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Human Molecular Genetics, 2002, Vol. 11, No. 20 2377-2384
© 2002 Oxford University Press

Molecular genetics of calcium sensing in bone cells

Jesús Purroy1 and Nigel K. Spurr2,*

1Discovery Genetics, GlaxoSmithKline, New Frontiers Science Park, Harlow, Essex CM19 5AW, UK and 2Discovery Genetics, GlaxoSmithKline, Five Moore Drive, PO Box 13398, Research Triangle Park, NC 27709, USA

Received August 1, 2002; Accepted August 5, 2002

The molecular mechanisms regulating bone remodelling are only partially understood. One of the controversial issues discussed during the past few years is the role that calcium signalling plays in this process and, in particular, in the functioning of the osteoclast. Calcium is involved in the recruitment and activation of osteoclasts and their subsequent detachment from bone. Parathyroid hormone and vitamin D are part of a systemic mechanism regulating calcium availability, storage and disposal. But there are conflicting results suggesting the presence of a local calcium-sensing mechanism in osteoclasts, in osteoblasts or in both. If this system could be characterized, it would be of therapeutic relevance for diseases such as postmenopausal osteoporosis and rheumatoid arthritis. Genetic data, animal models and cell-based assays have not yet been used to their full extent in this area. Here we review the available data and outline possible future strategies.

* To whom correspondence should be addressed. Tel.: +1 9194833435; Fax: +1 9193154174; Email: nigel_k_spurr{at}gsk.com


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