ArticleOncogene2006
Molecular mechanisms of hyperplasia induction by human papillomavirus E7.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
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- Human cytomegalovirus-encoded viral cyclin-dependent kinase (v-CDK) UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 and p130 proteins.The Journal of biological chemistry · 2017Article
- Deficiencies in Cellular Processes Modulated by the Retinoblastoma Protein Do Not Account for Reduced Human Cytomegalovirus Replication in Its Absence.Journal of virology · 2015Article
- The retinoblastoma tumor suppressor promotes efficient human cytomegalovirus lytic replication.Journal of virology · 2015Article
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- HPV18 E1^E4 is assembled into aggresome-like compartment and involved in sequestration of viral oncoproteins.Frontiers in microbiology · 2013Article
- Nonconserved lysine residues attenuate the biological function of the low-risk human papillomavirus E7 protein.Journal of virology · 2011Article
- p63 maintains keratinocyte proliferative capacity through regulation of Skp2-p130 levels.Journal of cell science · 2011Article
- Novel human papillomavirus type 18 replicon and its application in screening the antiviral effects of cytokines.Cancer science · 2010Article
- Human papillomavirus 16 E6 variants differ in their dysregulation of human keratinocyte differentiation and apoptosis.Virology · 2009Article
- Ras modifies proliferation and invasiveness of cells expressing human papillomavirus oncoproteins.Journal of virology · 2008Article
- Casein kinase II motif-dependent phosphorylation of human papillomavirus E7 protein promotes p130 degradation and S-phase induction in differentiated human keratinocytes.Journal of virology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infections of human papillomavirus (HPV) induce a variety of benign tumors, such as warts and condylomas. During the process of aberrant cell proliferation, genetic mutations are accumulated in the cells, from which malignant tumor cells arise. The viral oncoproteins E6 and E7 are known to help disrupt the cell cycle checkpoint machinery and accelerate chromosomal instability, events which are critical in malignant conversion. However, the mechanisms involved in the hyperplasia caused by HPV infection have remained unknown. We analysed the effects of regulatory genes of HPV18, a typical high-risk-type HPV, on the formation of the epithelial organ by using an organotypic culture system, and found that E7 had potent activity to induce hyperplasia, to which the disruption of the pRb pathway was well correlated. However, analysis with the E7 variants indicated that other pocket proteins are also involved in the activity.
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