IkB-alpha-specific transcript regulation by the C-terminal end of c-Rel.
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-alpha mRNA expression. Moreover, ectopic expression of IkB-alpha, along with the C-terminal truncated c-Rel, abrogates hyperactivity of this mutant. IkB-alpha 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-alpha mRNA expression and is dispensable for IL-2 gene expression.
Iwai
Kazuyuki
K
Program in Molecular Immunology, Institute of Molecular Medicine and Genetics, Medical College of Georgia, 1120, 15th Street, Augusta, GA 30912-2600, USA.
Lee
Byung Rho
BR
Hashiguchi
Masaaki
M
Fukushima
Atsuki
A
Iwashima
Makio
M
D005786:Gene Expression Regulation; D006801:Humans; D020672:I-kappa B Proteins / Q000235:genetics* / Q000502:physiology; D007376:Interleukin-2 / Q000235:genetics* / Q000378:metabolism; D019169:Jurkat Cells; D009154:Mutation / Q000235:genetics; D000072000:NF-KappaB Inhibitor alpha; D011401:Promoter Regions, Genetic / Q000235:genetics; D020569:Proto-Oncogene Proteins c-rel / Q000737:chemistry* / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D017384:Sequence Deletion / Q000235:genetics; D013601:T-Lymphocytes / Q000737:chemistry / Q000378:metabolism; D014162:Transfection
D020672:I-kappa B Proteins; D007376:Interleukin-2; C000606204:NFKBIA protein, human; D020569:Proto-Oncogene Proteins c-rel; D012333:RNA, Messenger; D000072000:NF-KappaB Inhibitor alpha