Phospholipase C-γ is required for agonist-induced Ca2+ entry

被引：160

作者：

Patterson, RL

van Rossum, DB

Ford, DL

Hurt, KJ

Bae, SS

Suh, PG

Kurosaki, T

Snyder, SH ^{[1
]}

Gill, DL

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA

[4] Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA

[5] Pohang Univ Sci & Technol, Dept Life Sci, Kyungbuk 790784, South Korea

[6] Kansai Med Univ, Dept Mol Genet, Moriguchi, Osaka 5708506, Japan

来源：

CELL | 2002年 / 111卷 / 04期

关键词：

D O I：

10.1016/S0092-8674(02)01045-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We report here that PLC-gamma isoforms are required for agonist-induced Ca2+ entry (ACE). Overexpressed wild-type PLC-gamma1 or a lipase-inactive mutant PLC-gamma1 each augmented ACE in PC12 cells, while a deletion mutant lacking the region containing the SH3 domain of PLC-gamma1 was ineffective. RNA interference to deplete either PLC-gamma1 or PLC-gamma2 in PC12 and A7r5 cells inhibited ACE. In DT40 B lymphocytes expressing only PLC-gamma2, overexpressed muscarinic M5 receptors (M5R) activated ACE. Using DT40 PLC-gamma2 knockout cells, M5R stimulation of ER Ca2+ store release was unaffected, but ACE was abolished. Normal ACE was restored by transient expression of PLC-gamma2 or a lipase-inactive PLC-gamma2 mutant. The results indicate a lipase-independent role of PLC-gamma in the physiological agonist-induced activation of Ca2+ entry.

引用

页码：529 / 541

页数：13

共 59 条

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