Background：Wiskott-Aldrich syndrome(WAS) Homo sapiens 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 t
仕様
サイズ：100ul
Source：Rabbit
Applications：WB,IHC-p,ELISA
Species reactivity：Human,Mouse
Immunogen：The antiserum was produced against synthesized peptide derived from human WASP around the phosphorylation site of Tyr290. AA range:256-305
Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
