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

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An update on nuclear calcium signalling

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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