Background:

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.

Classification:

Primary antibody

Alternative names:

WAS; IMD2; Wiskott-Aldrich syndrome protein; WASp

Species reactivity:

Human;Mouse

Host:

Rabbit

Isotype:

IgG

Immunogen:

The antiserum was produced against synthesized peptide derived from human WASP. AA range:256-305

Concentration:

1 mg/ml

Molecular weight:

52913

Applications:

WB, IHC-p, ELISA

Storage:

-20°C for one year

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