Modulation of HIV-LTR activity by ras oncogenes.
Cotransfection of NIH 3T3 cells with a mammalian expression vector containing a v-Ha-ras gene, together with a plasmid carrying the human immunodeficiency virus (HIV) long terminal repeat (LTR) linked to the chloramphenicol acetyl transferase (CAT) reporter gene, significantly stimulated CAT activity. High HIV LTR activation was also observed in cell lines carrying stably transfected ras oncogenes, activated by point mutation or amplification. By contrast an inactivated form of ras (Ha-ras Asn-17) did not stimulate the HIV-LTR but strongly inhibited its basal activity. Activation of the p21ras protein may thus be one of the signals that regulate LTR driven transcription during HIV infection.
Lembo
D
D
Institute of Microbiology of Novara, Institute of Microbiology of Turin, University of Turin, Italy.
Angeretti
A
A
Gaboli
M
M
Cavallo
R
R
Landolfo
S
S
D016475:3T3 Cells; D000818:Animals; D015500:Chloramphenicol O-Acetyltransferase / Q000096:biosynthesis / Q000235:genetics; D017930:Genes, Reporter / Q000235:genetics; D011905:Genes, ras / Q000502:physiology*; D016325:HIV Long Terminal Repeat / Q000235:genetics*; D051379:Mice; D015689:Oncogene Protein p21(ras) / Q000502:physiology; D017354:Point Mutation / Q000502:physiology; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis; D015533:Transcriptional Activation / Q000235:genetics*; D014162:Transfection
D011993:Recombinant Fusion Proteins; D015500:Chloramphenicol O-Acetyltransferase; D015689:Oncogene Protein p21(ras)