The Wiskott-Aldrich syndrome (WAS) family of proteins
share similar domain structure, and are involved in transduction of
signals from receptors on the cell surface to the actin
cytoskeleton. The presence of a number of different motifs
suggests that they are regulated by a number of different stimuli,
and interact with multiple proteins. Recent studies have
demonstrated that these proteins, directly or indirectly, associate
with the small GTPase, Cdc42, known to regulate formation of actin
filaments, and the cytoskeletal organizing complex, Arp2/3.
Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive
disease characterized by immune dysregulation and
microthrombocytopenia, and is caused by mutations in the WAS gene.
The WAS gene product is a cytoplasmic protein, expressed
exclusively in hematopoietic cells, which show signalling and
cytoskeletal abnormalities in WAS patients. A transcript variant
arising as a result of alternative promoter usage, and containing a
different 5' UTR sequence, has been described, however, its
full-length nature is not known.1) Burns, S.O., et al. Blood 115(26):5355-5365(2010)
Immunogen
This WAS antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 205-234 amino acids from the Central region of human WAS.
Western blot analysis in K562 cell line lysates (35ug/lane).
Application Notes
For WB starting dilution is: 1:1000:
Additional Information
Form
Liquid
Storage Instructions
Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.