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PMID: 2157136 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Postinduction turnoff of beta-interferon gene expression.

Molecular and cellular biology ·Vol. 10 ·No. 4 ·1990-04-00 ·Pages 1329-37

Whittemore LA, Maniatis T

Abstract

Viral induction of the human beta-interferon (IFN-beta) gene leads to a transient accumulation of high levels of IFN-beta mRNA. Previous studies have shown that the increase in IFN-beta mRNA levels after induction is due to an increase in the rate of IFN-beta gene transcription. In this paper, we show that the rapid postinduction decrease in the level of IFN-beta mRNA is due to a combination of transcriptional repression and rapid turnover of the mRNA. This transcriptional repression can be blocked with cycloheximide, suggesting that the synthesis of a virus-inducible repressor is necessary for the postinduction turnoff of the IFN-beta gene. Analysis of the sequence requirements for IFN-beta mRNA instability revealed two regions capable of destabilizing a heterologous mRNA. One destabilizer is an AU-rich sequence in the 3' untranslated region, and the other is located 5' to the translation stop codon.

MeSH Terms
Animals Base Sequence Cell Line Cell Transformation, Viral Cells, Cultured Cycloheximide/pharmacology Gene Expression Regulation Interferon Type I/genetics Molecular Sequence Data Parainfluenza Virus 1, Human/genetics Plasmids Poly I-C/pharmacology RNA, Messenger/genetics Transcription, Genetic/drug effects Transfection
Chemicals
Interferon Type I RNA, Messenger Cycloheximide Poly I-C
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Whittemore L A
Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.
Maniatis T
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
Published
1990-04-00
Pages
1329-37
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC362234
Subset
IM
Grants
PHS HHS · A1-20642 · United States
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