| Literature DB >> 2475256 |
H Harada1, T Fujita, M Miyamoto, Y Kimura, M Maruyama, A Furia, T Miyata, T Taniguchi.
Abstract
Viral infections commonly induce expression of type I interferon (IFN) genes. The induction is transient and involves transcriptional activation wherein a positive factor, IRF-1, binds to upstream regulatory cis elements. In the present study we report the isolation of a cDNA encoding a novel factor, termed IRF-2, that interacts with the same nucleotide sequence elements as IRF-1. Both genes are inducible not only by virus but also by IFN. Unlike IRF-1, IRF-2 does not function as an activator; rather, it suppresses the function of IRF-1 under certain circumstances. Our results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.Entities:
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Year: 1989 PMID: 2475256 DOI: 10.1016/0092-8674(89)90107-4
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582