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

Transient expression of chloramphenicol acetyltransferase (CAT) was used to study Marek's diseases virus (MDV)-mediated transactivation of the Rous sarcoma virus long terminal repeat (RSV-LTR) promoter. Cotransfection experiments in primary avian cells were conducted using MDV high-molecular-weight DNA and plasmid pRSVcat. Increased CAT activity, relative to controls, was consistently observed in the presence of MDV. Enhanced CAT activity, expressed via the RSV-LTR promoter, was strictly dependent on the presence of MDV DNA or virus, suggesting that activation of the RSV-LTR promoter was due to factors expressed in MDV-infected cells. Differences in transactivation efficiency were observed between various strains and the serotypes of MDV. In particular, high- and low-passage pairs of serotype 1 MDV showed marked differences in their ability to increase CAT activity in pRSVcat-transfected cells. Attenuation of viral pathogenicity and decreased expression of some cell surface glycoproteins occur in high-passage MDV strains. Decreased transactivation ability in these same strains suggests that continuous passage in culture and attenuation may perturb a regulatory mechanism operating by transcriptional control. In addition, transactivation of the RSV-LTR promoter suggests that increased incidence of avian leukosis following vaccination by MDV may be due to MDV-mediated transactivation of endogenous ALV proviral LTR promoters. MDV-mediated transactivation was not limited to the RSV-LTR promoter. Serotype 3 MDV (HVT) efficiently transactivated the herpes simplex virus (HSV) alpha 4 (ICP4) and beta-TK promoters as well as the human cytomegalovirus (hCMV) immediate early promoter.
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PMID:Transactivation of the Rous sarcoma virus long terminal repeat promoter by Marek's disease virus. 217 59

Transgenic mouse lines have been developed that express the tv-a receptor under the control of the chicken beta-actin promoter. These mice express the tv-a receptor in most or all tissues and in the early embryo. An avian leukosis virus (ALV)-based retroviral vector system was used for the efficient delivery of genes into preimplantation mouse embryos from these transgenic lines. Experimental animals could be generated quickly and easily by infecting susceptible blastocysts with ALV-based retroviral vectors. Expression of the delivered genes was controlled by either the constitutive viral promoter contained in the long terminal repeat or an internal nonviral tissue-specific promoter. Mating the infected founder chimeric animals produced animals that carry the ALV provirus as a transgene. A subset of the integrated proviruses expressed the chloramphenicol acetyltransferase reporter gene from either the promoter in the long terminal repeat or an internal promoter, which we believe indicates that many of the sites that are accessible to viral DNA insertion in preimplantation embryos are incompatible with expression in older animals. This approach should prove useful for studies on murine cell lineage and development, providing models for studying oncogenesis, and testing gene therapy strategies.
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PMID:Expression of transduced genes in mice generated by infecting blastocysts with avian leukosis virus-based retroviral vectors. 864 6