TRPM4 regulates calcium oscillations after T cell activation

被引：260

作者：

Launay, P

Cheng, H

Srivatsan, S

Penner, R

Fleig, A

Kinet, JP

机构：

[1] Harvard Univ, Sch Med, Boston, MA 02215 USA

[2] Univ Hawaii, Queens Med Ctr, Biomed Res Ctr, Lab Cell & Mol Signaling, Honolulu, HI 96813 USA

[3] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96813 USA

[4] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA

来源：

SCIENCE | 2004年 / 306卷 / 5700期

关键词：

D O I：

10.1126/science.1098845

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

TRPM4 has recently been described as a calcium-activated nonselective (CAN) cation channel that mediates membrane depolarization. However, the functional importance of TRPM4 in the context of calcium (Ca2+) signaling and its effect on cellular responses are not known. Here, the molecular inhibition of endogenous TRPM4 in T cells was shown to suppress TRPM4 currents, with a profound influence on receptor-mediated Ca2+ mobilization. Agonist-mediated oscillations in intracellutar Ca2+ concentration ([Ca2+](i)), which are driven by store-operated Ca2+ influx, were transformed into a sustained elevation in [Ca2+](i). This increase in Ca2+ influx enhanced interleukin-2 production. Thus, TRPM4-mediated depolarization modulates Ca2+ oscillations, with downstream effects on cytokine production in T lymphocytes.

引用

页码：1374 / 1377

页数：4

共 19 条

[1] Timeline - Jurkat T cells and development of the T-cell receptor signalling paradigm [J].