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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. Additionally we are shipping and many more products for this protein.
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Authors show that knock-down of WASp (show WASL Antibodies) or expression of Y102F mutant of WASp (show WASL Antibodies) decreases colony formation and in vivo tumor growth. Results show that WASp (show WASL Antibodies) is a novel substrate of ALK (show ALK Antibodies) and has a critical role in regulating invasiveness and oncogenesis of ALCL.
this study describes an Iranian boy with Wiskott-Aldrich syndrome (show WASL Antibodies) with a novel WASP (show WASL Antibodies) mutation
The inducible recruitment of WASp (show WASL Antibodies) to the TCR-CD3 (show CD3 Antibodies) complex is partially dependent of tyrosine phosphorylation of Cd3e (show CD3E Antibodies).
retrospectively investigated the outcome of hematopoietic stem cell transplantation in a cohort of 24 patients with the X-linked thrombocytopenia phenotype and mutations in the WAS gene
This suggests that N-WASP's failure to compensate for WASP (show WASL Antibodies) in rescuing chemotaxis could be due to the absence of this I30 region.
N-WASP (show WASL Antibodies) is downregulated in clear cell renal cell carcinoma (show MOK Antibodies)
Studies indicate that mutations in the Wiskott-Aldrich syndrome protein (WASp) gene cause a continuum of clinical symptoms ranging from intermittent X-linked thrombocytopenia to full classical Wiskott-Aldrich syndrome (show WASL Antibodies) (WAS).
Platelet actin nodule formation is dependent on WASp (show WASL Antibodies) and the ARP2 (show ACTR2 Antibodies)/3 complex.
conclude that tyrosine phosphorylation of WIP is a crucial regulator of WASP stability and function as an actin-nucleation-promoting factor
WASP (show WASL Antibodies), RUNX1 (show RUNX1 Antibodies), and ANKRD26 (show ANKRD26 Antibodies) genes are important for normal TPO (show THPO Antibodies) signaling and the network underlying thrombopoiesis.
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.
, thrombocytopenia 1 (X-linked)
, wiskott-Aldrich syndrome protein