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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Regulation of the human interleukin-2 receptor alpha chain promoter: activation of a nonfunctional promoter by the transactivator gene of HTLV-I.

We have characterized regulatory regions of the human IL-2 receptor alpha chain (IL2R alpha) promoter. 5' deletion constructs extending to -327 directed CAT expression in HTLV-I-infected T cells, which express IL2R alpha constitutively, and in Jurkat cells, which express IL2R alpha only after induction. Deletions to -267 and -265 were active only in HTLV-I-transformed T cells, but their activity in Jurkat cells was restored by cotransfection of a construct expressing the HTLV-I transactivator protein (tat-I). However, HTLV-I-infected human osteosarcoma cells do not express IL2R alpha-CAT constructs. Thus cell-type-specific factors are required for IL2R alpha expression, and direct or indirect interaction(s) between tat-I and a specific region of the IL2R alpha promoter may cause altered regulation. Tat-I also augments IL2-CAT expression under some conditions, suggesting possible autocrine or paracrine mechanisms for HTLV-I-induced leukemogenesis.[1]

References

  1. Regulation of the human interleukin-2 receptor alpha chain promoter: activation of a nonfunctional promoter by the transactivator gene of HTLV-I. Cross, S.L., Feinberg, M.B., Wolf, J.B., Holbrook, N.J., Wong-Staal, F., Leonard, W.J. Cell (1987) [Pubmed]
 
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