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Double‐stranded RNA activates binding of NF‐kappa B to an inducible element in the human beta‐interferon promoter.
Author(s) -
Visvanathan K. V.,
Goodbourn S.
Publication year - 1989
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1989.tb03483.x
Subject(s) - biology , transcription factor , microbiology and biotechnology , nfkb1 , rna silencing , interferon , transcription (linguistics) , rna , response element , gene , gene expression , promoter , rna interference , genetics , linguistics , philosophy
The human beta‐interferon promoter contains at least two positive acting domains (PRD I and PRD II). PRD I has been previously shown to stimulate basal transcription and to respond to induction by double‐stranded RNA (dsRNA). Here we show that PRD II functions independently as a constitutive element that also responds to induction. A cellular factor that specifically binds to PRD II has been identified, and the levels of this factor increase markedly in extracts from cells treated with dsRNA. The inducible factor has a binding specificity that is indistinguishable from the transcription factor NF‐kappa B. As has been shown for NF‐kappa B, the PRD II‐specific factor can be activated in uninduced extracts by treatment with detergent, suggesting that the inactive state is due to association with an inhibitory factor. Induction by dsRNA therefore provides a novel means for the post‐translational activation of NF‐kappa B. Potential binding sites for NF‐kappa B are present in the 5′ flanking regions of a number of genes involved in the immune response, several of which are inducible by dsRNA. These findings demonstrate a role for NF‐kappa B in the physiological activation of genes in non‐lymphoid cells.