Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10872925 | FEBS Letters | 2005 | 4 Pages |
Abstract
The NF-kB family transcription factor c-Rel is a critical molecule for inducing expression of cytokine genes by T cells. Here, we report that a deletion of the C-terminal end, similar to the deletion in the highly oncogenic chicken v-Rel gene, renders c-Rel hyperactive toward cytokine gene promoters. At the same time, this mutation dramatically reduced c-Rel activity in induction of IkB-α mRNA expression. Moreover, ectopic expression of IkB-α, along with the C-terminal truncated c-Rel, abrogates hyperactivity of this mutant. IkB-α co-expression did not affect the function of wild-type c-Rel. The data demonstrate that the C-terminal end of c-Rel has specific activity for IkB-α mRNA expression and is dispensable for IL-2 gene expression.
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Authors
Kazuyuki Iwai, Byung Rho Lee, Masaaki Hashiguchi, Atsuki Fukushima, Makio Iwashima,