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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.
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页码:2337 / 2350
页数:14
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