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WAS

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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. 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.

Derivation:
Mouse
Species Reactivity:
Human
Type:
IgG
Application:
ELISA, WB, IP, FuncS
Derivation:
Mouse
Species Reactivity:
Human
Type:
Fab
Application:
ELISA, FuncS
Derivation:
Mouse
Species Reactivity:
Human
Type:
scFv
Application:
ELISA, WB, Neut, FuncS
Derivation:
Phage display library screening
Species Reactivity:
Human
Type:
IgG
Application:
ICC, IHC-P, WB
Species Reactivity:
mouse
Type:
scFv-(D-Arg)9
Application:
ELISA, WB, ICC, FuncS
Species Reactivity:
mouse
Type:
scFv-(+36GFP)
Application:
WB, ICC, FuncS
Species Reactivity:
mouse
Type:
scFv-Tat
Application:
ICC, Neut, FuncS
Species Reactivity:
Human
Application:
WB
Species Reactivity:
Human
Type:
Chicken antibody
Application:
WB
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