WAS Antilichaam

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.

7454

P42768

Human

Recombinant fusion protein containing a sequence corresponding to amino acids 60-250 of human WAS (NP_000368.1) .

Unconjugated

Primary Antibodies

Cell Cycle, Immunology, Signal Transduction

Affinity purification

HL-60

Batch dependent

PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

None

Blue Ice

Store at -20˚ C. Avoid freeze / thaw cycles.

Observed: 62kDa

IgG

WAS

THP-1

Ramos

Wiskott-Aldrich syndrome

Homo sapiens

WAS, THC, IMD2, WASP, Wiskott-Aldrich syndrome (eczema-thrombocytopenia), thrombocytopenia 1 (X-linked), Wiskott-Aldrich syndrome (eczema-thrombocytopenia) protein

WB, IF

Liquid