Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

WASP (D9C8) Rabbit mAb #4271

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 60 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

WASP (D9C8) Rabbit mAb detects endogenous levels of total WASP protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to central residues of human WASP.

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat, Raji and Ramos cells using WASP (D9C8) Rabbit mAb.

Background

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).

  1. Millard, T.H. et al. (2004) Biochem J. 380, 1-17.
  2. Yan, C. et al. (2003) EMBO J. 22, 3602-3612.
  3. Snapper, S.B. et al. (2001) Nat. Cell Biol. 3, 897-904.
  4. Zhang, J. et al. (1999) J. Exp. Med. 190, 1329-4132.
  5. Suetsugu, S. et al. (1999) Biochem. Biophys. Res. Commun. 260, 296-302.
  6. Sossey-Alaoui, K. et al. (2002) Oncogene 21, 5967-5974.
  7. Sossey-Alaoui, K. et al. (2005) Exp. Cell Res. 308, 135-145.
  8. Sossey-Alaoui, K. et al. (2007) Am J Pathol 170, 2112-21.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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