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Modulation of HIV-LTR activity by ras oncogenes
D Lembo1, A Angeretti, M Gaboli
1Institute of Microbiology of Novara, Institute of Microbiology of Turin, University of Turin, Italy.
The New Microbiologica
|April 1, 1995
Summary
The ras oncogene activates human immunodeficiency virus (HIV) long terminal repeat (LTR) transcription. Inactivated ras inhibits HIV LTR activity, suggesting ras signaling regulates HIV infection.
Area of Science:
- Molecular Biology
- Virology
- Oncology
Background:
- The human immunodeficiency virus (HIV) long terminal repeat (LTR) controls viral gene expression.
- Ras oncogenes are implicated in cellular transformation and signaling pathways.
Purpose of the Study:
- To investigate the role of the ras oncogene in regulating HIV LTR-driven transcription.
Main Methods:
- Cotransfection of NIH 3T3 cells with v-Ha-ras and an HIV LTR-chloramphenicol acetyl transferase (CAT) reporter plasmid.
- Analysis of CAT activity in cell lines with stably transfected ras oncogenes (point mutation or amplification).
- Assessment of an inactivated ras mutant (Ha-ras Asn-17) on HIV LTR activity.
Main Results:
- Expression of v-Ha-ras significantly stimulated CAT activity, indicating HIV LTR activation.
- Stably transfected ras oncogenes also showed high HIV LTR activation.
- The inactivated Ha-ras Asn-17 mutant failed to stimulate but inhibited basal HIV LTR activity.
Conclusions:
- Activation of the p21ras protein is a key signal regulating HIV LTR-driven transcription.
- Ras signaling pathways play a significant role in the regulation of HIV transcription during infection.