ArticleJournal of virology2006
E2 proteins from high- and low-risk human papillomavirus types differ in their ability to bind p53 and induce apoptotic cell death.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Human Papillomavirus 16 E2 as an Apoptosis-Inducing Protein for Cancer Treatment: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- The Exploration of Therapeutic Antivirals for Human Papillomavirus in the Last 40 Years: Bibliometric Research.Pathogens (Basel, Switzerland) · 2026Article
- Navigating therapeutic strategies: HPV classification in head and neck cancer.British journal of cancer · 2024Review
- Article
- Review
- Human papillomavirus 16 E2 blocks cellular senescence in response to activation of the DNA damage response.Virology · 2022Article
- A Critical Role for p53 during the HPV16 Life Cycle.Microbiology spectrum · 2022Article
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs.Nucleic acids research · 2022Article
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- How Enhancing Immunity to Low-Risk HPV Could Cure Recurrent Respiratory Papillomatosis.The Laryngoscope · 2021Review
- Review
- Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift?Viruses · 2017Review
- HPV positive neuroendocrine cervical cancer cells are dependent on Myc but not E6/E7 viral oncogenes.Scientific reports · 2017Article
- Article
- Insights into the mechanism of human papillomavirus E2-induced procaspase-8 activation and cell death.Scientific reports · 2016Article
- Re-expression of HPV16 E2 in SiHa (human cervical cancer) cells potentiates NF-κB activation induced by TNF-α concurrently increasing senescence and survival.Bioscience reports · 2015Article
- Effects of Methylation Status of CpG Sites within the HPV16 Long Control Region on HPV16-Positive Head and Neck Cancer Cells.PloS one · 2015Article
- Regulation of human genome expression and RNA splicing by human papillomavirus 16 E2 protein.Virology · 2014Article
- 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
- Structural insights into a wildtype domain of the oncoprotein E6 and its interaction with a PDZ domain.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The E2 proteins from oncogenic (high-risk) human papillomaviruses (HPVs) can induce apoptotic cell death in both HPV-transformed and non-HPV-transformed cells. Here we show that the E2 proteins from HPV type 6 (HPV6) and HPV11, two nononcogenic (low-risk) HPV types, fail to induce apoptosis. Unlike the high-risk HPV16 E2 protein, these low-risk E2 proteins fail to bind p53 and fail to induce p53-dependent transcription activation. Interestingly, neither the ability of p53 to activate transcription nor the ability of p53 to bind DNA, are required for HPV16 E2-induced apoptosis in non-HPV-transformed cells. However, mutations that reduce the binding of the HPV16 E2 protein to p53 inhibit E2-induced apoptosis in non-HPV-transformed cells. In contrast, the interaction between HPV16 E2 and p53 is not required for this E2 protein to induce apoptosis in HPV-transformed cells. Thus, our data suggest that this high-risk HPV E2 protein induces apoptosis via two pathways. One pathway involves the binding of E2 to p53 and can operate in both HPV-transformed and non-HPV-transformed cells. The second pathway requires the binding of E2 to the viral genome and can only operate in HPV-transformed cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.