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IkB‐α‐specific transcript regulation by the C‐terminal end of c‐Rel
Author(s) -
Iwai Kazuyuki,
Lee Byung Rho,
Hashiguchi Masaaki,
Fukushima Atsuki,
Iwashima Makio
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.11.060
Subject(s) - ectopic expression , biology , mutant , gene , microbiology and biotechnology , gene expression , transcription factor , regulation of gene expression , promoter , genetics , transcription (linguistics) , linguistics , philosophy
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.