1988
DOI: 10.1128/mcb.8.8.3397
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trans activation of type 1 interferon promoters by simian virus 40 T antigen.

Abstract: A human transient expression system was used to measure the influence of simian virus 40 T antigen and adenovirus Ela proteins on the activation of alpha interferon subtype 1 (IFN-a,) and IFN-1 promoters linked to the reporter chloramphenicol acetyltransferase gene. Large T-antigen production, amplified by expression plasmid replication in transfected 293 cells, was able to trans activate the IFN-, promoter 5-to 10-fold, increasing both the constitutive and Sendai virus-induced levels of expression. Surprising… Show more

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Cited by 18 publications
(13 citation statements)
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“…Binding of the labeled probes was also blocked by the IFN-/3 promoter element PRDII (Fig. 2 A, lane 13, B, lane 6, and C, lane 7), which binds NF-KB specifically and is functionally interchangeable with the KB sequence (9,18,19). We conclude that K1, K2, and K3 can specifically bind NF-KB.…”
Section: Methodsmentioning
confidence: 74%
“…Binding of the labeled probes was also blocked by the IFN-/3 promoter element PRDII (Fig. 2 A, lane 13, B, lane 6, and C, lane 7), which binds NF-KB specifically and is functionally interchangeable with the KB sequence (9,18,19). We conclude that K1, K2, and K3 can specifically bind NF-KB.…”
Section: Methodsmentioning
confidence: 74%
“…The results obtained here with the transiently expressed IFN-A4 or IFN-A11 promoter constructs correlate well with the endogenous expression patterns of the corresponding IFN-A genes in L929 cells. In contrast, the expression of endogenous human IFN-A genes, as well as the CAT activity of the SV-CAT reporter constructs containing the human IFN-A1 promoter, were undetectable upon NDV or Sendai virus induction of HeLa cells (7,57,58). This discrepancy may be due to the presence of a negative regulatory sequence located in the human IFN-A1 promoter between the two highly conserved motifs equivalent to C and D domains of murine IFN-A4.…”
Section: Discussionmentioning
confidence: 95%
“…Numerous studies have focused on the mechanisms by which the IFN‐β gene is transcriptionally activated upon viral infection of the cells [1, 2]. It is well established that several cis ‐acting DNA elements exist within the promoter region of the IFN‐β gene, and that these elements bind transcription factors such as IRF‐1, IRF‐2, ISGF3, NF‐κB, AFT‐2, c‐Jun and others [5–10]. In particular, much attention has been focused on the elements which function as virus‐inducible enhancer elements, which we originally termed IRF‐Es [11].…”
Section: Introductionmentioning
confidence: 99%