ArticleJournal of virology2011
Systematic analysis of the amino acid residues of human papillomavirus type 16 E7 conserved region 3 involved in dimerization and transformation.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- The effect of phosphorylation efficiency on the oncogenic properties of the protein E7 from high-risk HPV.Virus research · 2024Article
- Article
- HPV16 E7 Nucleotide Variants Found in Cancer-Free Subjects Affect E7 Protein Expression and Transformation.Cancers · 2022Article
- Characterization of the High-Affinity Fuzzy Complex between the Disordered Domain of the E7 Oncoprotein from High-Risk HPV and the TAZ2 Domain of CBP.Biochemistry · 2021Article
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
- Modeling and Molecular Dynamics of the 3D Structure of the HPV16 E7 Protein and Its Variants.International journal of molecular sciences · 2021Article
- Article
- Article
- Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Structural basis for recognition of the tumor suppressor protein PTPN14 by the oncoprotein E7 of human papillomavirus.PLoS biology · 2019Article
- The PTPN14 Tumor Suppressor Is a Degradation Target of Human Papillomavirus E7.Journal of virology · 2017Article
- Degenerate cysteine patterns mediate two redox sensing mechanisms in the papillomavirus E7 oncoprotein.Redox biology · 2017Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Structural investigation on the intrinsically disordered N-terminal region of HPV16 E7 protein.BMB reports · 2016Article
- The Human Papillomavirus 16 E7 Oncoprotein Attenuates AKT Signaling To Promote Internal Ribosome Entry Site-Dependent Translation and Expression of c-MYC.Journal of virology · 2016Article
- Article
- The high-risk HPV16 E7 oncoprotein mediates interaction between the transcriptional coactivator CBP and the retinoblastoma protein pRb.Journal of molecular biology · 2014Article
- Oncogenes and RNA splicing of human tumor viruses.Emerging microbes & infections · 2014Review
- Human papillomavirus E7 oncoprotein increases production of the anti-inflammatory interleukin-18 binding protein in keratinocytes.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The human papillomavirus (HPV) E7 oncoprotein exists as a dimer and acts by binding to many cellular factors, preventing or retargeting their function and thereby making the infected cell conducive for viral replication. Dimerization of E7 is attributed primarily to the C-terminal domain, referred to as conserved region 3 (CR3). CR3 is highly structured and is necessary for E7's transformation ability. It is also required for binding of numerous E7 cellular targets. To systematically analyze the molecular mechanisms by which HPV16 E7 CR3 contributes to carcinogenesis, we created a comprehensive panel of mutations in residues predicted to be exposed on the surface of CR3. We analyzed our novel collection of mutants, as well as mutants targeting predicted hydrophobic core residues of the dimer, for the ability to dimerize. The same set of mutants was also assessed functionally for transformation capability in a baby rat kidney cell assay in conjugation with activated ras. We show that some mutants of HPV16 E7 CR3 failed to dimerize yet were still able to transform baby rat kidney cells. Our results identify several novel E7 mutants that abrogate transformation and also indicate that E7 does not need to exist as a stable dimer in order to transform cells.
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