GO curators for mouse genes have assigned the following annotations to the gene product of Was. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known. [provided by RefSeq, Jul 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Was
participates in the following biological processes:
Benesch S et al. (2002) Phosphatidylinositol 4,5-biphosphate (PIP2)-induced vesicle movement depends on N-WASP and involves Nck, WIP, and Grb2. J Biol Chem, 277:37771-6. (PubMed:12147689)
Krawczyk C et al. (2000) Cbl-b is a negative regulator of receptor clustering and raft aggregation in T cells. Immunity, 13:463-73. (PubMed:11070165)
Ma T et al. (2008) Dramatic inhibition of osteoclast sealing ring formation and bone resorption in vitro by a WASP-peptide containing pTyr294 amino acid. J Mol Signal, 3:4. (PubMed:18289379)
Round JL et al. (2005) Dlgh1 coordinates actin polymerization, synaptic T cell receptor and lipid raft aggregation, and effector function in T cells. J Exp Med, 201:419-30. (PubMed:15699074)
Vignal E et al. (2000) Characterization of TCL, a new GTPase of the rho family related to TC10 andCcdc42. J Biol Chem, 275:36457-64. (PubMed:10967094)