ArticleOncogene1999
Papillomavirus E2 induces p53-independent apoptosis in HeLa cells.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 89 citations in OpenAlex.
- Human Papilloma Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Deep Sequencing Discovery and Profiling of Known and Novel miRNAs Produced in Response to DNA Damage in Rice.International journal of molecular sciences · 2021Article
- Carbon-ion irradiation overcomes HPV-integration/E2 gene-disruption induced radioresistance of cervical keratinocytes.Journal of radiation research · 2019Article
- A fully defined static suspension culture system for large-scale human embryonic stem cell production.Cell death & disease · 2018Article
- β-HPV 5 and 8 E6 disrupt homology dependent double strand break repair by attenuating BRCA1 and BRCA2 expression and foci formation.PLoS pathogens · 2015Article
- HPV16 E2-mediated potentiation of NF-κB activation induced by TNF-α involves parallel activation of STAT3 with a reduction in E2-induced apoptosis.Molecular and cellular biochemistry · 2014Article
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
- The modulation of apoptosis by oncogenic viruses.Virology journal · 2013Review
- The transcriptional regulator gene E2 of the Human Papillomavirus (HPV) 16 influences the radiosensitivity of cervical keratinocytes.Radiation oncology (London, England) · 2012Article
- Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation.Virology · 2012Article
- Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development.Journal of oncology · 2012Article
- HPV E6 proteins target Ubc9, the SUMO conjugating enzyme.Virus research · 2011Article
- Growth inhibition of HeLa cells is a conserved feature of high-risk human papillomavirus E8^E2C proteins and can also be achieved by an artificial repressor protein.Journal of virology · 2011Article
- A new E6/P63 pathway, together with a strong E7/E2F mitotic pathway, modulates the transcriptome in cervical cancer cells.Journal of virology · 2007Article
- Cell cycle arrest and apoptosis induced by the coronavirus infectious bronchitis virus in the absence of p53.Virology · 2007Article
- Human papillomavirus E7 repression in cervical carcinoma cells initiates a transcriptional cascade driven by the retinoblastoma family, resulting in senescence.Journal of virology · 2007Article
- Inhibition of Bax activity is crucial for the antiapoptotic function of the human papillomavirus E6 oncoprotein.Oncogene · 2006Article
- E2 proteins from high- and low-risk human papillomavirus types differ in their ability to bind p53 and induce apoptotic cell death.Journal of virology · 2006Article
- The human DEK proto-oncogene is a senescence inhibitor and an upregulated target of high-risk human papillomavirus E7.Journal of virology · 2005Article
- Crosstalk between the human papillomavirus E2 transcriptional activator and the E6 oncoprotein.Oncogene · 2005Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that expression of the papillomavirus E2 protein in HeLa cells induces p53 accumulation and causes both cell cycle arrest and apoptosis. In contrast to growth arrest, onset of apoptosis was not correlated with an increase of p53 transcriptional activity. In the present study, we conducted biochemical and genetic experiments in order to determine whether E2-induced apoptosis was independent of p53 induction. We showed that E2 did not alter the transcription of Bax, a known p53-activated cell death inducer. The time course of apoptotic cell death preceded p53 induction by several hours. Overexpression of the HPV18 E6 oncogene prevented E2-mediated p53 accumulation, but did not alter the rate of cell death. Finally, point mutants of the HPV18 E2 transactivation domain induced apoptosis, although they were unable to induce high p53 accumulation or cell cycle arrest. In addition, the results obtained with these mutants indicated that both transcriptional activation and replication functions of E2 were dispensable for the induction of cell death. These observations show that E2-induced apoptosis is an early event, independent of p53 accumulation and unrelated to downstream p53-dependent transcriptional events.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.