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First published online July 1, 2009
doi: 10.1242/jcs.028100

Journal of Cell Science 122, 2337-2350 (2009)
Published by The Company of Biologists 2009
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Commentary

An update on nuclear calcium signalling

Martin D. Bootman1, Claire Fearnley1, Ioannis Smyrnias1, Fraser MacDonald2 and H. Llewelyn Roderick1,3,*

1 Laboratory of Molecular Signalling, The Babraham Institute, Babraham, Cambridge CB22 3AT, UK
2 KCL Dental Institute, Department of Orthodontics, St Thomas Street, London SE1 9RT, UK
3 Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK

* Authors for correspondence (e-mails: martin.bootman{at}bbsrc.ac.uk; llewelyn.roderick{at}bbsrc.ac.uk)

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.

Key words: Calcium, Gene transcription, InsP3, Nucleus, Paclitaxel, Ryanodine, Signalling, Spindle checkpoint, Taxol


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