RETRACTED: Requirement of voltage-gated calcium channel β4 subunit for T lymphocyte functions (Retracted Article. See vol 310, pg 1903, 2005)

被引:19
作者
Badou, A
Basavappa, S
Desai, R
Peng, YQ
Matza, D
Mehal, WZ
Kaczmarek, LK
Boulpaep, EL
Flavell, RA [1 ]
机构
[1] Yale Univ, Sch Med, Howard Hughes Med Inst, Immunobiol Sect, New Haven, CT 06510 USA
[2] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06510 USA
[3] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA
[4] Univ Rochester, Sch Med, Dept Med Pharmacol & Physiol, Digest Dis Unit, Rochester, NY 14627 USA
关键词
D O I
10.1126/science.1100582
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
Calcium is known to play vital roles in diverse physiological processes, and it is known that voltage-gated calcium channels (Ca-v) mediate calcium influx in excitable cells. However, no consensus exists on the molecular identity of the calcium channels present in nonexcitable cells such as T lymphocytes. Here, we demonstrate that T lymphocytes express both regulatory beta(4) and pore-forming Ca(v)1 alpha(1) subunits of Ca-v channels. Ca-v beta(4)-mutant T lymphocytes fail to acquire normal functions and display impairment in the calcium response, activation of the transcription factor NFAT, and cytokine production. Although Ca(v)1 channels of lymphocytes retain their voltage dependency, T cell receptor stimulation dramatically increases channel opening, providing a new mechanism for calcium entry in lymphocytes.
引用
收藏
页码:117 / 121
页数:5
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