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Updated: Aug 19, 2026

Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
PP2A-dependent transactivation of the cyclin A promoter by SV40 ST is mediated by a cell cycle-regulated E2F site
Christine Skoczylas1, Berthold Henglein, Kathleen Rundell
1Department of Microbiology-Immunology, Northwestern University, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Abstract:
The Simian Virus 40 (SV40) small-t antigen (ST) plays an important role in driving cell proliferation, enhancing transformation by the large-T (LT) antigen. Potential targets of ST are the cyclin kinase inhibitor p27 and the cyclin A gene itself. Transactivation of the cyclin A promoter by ST depends on the interaction of ST with protein phosphatase 2A (PP2A) and occurs through a cell cycle-regulated E2F site near the transcription start site of the promoter. A third SV40 early protein, 17KT, also transactivates the cyclin A promoter but, in this case, transactivation depends on the dnaJ domain of the protein.
Insights
Simian Virus 40 (SV40) small-t antigen (ST) drives cell proliferation and enhances transformation. ST interacts with protein phosphatase 2A (PP2A) to activate the cyclin A promoter.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Simian Virus 40 (SV40) is a DNA tumor virus.
- The SV40 small-t antigen (ST) is implicated in viral oncogenesis and cell cycle regulation.
- Understanding ST's molecular mechanisms is crucial for cancer research.
Purpose of the Study:
- To elucidate the molecular mechanisms by which SV40 ST regulates cell proliferation.
- To identify the specific cellular targets and pathways modulated by ST.
- To investigate the role of protein phosphatase 2A (PP2A) in ST-mediated transactivation.
Main Methods:
- Analysis of SV40 ST interactions with cellular proteins.
- Reporter gene assays to measure promoter activity (e.g., cyclin A promoter).
- Cell cycle analysis and proliferation assays.
Main Results:
- SV40 ST enhances cell proliferation and transformation, partly by targeting p27 and cyclin A.
- ST-mediated transactivation of the cyclin A promoter requires interaction with PP2A.
- This activation occurs via a cell cycle-regulated E2F site on the cyclin A promoter.
Conclusions:
- SV40 ST utilizes PP2A to modulate the cyclin A promoter, contributing to cell cycle dysregulation.
- The findings provide insights into viral mechanisms of cell proliferation and transformation.
- ST's interaction with PP2A represents a key step in SV40-induced oncogenesis.
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