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WASP Antibody

Rabbit Monoclonal Antibody

  • WB - WASP Antibody AJ1819b
    A. Western blot analysis on (A) TF-1 and (B) U937 cell lysate using anti-WASP RabMAb (Cat. #AJ1819b), dilution 1:50,000.
  • IHC - WASP Antibody AJ1819b
    B. Immunohistochemical analysis ofparaffin-embedded human spleen using anti-WASP RabMAb (Cat. #AJ1819b).
Product Information
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
Primary Accession P42768
Reactivity Human
Host Rabbit
Clonality Monoclonal
Clone Names EP2541Y
Calculated MW 52913 Da
Gene ID 7454
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.
Dilution WB~~1:10000~50000
Format 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
StorageMaintain 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.
PrecautionsWASP Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name WAS
Synonyms IMD2
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
Research Areas
Citations (0)

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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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Cat# AJ1819b
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