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Guillaume Bompard¹ and Emmanuelle Caron²

¹ School of Biosciences, Division of Molecular Cell Biology, University of Birmingham, Birmingham B15 2TT, England, UK
² Centre for Molecular Microbiology and Infection and Department of Biological Sciences, Imperial College London, London SW7 2AZ, England, UK

Address correspondence to Guillaume Bompard, School of Biosciences, Division of Molecular Cell Biology, University of Birmingham, Birmingham B15 2TT, England, UK. Tel.: 44-121-414-2508. Fax: 44-121-414-5925. email: G.Bompard{at}bham.ac.uk

Abstract
Despite their homology, the regulation of WASP and WAVE, activators of Arp2/3-dependent actin polymerization, has always been thought to be different. Several recent studies have revealed new aspects of their regulation, highlighting its complexity and the crucial role of post-translational modifications. New data also suggest additional functions for WASP family proteins, pushing us to reconsider existing models.

Abbreviations used in this paper: Abi, Abl interactor; GBD, GTPase binding domain; Nap1, Nck-associated protein; PIR121, p53 inducible messenger RNA; SCAR, suppressor of cAMP receptor; WASP, WAVE, WASP family verprolin homologous; Wiskott-Aldrich syndrome protein; WHD, WASP homology domain.

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