Wiskott-Aldrich syndrome protein family member 2 (WASF2)

Wiskott-Aldrich syndrome protein family member 2 (WASF2/WAVE2) is a central regulator of actin cytoskeletal dynamics and cell motility. It acts downstream of receptor kinases and small GTPases like Rac, translating spatial signals into actin nucleation via the Arp2/3 complex[1][2][3]. WASF2 is a core subunit of the WAVE regulatory complex, required for lamellipodia formation and directional migration in diverse cells. Its activity is tightly regulated by kinase-mediated phosphorylation, lipid signaling, and association with proteins such as Abi1, Nap1, PIR121, and IRSp53. WASF2 functions are vital for cell–cell junctions in epithelia, integrin activation at immune synapses, and cytotoxic effector cell activity. Pathogenic bacteria and viruses can exploit WASF2-mediated actin remodeling for invasion. Aberrant WASF2 activity promotes tumor cell motility, invasion, metastasis, and therapy resistance, making it a putative therapeutic target and biomarker in aggressive cancers[1][2][3]. In humans, it is encoded by the WASF2 gene located on chromosome 1[3]. Summary of evidence base: Information is synthesized from Harmonizome (Ma'ayan Laboratory), GeneCards, UniProtKB, NCBI Gene, and Wikipedia, which together provide genomic, molecular, and functional annotation as well as disease roles for WASF2[1][2][3][6]. No direct references to approved drug interactions were found in the provided sources.

Other names

WAVE2Actin-binding protein WASF2SCAR2Protein WAVE-2Verprolin homology domain-containing protein 2WASP family protein member 2WASF4IMD2dJ393P12.2WASP family Verprolin-homologous protein 2suppressor of cyclic-AMP receptor (WASP-family)

No approved drugs; mechanistically could be targeted to inhibit actin polymerization, cell migration, or block protein–protein interactions with Rac, Arp2/3, Abi1, Nap1, PIR121