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)

Promiscuous transcriptional activity of the reticuloendotheliosis virus (REV) long terminal repeat (LTR) was detected in transient expression assays using LTR-chloramphenicol acetyltransferase-encoding gene chimeras, and cells of diverse species and tissue type; levels of expression from two different REV LTRs correlate with reports of pathogenicity of the respective viruses in vivo. REVs do not encode a transactivator targeted to the viral LTR, and cells infected with Marek's disease virus, a herpesvirus with an overlapping host range, do not express factors that preferentially enhance expression from REV or avian sarcoma/leukemia virus LTRs. REV LTRs work efficiently in human lymphoid cells, and are viable alternatives to promoters commonly used for expression of cloned genes. They may also prove useful in the identification of new, ubiquitous cellular transcription factors.
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PMID:Reticuloendotheliosis virus long terminal repeat elements are efficient promoters in cells of various species and tissue origin, including human lymphoid cells. 133 12

Avian retrovirus vectors, with potential for use in avian transformation, were constructed to evaluate the relative efficiency of promoters placed internal to the viral long terminal repeats (LTR). The vectors are replication-defective reticuloendotheliosis plasmids that contain the neomycin phosphotransferase gene under control of the 5' LTR and an internal promoter that directs expression of the chloramphenicol acetyltransferase gene. The internal promoters were the SV40 early, the mouse metallothionein I, and the human cytomegalovirus immediate early (HCMV-IE) promoters. Under transient conditions in QT6 cells, the HCMV-IE promoter construct was by far the strongest. However, expression dropped greatly from the HCMV-IE promoter after integration into the quail cell genome. Evidence suggests that the HCMV-IE promoter is selectively suppressed by methylation after stable transfection but not after infection.
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PMID:Gene expression from heterologous promoters in a replication-defective avian retrovirus vector in quail cells. 165 36

Reticuloendotheliosis viruses (Rev) replicate in chicken and dog cells, but not in rat cells. Amphotropic murine leukemia viruses (Am-MLV) replicate in chicken, dog, and rat cells. Transcription from the Rev long terminal repeat, determined by the chloramphenicol acetyltransferase assay, was not significantly different from transcription from the MLV long terminal repeat in rat cells. To determine further the step(s) in the retroviral life cycle that is blocked for Rev replication in rat cells, we took advantage of the wide host range of Am-MLV (S. Rasheed, M. B. Gardner, and E. Chan, J. Virol. 19:13-18, 1976) and the ability to form Rev-Am-MLV pseudotypes. Data from these pseudotypes indicate that the block to Rev replication in rat cells is posttranscriptional.
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PMID:Pseudotyped retroviral vectors reveal restrictions to reticuloendotheliosis virus replication in rat cells. 302 99