ArticleJournal of virology1996
Abrogation of growth arrest signals by human papillomavirus type 16 E7 is mediated by sequences required for transformation.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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.
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Who cites it
68 citing papers in PubMed.
- Inactivation of the RB1 and PTPN14 tumor suppressors cooperatively enables the carcinogenic activity of the human papillomavirus E7 oncoprotein.bioRxiv : the preprint server for biology · 2026Article
- Structurally-optimised HPV16 E7/E6 mRNA-LPP mediates dose-sparing efficacy via tumour microenvironment reprogramming.Molecular biomedicine · 2026Article
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- A safe and potentiated multi-type HPV L2-E7 nanoparticle vaccine with combined prophylactic and therapeutic activity.NPJ vaccines · 2024Article
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Genome composition-based deep learning predicts oncogenic potential of HPVs.Frontiers in cellular and infection microbiology · 2024Article
- CDK4/6 inhibition enhances SHP2 inhibitor efficacy and is dependent upon RB function in malignant peripheral nerve sheath tumors.Science advances · 2023Article
- CDK4/6 inhibition enhances SHP2 inhibitor efficacy and is dependent upon restoration of RB function in malignant peripheral nerve sheath tumors.bioRxiv : the preprint server for biology · 2023Article
- Human Papillomavirus 42 Drives Digital Papillary Adenocarcinoma and Elicits a Germ Cell-like Program Conserved in HPV-Positive Cancers.Cancer discovery · 2023Article
- Construction and immune effect of an HPV16/18/58 trivalent therapeutic adenovirus vector vaccine.Infectious agents and cancer · 2022Article
- Human papillomavirus E6 and E7: What remains?Tumour virus research · 2021Review
- Article
- Molecular pathways in the development of HPV-induced cervical cancer.EXCLI journal · 2021Review
- KDM6A-Mediated Expression of the Long Noncoding RNA DINO Causes TP53 Tumor Suppressor Stabilization in Human Papillomavirus 16 E7-Expressing Cells.Journal of virology · 2020Article
- Human papillomavirus 16 promotes microhomology-mediated end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- HPV-16 E7 expression up-regulates phospholipase D activity and promotes rapamycin resistance in a pRB-dependent manner.BMC cancer · 2018Article
- Mechanisms by which HPV Induces a Replication Competent Environment in Differentiating Keratinocytes.Viruses · 2017Review
- Spontaneous and Vaccine-Induced Clearance of Mus Musculus Papillomavirus 1 Infection.Journal of virology · 2017Article
- Cdc6 contributes to abrogating the G1 checkpoint under hypoxic conditions in HPV E7 expressing cells.Scientific reports · 2017Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cells arrest in the G1 or G0 phase of the cell cycle in response to a variety of negative growth signals that induce arrest by different molecular pathways. The ability of human papillomavirus (HPV) oncogenes to bypass these signals and allow cells to progress into the S phase probably contributes to the neoplastic potential of the virus. The E7 protein of HPV-16 was able to disrupt the response of epithelial cells to three different negative growth arrest signals: quiescence imposed upon suprabasal epithelial cells, G1 arrest induced by DNA damage, and inhibition of DNA synthesis caused by treatment with transforming growth factor beta. The same set of mutated E7 proteins was able to abrogate all three growth arrest signals. Mutant proteins that failed to abrogate growth arrest signals were transformation deficient and included E7 proteins that bound retinoblastoma protein in vitro. In contrast, HPV-16 E6 was able to bypass only DNA damage-induced G1 arrest, not suprabasal quiescence or transforming growth factor beta-induced arrest. The E6 and E7 proteins from the low-risk virus HPV-6 were not able to bypass any of the growth arrest signals.
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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.