Applications: WB, ELISA, Flow, IHC, IHC-P, CyTOF-ready
Host: Mouse Monoclonal
Species: Hu, Mu
Applications: WB, ICC
Host: Goat Polyclonal
Applications: WB, ELISA, PA
Applications: RNAi, RNAi SP
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.
Bioinformatics Tool for WASP
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|"Actin the Fool" about Cytoskeleton Structure
Actins are highly conserved, commonly found and abundant proteins involved in several types of cell motility as well as cytoskeleton maintenance. In vertebrate species, three main groups of actin isoforms, the alpha, beta and gamma, have been identifi... Read more.