An update on nuclear calcium signalling

被引:159
作者
Bootman, Martin D. [1 ]
Fearnley, Claire [1 ]
Smyrnias, Ioannis [1 ]
MacDonald, Fraser [2 ]
Roderick, H. Llewelyn [1 ,3 ]
机构
[1] Babraham Inst, Mol Signalling Lab, Cambridge CB22 3AT, England
[2] KCL Dent Inst, Dept Orthodont, London SE1 9RT, England
[3] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1PD, England
基金
英国生物技术与生命科学研究理事会;
关键词
Calcium; Gene transcription; InsP(3); Nucleus; Paclitaxel; Ryanodine; Signalling; Spindle checkpoint; Taxol; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; PHOSPHOLIPASE-C; PORE COMPLEX; CA2+ OSCILLATIONS; CYTOSOLIC CA2+; CYTOPLASMIC CALCIUM; RYANODINE RECEPTORS; CALMODULIN COMPLEX; INSP(3) RECEPTOR; PLASMA-MEMBRANE;
D O I
10.1242/jcs.028100
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Over the past 15 years or so, numerous studies have sought to characterise how nuclear calcium (Ca2+) signals are generated and reversed, and to understand how events that occur in the nucleoplasm influence cellular Ca2+ activity, and vice versa. In this Commentary, we describe mechanisms of nuclear Ca2+ signalling and discuss what is known about the origin and physiological significance of nuclear Ca2+ transients. In particular, we focus on the idea that the nucleus has an autonomous Ca2+ signalling system that can generate its own Ca2+ transients that modulate processes such as gene transcription. We also discuss the role of nuclear pores and the nuclear envelope in controlling ion flux into the nucleoplasm.
引用
收藏
页码:2337 / 2350
页数:14
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