Phospho-WASP (Y290) Polyclonal Antibody, 100µg, (ATB-P0679)

Description

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. [provided by RefSeq, Jul 2008]

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.

Product datasheet:

Overview
Product Description	Phospho-WASP (Y290) Polyclonal Antibody, 100µg, (ATB-P0679)
Image
Species Reactivities	Human,Mouse
Immunogen	Synthesized peptide derived from human WASP around the phosphorylation site of Y290.
Properties
Form	Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Storage Instructions	-20°C/1 year
Clonality	Polyclonal

References:

1. Disruption of hSWI/SNF complexes in T cells by WAS mutations distinguishes X-linked thrombocytopenia from Wiskott-Aldrich syndrome. Sarkar K, et al. Blood, 2014 Nov 27. PMID 25253772
2. Synthetic variants of mycolactone bind and activate Wiskott-Aldrich syndrome proteins. Chany AC, et al. J Med Chem, 2014 Sep 11. PMID 25158122
3. X-linked thrombocytopenia in three males with normal sized platelets due to novel WAS gene mutations. Mantadakis E, et al. Pediatr Blood Cancer, 2014 Dec. PMID 25154619
4. Wiskott-Aldrich Syndrome causing mutation, Pro373Ser restricts conformational changes essential for WASP activity in T-cells. Jain N, et al. Biochim Biophys Acta, 2014 Apr. PMID 24440360
5. Wiskott-Aldrich Syndrome protein deficiency perturbs the homeostasis of B-cell compartment in humans. Castiello MC, et al. J Autoimmun, 2014 May. PMID 24369837 Free PMC Article
6. Isolation of a novel gene mutated in Wiskott-Aldrich syndrome.
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   Cell 78:635-644(1994) [PubMed] [Europe PMC] Cited for: NUCLEOTIDE SEQUENCE [GENOMIC DNA / MRNA], TISSUE SPECIFICITY. Tissue: T-cell.
7. Erratum
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8. Identification of mutations in the Wiskott-Aldrich syndrome gene and characterization of a polymorphic dinucleotide repeat at DXS6940, adjacent to the disease gene.
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   Proc. Natl. Acad. Sci. U.S.A. 92:4706-4710(1995) [PubMed] [Europe PMC] Cited for: NUCLEOTIDE SEQUENCE [MRNA], VARIANTS WAS TRP-43; MET-45; LEU-58; LYS-133 AND THR-134.
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    Cited for: NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA].