WAS antibody
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Description
Wiskott-Aldrich Syndrome protein(WASP) regulates actin cytoskeleton in hematopoietic cells and defects in WASP cause Wiskott-Aldrich Syndrome(WAS), an X-linked immunodeficiency and autoimmunity disorder of childhood.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Wiskott-Aldrich syndrome(eczema-thrombocytopenia) (WAS) |
| Host | Rabbit |
| Reactivity | Human, Mouse |
| Recommended Dilution | WB: 1:200-1:2000;IHC: 1:20-1:200;IP: 1:200-1:2000 |
| Clonality | polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | 53 kDa |
| Purity | ≥95% as determined by SDS-PAGE |
| Purification | Immunogen affinity purified |
| Size 1 | 100µg |
| Form | liquid |
| Tested Applications | ELISA, IP, WB, IHC |
| Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
| UniProt ID | P42768 |
| Alias | Actin nucleation-promoting factor WAS,Wiskott-Aldrich syndrome protein (WASp),WAS,IMD2 |
| Background | Antibody anti-WAS |
| Status | RUO |
| Note | Mol. Weight 53-62 kDa |
Descripción
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WAS antibody
Wiskott-Aldrich Syndrome protein(WASP) regulates actin cytoskeleton in hematopoietic cells and defects in WASP cause Wiskott-Aldrich Syndrome(WAS), an X-linked immunodeficiency and autoimmunity disorder of childhood.
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Wiskott-Aldrich Syndrome (WAS) Antibody
WAS Antibody is a Rabbit Polyclonal antibody against WAS. Wiskott-Aldrich syndrome proteins (WASPs) mediate actin dynamics by activating the Arp2/3 actin nucleation complex in response to activated Rho family GTPases. In mammals, five WASP family members have been described. Hematopoietic WASP and ubiquitously expressed N-WASP are autoinhibited in unstimulated cells. Upon stimulation they are activated by cdc42, which relieves the autoinhibition in conjunction with phosphatidyl inositol 4,5-bisphosphate. Three WAVE (Wasf, SCAR) family proteins are similar in sequence to WASP and N-WASP but lack the WASP/N-WASP autoinhibition domains and are indirectly activated by Rac (reviewed in 1). Both WASP and WAVE functions appear to be essential, as knockout of either N-WASP or Scar-2 in mice results in cardiac and neuronal defects and embryonic lethality (2,3). Loss of WASP results in immune system defects and fewer immune cells (4). WAVE-2 (WASF2) is widely distributed, while WAVE-1 and WAVE-3 are strongly expressed in brain (5). WAVE-3 may act as a tumor suppressor in neuroblastoma, a childhood disease of the sympathetic nervous system (6). Increased expression of WAVE-3 is seen in breast cancer, and studies in breast adenocarcinoma cells indicate that WAVE-3 regulates breast cancer progression, invasion and metastasis through the p38 mitogen-activated protein kinase (MAPK) pathway (7,8).
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