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Updated: Aug 19, 2026

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
Published on: July 24, 2010
Molecular interactions of 'high risk' human papillomaviruses E6 and E7 oncoproteins: implications for tumour
Oishee Chakrabarti1, Sudhir Krishna
1National Centre for Biological Sciences, Tata Institute of Fundamental Research, UAS-GKVK Campus, Bangalore 560 065, India. oishee@ncbs.res.in
Abstract:
The aetiology of cervical cancer has been primarily attributed to human papillomaviruses (HPVs). These are characterized by the persistent expression of the two oncogenes, E6 and E7. Experimental studies show that E6 and E7 genes of the high risk HPVs deregulate key cell cycle controls. Recent work has uncovered new cellular partners for these proteins that throw light on many of the pathways and processes in which these viral proteins intervene. This review focuses on the regulation of host proteins by the viral oncoproteins and consequence of such interactions on cell survival, proliferation, differentiation and apoptosis.
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