ArticleJournal of virology2004
Human papillomavirus type 16 E6 promotes retinoblastoma protein phosphorylation and cell cycle progression.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 47 citations in OpenAlex.
- Lyon IARC Polyomavirus Displays Transforming Activities in Primary Human Cells.Journal of virology · 2022Article
- 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
- Human papillomavirus molecular biology and disease association.Reviews in medical virology · 2015Review
- Beta human papillomavirus E6 expression inhibits stabilization of p53 and increases tolerance of genomic instability.Journal of virology · 2014Article
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
- Polyomavirus-associated Trichodysplasia spinulosa involves hyperproliferation, pRB phosphorylation and upregulation of p16 and p21.PloS one · 2014Article
- The human papillomavirus type 16 E7 oncoprotein induces a transcriptional repressor complex on the Toll-like receptor 9 promoter.The Journal of experimental medicine · 2013Article
- Screening of drugs to counteract human papillomavirus 16 E6 repression of E-cadherin expression.Investigational new drugs · 2012Article
- Article
- Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.Virology · 2012Review
- Tumour-associated antigens: considerations for their use in tumour immunotherapy.International journal of hematology · 2011Review
- Article
- E6-associated protein is required for human papillomavirus type 16 E6 to cause cervical cancer in mice.Cancer research · 2010Article
- Review
- p53 Loss synergizes with estrogen and papillomaviral oncogenes to induce cervical and breast cancers.Cancer research · 2008Article
- The human papillomavirus E6 oncogene dysregulates the cell cycle and contributes to cervical carcinogenesis through two independent activities.Cancer research · 2007Article
- Skin hyperproliferation and susceptibility to chemical carcinogenesis in transgenic mice expressing E6 and E7 of human papillomavirus type 38.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
We show that E6 proteins from benign human papillomavirus type 1 (HPV1) and oncogenic HPV16 have the ability to alter the regulation of the G(1)/S transition of the cell cycle in primary human fibroblasts. Overexpression of both viral proteins induces cellular proliferation, retinoblastoma (pRb) phosphorylation, and accumulation of products of genes that are negatively regulated by pRb, such as p16(INK4a), CDC2, E2F-1, and cyclin A. Hyperphosphorylated forms of pRb are present in E6-expressing cells even in the presence of ectopic levels of p16(INK4a). The E6 proteins strongly increased the cyclin A/cyclin-dependent kinase 2 (CDK2) activity, which is involved in pRb phosphorylation. In addition, mRNA and protein levels of the CDK2 inhibitor p21(WAF1/CIP1) were strongly down-regulated in cells expressing E6 proteins. The down-regulation of the p21(WAF1/CIP1) gene appears to be independent of p53 inactivation, since HPV1 E6 and an HPV16 E6 mutant unable to target p53 were fully competent in decreasing p21(WAF1/CIP1) levels. E6 from HPV1 and HPV16 also enabled cells to overcome the G(1) arrest imposed by oncogenic ras. Immunofluorescence staining of cells coexpressing ras and E6 from either HPV16 or HPV1 revealed that antiproliferative (p16(INK4a)) and proliferative (Ki67) markers were coexpressed in the same cells. Together, these data underline a novel activity of E6 that is not mediated by inactivation of p53.
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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.