Anti-WASP Antibody Picoband® Fluoro488 Conjugated

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, ly or inly, 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.

Actin, Actin Binding Proteins, Actin, etc., Cytoskeleton, Cytoskeleton/ECM, Microfilaments, Signal Transduction, Subcellular Markers, Tags & Cell Markers

Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria. .

1. Jin, Y.; Mazza, C.; Christie, J.; Giliani, S.; Fiorini, M.; Mella, P.; Gandellini, F.; Stewart, D.; Zhu, Q.; Nelson, D. L.; Notarangelo, L. D.; Ochs, H. D. (2004) . Mutations of the Wiskott-Aldrich Syndrome Protein (WASP) : hotspots, effect on transcription, and translation and phenotype/genotype correlation. Blood104 (13) : 4010–4019. 2. Radl, J.; Dooren, L. H.; Morell, A.; Skvaril, F.; Vossen, J. M.; Uittenbogaart, C. H. (1976) . Immunoglobulins and transient paraproteins in sera of patients with the Wiskott-Aldrich syndrome: a follow-up study. Clinical and experimental immunology 25 (2) : 256–263.