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Was  -  Wiskott-Aldrich syndrome homolog (human)

Mus musculus

Synonyms: U42471, WASp, Wasp, Wiskott-Aldrich syndrome protein homolog
 
 
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Disease relevance of Was

 

High impact information on Was

  • Genetics. Was Lamarck just a little bit right [4]?
  • WASp-deficient thymocytes and T cells also exhibited impaired proliferation and interleukin (IL)-2 production in response to T cell antigen receptor (TCR) stimulation, but proliferated normally in response to phorbol ester/ionomycin [1].
  • Together, these results provide evidence of roles for WASp in driving lymphocyte development, as well as in the translation of antigen receptor stimulation to proliferative or apoptotic responses, cytokine production, and cytoskeletal rearrangement [1].
  • The data also reveal a role for WASp in modulating endocytosis and phagocytosis and, accordingly, suggest that the immune deficit conferred by WASp deficiency reflects the disruption of a broad range of cellular behaviors [1].
  • WASp verprolin homology, cofilin homology, and acidic region domain-mediated actin polymerization is required for T cell development [5].
 

Biological context of Was

  • Musculus/M. spretus backcross placed the Wasp locus near the centromere of the mouse X chromosome, inseparable from Gata1, Tcfe3, and scurfy (sf) [6].
  • Here we demonstrate that T cell-restricted expression of VCA domain-deleted WASp (WASpdeltaVCA) in WAS(-/-) mice engenders a severe early block in T lymphopoiesis associated with impaired T cell antigen receptor alphabeta expression and a consequent failure to generate single-positive CD4(+) and CD8(+) T cells [5].
 

Anatomical context of Was

 

Associations of Was with chemical compounds

  • Furthermore, following systemic challenge with lipopolysaccharide (LPS) or toxoplasma-derived antigen, WASp-null DCs showed incomplete redistribution to T-cell areas in the spleen [3].
  • 5'-D Was adaptive to changes in age (1 to 8-10 wk), environmental temperature (14, 25, and 33 degrees C), and thyroid hormone status in both lean and obese mice [9].
 

Regulatory relationships of Was

 

Other interactions of Was

  • Although the VCA domain imbues WASp and other WASp family members with the capacity to modulate cytoskeletal organization, little is known about the impact of this domain activity on lymphoid cell function [5].
  • On fibronectin-coated surfaces, WASp-null immature murine DCs exhibited defects both of attachment and detachment, resulting in impaired net translocation compared with normal cells [3].
  • The chemokinetic response to CCL21, which is critical for normal lymphatic trafficking, was also abrogated in the absence of WASp [3].
  • These results suggest that CD4(+) T cell cytokines require a specialized, WASp-dependent pathway for cellular traffic and/or vesicle release that is distinct from that required for chemokine release [8].

References

  1. Antigen receptor-induced activation and cytoskeletal rearrangement are impaired in Wiskott-Aldrich syndrome protein-deficient lymphocytes. Zhang, J., Shehabeldin, A., da Cruz, L.A., Butler, J., Somani, A.K., McGavin, M., Kozieradzki, I., dos Santos, A.O., Nagy, A., Grinstein, S., Penninger, J.M., Siminovitch, K.A. J. Exp. Med. (1999) [Pubmed]
  2. WASp deficiency in mice results in failure to form osteoclast sealing zones and defects in bone resorption. Calle, Y., Jones, G.E., Jagger, C., Fuller, K., Blundell, M.P., Chow, J., Chambers, T., Thrasher, A.J. Blood (2004) [Pubmed]
  3. Impaired dendritic-cell homing in vivo in the absence of Wiskott-Aldrich syndrome protein. de Noronha, S., Hardy, S., Sinclair, J., Blundell, M.P., Strid, J., Schulz, O., Zwirner, J., Jones, G.E., Katz, D.R., Kinnon, C., Thrasher, A.J. Blood (2005) [Pubmed]
  4. Genetics. Was Lamarck just a little bit right? Balter, M. Science (2000) [Pubmed]
  5. WASp verprolin homology, cofilin homology, and acidic region domain-mediated actin polymerization is required for T cell development. Zhang, J., Shi, F., Badour, K., Deng, Y., McGavin, M.K., Siminovitch, K.A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  6. The mouse homolog of the Wiskott-Aldrich syndrome protein (WASP) gene is highly conserved and maps near the scurfy (sf) mutation on the X chromosome. Derry, J.M., Wiedemann, P., Blair, P., Wang, Y., Kerns, J.A., Lemahieu, V., Godfrey, V.L., Wilkinson, J.E., Francke, U. Genomics (1995) [Pubmed]
  7. Wiskott-Aldrich syndrome protein deficiency leads to reduced B-cell adhesion, migration, and homing, and a delayed humoral immune response. Westerberg, L., Larsson, M., Hardy, S.J., Fernández, C., Thrasher, A.J., Severinson, E. Blood (2005) [Pubmed]
  8. Cutting edge: selective requirement for the Wiskott-Aldrich syndrome protein in cytokine, but not chemokine, secretion by CD4+ T cells. Morales-Tirado, V., Johannson, S., Hanson, E., Howell, A., Zhang, J., Siminovitch, K.A., Fowell, D.J. J. Immunol. (2004) [Pubmed]
  9. Regulation of iodothyronine 5'-deiodination in lean and obese (ob/ob) mice. Hillgartner, F.B., Romsos, D.R. Am. J. Physiol. (1985) [Pubmed]
  10. A Potential Excitability Was Induced by Basic Fibroblast Growth Factor during Early Differentiation of Neurons from Mouse Embryonic Stem Cells in vitro. Enming, Z., Liangqiang, C., Yi, Y., Xiaoxiang, Z. Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference (2005) [Pubmed]
 
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