Anti-Human WAS Antibody Pair

Product Description: The Wiskott-Aldrich Syndrome Protein (WASP) is a key actin nucleation-promoting factor that regulates the dynamics of the actin cytoskeleton through activation of the Arp2/3 complex. WASP facilitates the formation of branched actin filaments, crucial for cellular processes such as endocytosis, cell migration, and immune synapse formation. Its activity is tightly regulated by interactions with Rho-family GTPases and its conserved WH2-Central-Acidic (WCA) domain, which binds actin monomers and the Arp2/3 complex. WASP's efficiency in actin nucleation varies among family members due to differences in their acidic C-terminal residues, influencing the architecture of actin networks they produce. Mutations in the WAS gene disrupt normal WASP function, leading to diseases like Wiskott-Aldrich Syndrome (WAS), an X-linked disorder characterized by immune deficiencies, thrombocytopenia, and eczema. These mutations often result in unregulated actin polymerization, impairing hematopoietic cell functions and increasing susceptibility to infections. Protein Function: Effector protein for Rho-type GTPases that regulates actin filament reorganization via its interaction with the Arp2/3 complex (PubMed:12235133, PubMed:12769847, PubMed:16275905). Important for efficient actin polymerization (PubMed:12235133, PubMed:16275905, PubMed:8625410). Possible regulator of lymphocyte and platelet function (PubMed:9405671). Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria (PubMed:18650809). In addition to its role in the cytoplasmic cytoskeleton, also promotes actin polymerization in the nucleus, thereby regulating gene transcription and repair of damaged DNA (PubMed:20574068). Promotes homologous recombination (HR) repair in response to DNA damage by promoting nuclear actin polymerization, leading to drive motility of double-strand breaks (DSBs) (PubMed:29925947) [The Uniprot Consortium]