|Application ||WB, IHC|
|Calculated MW||52913 Da|
|Other Names||Wiskott-Aldrich syndrome protein, WASp, WAS, IMD2|
|Target/Specificity||A synthetic peptide corresponding to residues near the C-terminus of human WASP was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||WASP Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria.|
|Cellular Location||Cytoplasm, cytoskeleton.|
|Tissue Location||Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen|
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Provided below are standard protocols that you may find useful for product applications.
The Wiskott-Aldrich syndrome (WAS) is an X-chromosome-linked recessive disease characterized by eczema, thrombocytopenia, and immunodeficiency (1). WAS is an immunodeficiency disorder with the most severe pathology in the T lymphocytes and platelets. The disease arises from mutations in the gene encoding the WAS protein (WASP). T lymphocytes of affected males with WAS exhibit a severe disturbance of the actin cytoskeleton, suggesting that the WASP could regulate its organization. Data suggest that the WASP might function as a signal transduction adaptor downstream of Cdc42, and in affected males, the cytoskeletal abnormalities may result from a defect in Cdc42 signaling (2). WASP is a key regulator of the Arp2/3 complex and the actin cytoskeleton in hematopoietic cells. WASP is capable of forming an auto-inhibited conformation, which can be disrupted by binding of Cdc42 and phosphatidylinositol 4,5-bisphosphate, leading to its activation. Stimulation of the collagen receptor on platelets and crosslinking the B-cell receptor induce tyrosine phosphorylation of WASP (3).
1. Smith FJ, et al. Biochem Biophys Res Commun. 297(4):818-27, 2002.
2. Adley BP, et al. Anal Qnt Cytol Histol 28(4):228-36, 2006
3. Coons SW, et al. Endocr Pathol 16(3):201-10, 2005
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