|Reactivity||Human Mouse Rat|
|Tested applications||WB IHC IF|
|Recommended Dilution||WB 1:500 - 1:2000
IHC 1:50 - 1:200
IF 1:10 - 1:100|
|Observed MW||Refer to Figures|
|Immunogen||Recombinant protein of human WAS|
|Storage Buffer||Store at -20℃. Avoid freeze / thaw cycles.
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.|
Western blot analysis of extracts of various cell lines, using WAS antibody.
Immunofluorescence analysis of U2OS cell using WAS antibody. Blue: DAPI for nuclear staining.
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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