ArticleJournal of molecular biology2014
The high-risk HPV16 E7 oncoprotein mediates interaction between the transcriptional coactivator CBP and the retinoblastoma protein pRb.
Article in Journal of molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 85 citations in OpenAlex.
- Anal HPV in Kidney Transplant Recipients: A Closer Look at Pathogenesis and Clinical Management.Pathogens (Basel, Switzerland) · 2026Review
- Plant Bioactive Constituents and Their Potential Benefits in HPV-Positive Oropharyngeal Squamous Cell Carcinoma-A Narrative Review.Current issues in molecular biology · 2026Review
- Synergistic Interaction Between HPV-16 E7 Oncoprotein and Severe Vitamin A Deficiency in Regulating Adaptive Immunity in a Preclinical Cervical Cancer Model.Journal of medical virology · 2026Article
- Therapeutic resistance in HPV-positive oropharyngeal squamous cell carcinoma: molecular mechanisms, clinical challenges, and precision strategies.Frontiers in genetics · 2026Review
- Post-translational modifications in retinoblastoma: mechanisms, immune regulation, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- Decoding the relationships among miRNA, HPV infection, and tumor suppressor gene expression in breast cancer patients.Scientific reports · 2025Article
- Review
- KAT8 facilitates the proliferation of cancer cells through enhancing E7 function in HPV-associated cervical cancer.Acta biochimica et biophysica Sinica · 2025Article
- Regulation of Granzymes A and B by High-Risk HPV: Impact on Immune Evasion and Carcinogenesis.Viruses · 2025Review
- Curcumin, EGCG and apigenin in cervical cancer: mechanistic insights and therapeutic potential.Frontiers in pharmacology · 2025Review
- The effect of phosphorylation efficiency on the oncogenic properties of the protein E7 from high-risk HPV.Virus research · 2024Article
- Review
- Vital for Viruses: Intrinsically Disordered Proteins.Journal of molecular biology · 2023Review
- Post-translational modifications on the retinoblastoma protein.Journal of biomedical science · 2022Review
- High Risk-Human Papillomavirus in HNSCC: Present and Future Challenges for Epigenetic Therapies.International journal of molecular sciences · 2022Review
- 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
- Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021Review
- Human papillomavirus E6 and E7: What remains?Tumour virus research · 2021Review
- Viral Manipulation of the Host Epigenome as a Driver of Virus-Induced Oncogenesis.Microorganisms · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The oncoprotein E7 from human papillomavirus (HPV) strains that confer high cancer risk mediates cell transformation by deregulating host cellular processes and activating viral gene expression through recruitment of cellular proteins such as the retinoblastoma protein (pRb) and the cyclic-AMP response element binding binding protein (CBP) and its paralog p300. Here we show that the intrinsically disordered N-terminal region of E7 from high-risk HPV16 binds the TAZ2 domain of CBP with greater affinity than E7 from low-risk HPV6b. HPV E7 and the tumor suppressor p53 compete for binding to TAZ2. The TAZ2 binding site in E7 overlaps the LxCxE motif that is crucial for interaction with pRb. While TAZ2 and pRb compete for binding to a monomeric E7 polypeptide, the full-length E7 dimer mediates an interaction between TAZ2 and pRb by promoting formation of a ternary complex. Cell-based assays show that expression of full-length HPV16 E7 promotes increased pRb acetylation and that this response depends both on the presence of CBP/p300 and on the ability of E7 to form a dimer. These observations suggest a model for the oncogenic effect of high-risk HPV16 E7. The disordered region of one E7 molecule in the homodimer interacts with the pocket domain of pRb, while the same region of the other E7 molecule binds the TAZ2 domain of CBP/p300. Through its ability to dimerize, E7 recruits CBP/p300 and pRb into a ternary complex, bringing the histone acetyltransferase domain of CBP/p300 into proximity to pRb and promoting acetylation, leading to disruption of cell cycle control.
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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.