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)

Vesicular stomatitis virus infection causes a rapid and potent inhibition of both host transcription and translation. Recently, the viral matrix (M) protein was shown to inhibit host-directed transcription in vivo in the absence of any other viral component (B. L. Black and D. S. Lyles, J. Virol. 66:4058-4064, 1992). The goal of this study was to determine the effect of M protein on host-directed translation. In vitro-transcribed mRNAs encoding M protein and chloramphenicol acetyltransferase (CAT) were cotransfected into BHK cells to determine the effect of M protein expression on translation of CAT mRNA. The results presented here show that M protein did not inhibit host-directed translation of CAT mRNA. On the contrary, this study gave the unexpected result that M protein actually stimulated host-directed translation under the same conditions in which it potently inhibited host-directed transcription. Under these conditions, the combined effect on host gene expression was a greater-than-20-fold inhibition. Furthermore, the enhancement of host translation mediated by M protein was genetically correlated with M protein's ability to inhibit host transcription. Thus, the results of this study establish that M protein does not inhibit host protein synthesis under the same conditions in which it potently inhibits host transcription and suggest that the inhibition of transcription and that of translation by vesicular stomatitis virus require separate viral gene products.
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PMID:Effect of vesicular stomatitis virus matrix protein on host-directed translation in vivo. 825 71

Vesicular stomatitis virus (VSV) mutant T1026R1 of the Indiana (IN) serotype is a good inducer of interferon (IFN). This mutant was used to study the activation of NF-kappaB, a transcription factor necessary for IFN induction, in mouse L929 cells that were stably transfected with a chimeric gene containing the human IFN-beta gene promoter attached to the chloramphenicol acetyltransferase (CAT) coding sequence. NF-kappaB DNA binding activity was detected as early as 30 min after virus adsorption in nuclear extracts, increased up to 4 hr, and then remained constant for at least 6 additional hr. The kinetics of CAT expression correlated with the kinetics of NF-kappaB nuclear DNA binding activity. Virus entry and delivery of viral components into the cytoplasm were required for NF-kappaB activation. Exposure of T1026R1 to one hit of UV irradiation nearly completely reduced NF-kappaB activation. In cells infected with wild-type (wt) VSV (IN), a noninducer of IFN, NF-kappaB DNA binding activity in the nucleus was delayed for several hours after virus adsorption. Coinfection of wt VSV and T1026R1 resulted in the reduction of T1026R1-promoted NF-kappaB activation. This inhibitory activity of wt VSV was abolished by one hit of UV irradiation. Under similar conditions expression of the CAT gene was more UV resistant, suggesting that IFN gene expression is regulated at multiple levels.
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PMID:NF-kappaB activation Is delayed in mouse L929 cells infected with interferon suppressing, but not inducing, vesicular stomatitis virus strains. 861 43