Previous Article | Next Article ![]()
Molecular and Cellular Biology, February 2003, p. 826-830, Vol. 23, No. 3
0270-7306/03/$08.00+0 DOI: 10.1128/MCB.23.3.826-830.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Department of Immunology and Molecular Pathology, Windeyer Institute of Medical Sciences, University College London, London W1T 4JF,1 Centre for Molecular Medicine, The Rayne Institute, London WC1E 6JJ, United Kingdom2
Received 10 June 2002/ Returned for modification 31 July 2002/ Accepted 7 November 2002
Grancalcin, one of the penta-EF-hand Ca2+ binding proteins, is expressed at high levels in polymorphonuclear granulocytes (neutrophils). EF-hand proteins are implicated in the regulation of diverse processes including cell migration, apoptosis, and mobilization of neutrophil effector functions. To determine the role of grancalcin in vivo, we inactivated the gene encoding grancalcin (Gca) in embryonic stem cells and generated grancalcin-deficient mice. Homozygous Gca mutants appeared healthy and reproduced normally. Leukocyte recruitment into the peritoneal cavity upon induction of inflammation was not significantly affected by the absence of grancalcin. The mutants also resisted systemic fungal infection similarly to wild-type mice, and in vitro killing of Staphylococcus aureus by inflammatory cells was not significantly impaired. While marginally increased survival rates of mutants faced with endotoxic shock may indicate a contribution of grancalcin to immunopathogenesis, it is not essential for vital leukocyte effector functions required to control microbial infections.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»