 × 10-倍）。CARDα1-和CARDα1β-Ba 2+电流均对1，4-二氢吡啶（DHP）激动剂Bay K 8644敏感（增加5至8倍）。CARDα1-和CARDα1β-Ba 2+电流的激活动力学相当。CARDα1β）-Ba 2+电流的失活时间过程更快（3 - 4倍）。我们的结论是，β亚基在心脏中的主要作用是调节L-型电流密度，并提出了几条证据表明，SKMα 1和CARDα 1是由β亚基的差异调节。
Functional properties of a rabbit cardiac α1Ca2+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 CARDα1subunit 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 SKMα1and CARDα1are differentially regulated by the β subunit.