ArticleJournal of virology1991
Biochemical and biological differences between E7 oncoproteins of the high- and low-risk human papillomavirus types are determined by amino-terminal sequences.
Article in Journal of virology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 111 citations in OpenAlex.
- 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
- Detection and genotyping of CMV and HPV in tumors and fallopian tubes from epithelial ovarian cancer patients.Scientific reports · 2019Article
- Comparative analysis of HPV16 gene expression profiles in cervical and in oropharyngeal squamous cell carcinoma.Oncotarget · 2017Article
- Regulation of E2F1-induced apoptosis by poly(ADP-ribosyl)ation.Cell death and differentiation · 2015Article
- The papillomavirus E7 proteins.Virology · 2013Review
- Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.Virology · 2012Review
- Identification of key amino acid residues that determine the ability of high risk HPV16-E7 to dysregulate major histocompatibility complex class I expression.The Journal of biological chemistry · 2011Article
- The human papillomavirus E7 oncoprotein.Virology · 2009Review
- HUMAN PAPILLOMAVIRUS ASSOCIATION WITH HEAD AND NECK CANCERS: UNDERSTANDING VIRUS BIOLOGY AND USING IT IN THE DEVELOPMENT OF CANCER DIAGNOSTICS.Expert opinion on medical diagnostics · 2008Article
- Macrophages kill human papillomavirus type 16 E6-expressing tumor cells by tumor necrosis factor alpha- and nitric oxide-dependent mechanisms.Journal of virology · 2005Article
- Genetic analysis of high-risk e6 in episomal maintenance of human papillomavirus genomes in primary human keratinocytes.Journal of virology · 2002Article
- Human papillomavirus type 16 E7 maintains elevated levels of the cdc25A tyrosine phosphatase during deregulation of cell cycle arrest.Journal of virology · 2002Article
- Biological activities and molecular targets of the human papillomavirus E7 oncoprotein.Oncogene · 2001Review
- Biology of human papillomaviruses.International journal of experimental pathology · 2001Review
- The human papillomavirus type 16 E6 oncoprotein can down-regulate p53 activity by targeting the transcriptional coactivator CBP/p300.Journal of virology · 1999Article
- Intranuclear localization of human papillomavirus 16 E7 during transformation and preferential binding of E7 to the Rb family member p130.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Aetiology, pathogenesis, and pathology of cervical neoplasia.Journal of clinical pathology · 1998Review
- Initiation of DNA synthesis by human papillomavirus E7 oncoproteins is resistant to p21-mediated inhibition of cyclin E-cdk2 activity.Journal of virology · 1997Article
- Abrogation of growth arrest signals by human papillomavirus type 16 E7 is mediated by sequences required for transformation.Journal of virology · 1996Article
- Predicted alpha-helix/beta-sheet secondary structures for the zinc-binding motifs of human papillomavirus E7 and E6 proteins by consensus prediction averaging and spectroscopic studies of E7.The Biochemical journal · 1996Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Differences in the biological characteristics of the high-risk human papillomavirus type 16 (HPV-16) and the low-risk HPV-6 E7 proteins were analyzed and shown to correlate with certain biochemical properties. To ascertain which region of E7 conferred these properties, chimeric E7 genes were constructed by the exchange of the amino and carboxyl coding halves of the HPV-6 and HPV-16 E7 genes. The amino-terminal half of E7 determined the affinity for binding to the retinoblastoma protein pRB, the transformation properties, and the ability to abrogate transforming growth factor beta-mediated repression of the c-myc promoter. This region of E7 is therefore responsible for the biological and biochemical differences between the E7 proteins of the low-risk and the high-risk HPVs and consequently is one of the critical determinants distinguishing these two groups of viruses. Transcriptional transactivation of the adenovirus E2 promoter, in contrast, was a property shared by E7 proteins of both low-risk and high-risk HPVs.
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