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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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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 introduction of functional WASp (show WASL Antibodies) by GT corrected the alterations of both central and peripheral B cell tolerance checkpoints. WASp (show WASL Antibodies) plays an important role in the establishment and maintenance of B cell tolerance in humans.
We describe two Malay patients with classical Wiskott-Aldrich Syndrome (show WASL Antibodies) with two different mutations in the WASP (show WASL Antibodies) gene
we identify small ubiquitin-related modifier (SUMO)ylation as a novel posttranslational modification of WASp
studies discovered that HMGB1 (show HMGB1 Antibodies) suppressed phosphorylation, nuclear translocation, and activation of CREB (show CREB1 Antibodies), by inhibiting nuclear translocation of PKA catalytic subunit
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