WASL (gene)
Template:PBB Wiskott-Aldrich syndrome-like, also known as WASL, is a human gene.[1]
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. The WASL gene product is a homolog of WAS protein, however, unlike the latter, it is ubiquitously expressed and shows highest expression in neural tissues. It has been shown to bind Cdc42 directly, and induce formation of long actin microspikes.[1]
Interactions
WASL (gene) has been shown to interact with RHOQ,[2] NCK1,[3] Profilin 1,[4][5] Cortactin[6] and CDC42.[7][8]
References
- ^ a b "Entrez Gene: WASL Wiskott-Aldrich syndrome-like".
- ^ Abe, Tomoyuki (2003). "Small GTPase Tc10 and its homologue RhoT induce N-WASP-mediated long process formation and neurite outgrowth". J. Cell. Sci. 116 (Pt 1). England: 155–68. ISSN 0021-9533. PMID 12456725.
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ignored (help)CS1 maint: year (link) - ^ Rohatgi, R (2001). "Nck and phosphatidylinositol 4,5-bisphosphate synergistically activate actin polymerization through the N-WASP-Arp2/3 pathway". J. Biol. Chem. 276 (28). United States: 26448–52. doi:10.1074/jbc.M103856200. ISSN 0021-9258. PMID 11340081.
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ignored (help)CS1 maint: unflagged free DOI (link) CS1 maint: year (link) - ^ Mimuro, H (2000). "Profilin is required for sustaining efficient intra- and intercellular spreading of Shigella flexneri". J. Biol. Chem. 275 (37). UNITED STATES: 28893–901. doi:10.1074/jbc.M003882200. ISSN 0021-9258. PMID 10867004.
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