WAS Antibodies, cDNA Clones Research Reagents

WAS (WASP Actin Nucleation Promoting Factor, also known as THC; IMD2; SCNX; THC1; WASP; WASPA), located on Xp11.23, is a Protein Coding gene. The gene produces a 52913 Da protein composed of 502 amino acids. The Wiskott-Aldrich syndrome (WAS) family of proteins share a similar domain structure and are involved in the transduction of signals from receptors on the cell surface to the actin cytoskeleton. Several studies show that WAS protein (WASP) plays a key role in the function of certain lymphocyte subsets. Diseases such as Wiskott-Aldrich Syndrome and Thrombocytopenia 1 are associated with WAS.

WAS Antibody (1)

    WAS cDNA Clone (15)

    WAS qPCR Primer (1)

    WAS Background

    Wiskott-Aldrich syndrome (WAS) is an X-linked primary immunodeficiency disease characterized by microthrombocytopenia, eczema, immunodeficiency, and susceptibility to lymphoid malignancy. Loss-of-function mutations in the WAS gene have been identified to cause disorders with platelet defects including WAS and X-linked thrombocytopenia. The WAS disease is caused by alterations in the WAS protein (WASP), and 80% of the missense mutations are located in the WH1 domain, the region essential for interaction with the WASP-interacting protein (WIP). It has been suggested that loss of WASP-WIP interaction is causal to the disease. Several studies show that WAS protein (WASp) plays a key role in the function of certain lymphocyte subsets. T-cell dysfunction is thought to be central to the immunodeficiency state seen in patients with the Wiskott-Aldrich syndrome.

    WAS References

    • Zhang L, et al. (2020) Faecal microbial dysbiosis in children with wiskott-aldrich syndrome. Scand J Immunol 91 (1): e12805.
    • Sarkar K, et al. (2014) Disruption of hswi/snf complexes in t cells by was mutations distinguishes x-linked thrombocytopenia from wiskott-aldrich syndrome. Blood 124 (23): 3409-3419.
    • Rajmohan R, et al. (2009) Characterization of wiskott-aldrich syndrome (was) mutants using saccharomyces cerevisiae. FEMS Yeast Res 9 (8): 1226-1235.
    • Chatchatee P, et al. (2003) A novel termination codon mutation of the was gene in a thai family with wiskott-aldrich syndrome. Int J Mol Med 12 (6): 939-941.

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