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NF-kappa B-independent activation of beta-interferon expression in mouse F9 embryonal carcinoma cells.

作者信息

Ellis M J, Goodbourn S

机构信息

Gene Expression Laboratory, Imperial Cancer Research Fund, London, UK.

出版信息

Nucleic Acids Res. 1994 Oct 25;22(21):4489-96. doi: 10.1093/nar/22.21.4489.

Abstract

We have examined the behaviour of the beta-interferon promoter in mouse F9 embryonal carcinoma cells. In undifferentiated cells, the beta-interferon promoter is not responsive to dsRNA or to Sendai virus. In cells stimulated to differentiate into parietal endoderm by treatment with retinoic acid, the beta-interferon promoter responds to both inducers, but only Sendai virus can activate the transcription factor NF-kappa B previously thought to be essential for beta-interferon induction. Differentiated F9 cells therefore present an unprecedented situation in which induction of the beta-interferon gene does not require NF-kappa B. In addition to these differences, induction by dsRNA, but not by Sendai virus, is significantly enhanced by a pretreatment with interferon (priming). These observations suggest that paramyxo-viruses can participate in beta-interferon induction in a manner that is distinct from a simple generator of dsRNA. Analysis of the promoter requirements for induction in differentiated F9 cells suggests that induction is brought about by a novel mechanism using the currently identified regulatory domains.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3407/308484/bfcbbd14ad12/nar00045-0143-a.jpg

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