Abstract:
:High-risk human papillomavirus type 16 (HPV-16) and HPV-18 are associated with the majority of human cervical carcinomas, and two viral genes, HPV E6 and E7, are commonly found to be expressed in these cancers. The presence of HPV-16 E7 is sufficient to induce epidermal hyperplasia and epithelial tumors in transgenic mice. In this study, we have performed experiments in transgenic mice to determine which domains of E7 contribute to these in vivo properties. The human keratin 14 promoter was used to direct expression of mutant E7 genes to stratified squamous epithelia in mice. The E7 mutants chosen had either an in-frame deletion in the conserved region 2 (CR2) domain, which is required for binding of the retinoblastoma tumor suppressor protein (pRb) and pRb-like proteins, or an in-frame deletion in the E7 CR1 domain. The CR1 domain contributes to cellular transformation at a level other than pRb binding. Four lines of animals transgenic for an HPV-16 E7 harboring a CR1 deletion and five lines harboring a CR2 deletion were generated and were observed for overt and histological phenotypes. A detailed time course analysis was performed to monitor acute effects of wild-type versus mutant E7 on the epidermis, a site of high-level expression. In the transgenic mice with the wild-type E7 gene, age-dependent expression of HPV-16 E7 correlated with the severity of epidermal hyperplasia. Similar age-dependent patterns of expression of the mutant E7 genes failed to result in any phenotypes. In addition, the transgenic mice with a mutant E7 gene did not develop tumors. These experiments indicate that binding and inactivation of pRb and pRb-like proteins through the CR2 domain of E7 are necessary for induction of epidermal hyperplasia and carcinogenesis in mouse skin and also suggest a role for the CR1 domain in the induction of these phenotypes through as-yet-uncharacterized mechanisms.
journal_name
J Viroljournal_title
Journal of virologyauthors
Gulliver GA,Herber RL,Liem A,Lambert PFdoi
10.1128/JVI.71.8.5905-5914.1997subject
Has Abstractpub_date
1997-08-01 00:00:00pages
5905-14issue
8eissn
0022-538Xissn
1098-5514journal_volume
71pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:1992-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.66.6.3776-3783.1992
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.23.1.117-125.1977
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/jvi.77.8.4731-4738.2003
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.64.4.1517-1522.1990
更新日期:1990-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.55.2.475-482.1985
更新日期:1985-08-01 00:00:00
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2006-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2009-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.71.1.608-612.1997
更新日期:1997-01-01 00:00:00
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.75.17.8251-8258.2001
更新日期:2001-09-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.72.11.8613-8619.1998
更新日期:1998-11-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.74.9.4258-4263.2000
更新日期:2000-05-01 00:00:00
abstract::Virus-specific RNA synthesized in monkey cells after infection by both wild-type simian virus 40 (SV40) and the early SV40 temperature-sensitive mutant tsA58 has been analyzed. The fraction of SV40-specific RNA increased throughout infection with either wild-type SV40 or with tsA58 in direct proportion to the accumula...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.23.1.167-176.1977
更新日期:1977-07-01 00:00:00