WAS Antibody | 13-349

WAS Antibody | 13-349 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

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

Research Area: Cell Cycle, Immunology, Signal Transduction

Tested Application: WB, IF

Application: WB: 1:500 - 1:2000
IF: 1:10 - 1:100

Specificiy: N/A

Positive Control 1: HL-60

Positive Control 2: THP-1

Positive Control 3: Ramos

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: Observed: 62kDa

Validation: N/A

Isoform: N/A

Purification: Affinity purification

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

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

Concentration: N/A

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

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

User Note: Optimal dilutions for each application to be determined by the researcher.

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.