Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pretreatment of L929 cells with IFN enhances Sendai virus-mediated induction of IL-6, TNF-alpha, and IFNA and IFNB genes. The priming effect could be demonstrated at both the RNA and protein levels and the former did not require cellular protein synthesis. Priming increased the Sendai virus-mediated induction of a murine IFNA4 promoter-chloramphenicol acetyltransferase gene hybrid plasmid (A4CAT) in transiently transfected cells, and deletion analysis showed that the identical DNA sequence was required for the inducibility in primed and unprimed cells. Cotransfection of A4CAT plasmid with interferon regulatory factor-1 (IRF-1) expression plasmid increased CAT expression, however, the IRF-1-mediated expression was further enhanced by priming. These results show that the identical inducible element present in the promoter region of IFNA4 gene is required for both the inducibility and the priming effect; however, no direct correlation between the enhancement of expression of the IRF-1 gene and enhancement of expression of IFN, IL-6, and TNF-alpha genes in the primed cells was observed. We suggest that priming facilitates inducer-mediated posttranscriptional modulation of various transcriptional factors that play a role in stimulation of transcription of these genes.
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PMID:Priming does not change promoter sequence requirements for IFN induction or correlate with the expression of IFN regulatory factor-1. 768 28

We have studied the effects of lipopolysaccharide (LPS) on the Newcastle disease virus (NDV)-mediated induction of cytokine genes expression. Raw cells treated with LPS before or after virus infection showed down-regulation in the expression of interferon A and, to a lesser extent, interferon B genes. In contrast, induction of the interleukin (IL)-6 gene was enhanced. The effects of LPS were not a result of the suppression of virus replication, because the transcription of viral nucleocapsid gene was not affected. Consistent with these findings, LPS also suppressed the NDV-mediated induction of chloramphenicol acetyltransferase reporter gene driven by murine interferon A4 promoter in a transient transfection assay. Furthermore, LPS inhibited virus-mediated phosphorylation of interferon regulatory factor (IRF)-3 and the consequent translocation of IRF-3 from cytoplasm to nucleus. The LPS-mediated inhibition of IFNA gene expression was much weaker in infected Raw cells that constitutively overexpressed IRF-3. The nuclear translocation of IRF-7 in infected cells was also inhibited by LPS. These data suggest that LPS down-regulates the virus-mediated induction of IFNA genes by post-translationally targeting the IRF-3 and IRF-7 proteins.
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PMID:Lipopolysaccharide inhibits virus-mediated induction of interferon genes by disruption of nuclear transport of interferon regulatory factors 3 and 7. 1036 58