Literature DB >> 2845664

Functional dissociation of transforming genes of human papillomavirus type 16.

M Yutsudo1, Y Okamoto, A Hakura.   

Abstract

Human papillomavirus (HPV) type 16 is thought to be responsible for development of cervical carcinomas, but the mechanism of its carcinogenic action is unknown. To determine which viral genes are involved in cellular transformation, we constructed recombinant murine retrovirus DNAs containing various subgenomic fragments of the HPV 16 early region and examined their transforming activities. The results show that the E6 and E7 ORFs are the transforming genes of HPV 16; the former governs the tumorigenicity in nude mice and the latter influences cell growth properties such as saturation density and colony formation in soft agar. There may also be a tumor-suppressing gene in the E1-E2 ORF region, because the tumorigenic activity of recombinant DNA containing the E1 ORF and the 5' portion of the E2 ORF in addition to the E6 and E7 ORFs was much lower than that of recombinant DNA containing only the E6 and E7 ORFs.

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Year:  1988        PMID: 2845664     DOI: 10.1016/0042-6822(88)90532-6

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  25 in total

1.  Detection of transforming gene regions of human papillomavirus type 16 in cervical dysplasias by the polymerase chain reaction.

Authors:  J Czeglédy; M Evander; L Veres; L Gergely; G Wadell
Journal:  Med Microbiol Immunol       Date:  1991       Impact factor: 3.402

2.  Cellular aging is a critical determinant of primary cell resistance to v-src transformation.

Authors:  N Tavoloni; H Inoue
Journal:  J Virol       Date:  1997-01       Impact factor: 5.103

3.  The E6 and E7 genes of the human papillomavirus type 16 together are necessary and sufficient for transformation of primary human keratinocytes.

Authors:  K Münger; W C Phelps; V Bubb; P M Howley; R Schlegel
Journal:  J Virol       Date:  1989-10       Impact factor: 5.103

4.  Negative charge at the casein kinase II phosphorylation site is important for transformation but not for Rb protein binding by the E7 protein of human papillomavirus type 16.

Authors:  J M Firzlaff; B Lüscher; R N Eisenman
Journal:  Proc Natl Acad Sci U S A       Date:  1991-06-15       Impact factor: 11.205

5.  A cell mutant that exhibits temperature-dependent sensitivity to transformation by various oncogenes.

Authors:  S Kizaka; A Hakura
Journal:  Mol Cell Biol       Date:  1989-12       Impact factor: 4.272

6.  Retrospective analysis of HPV 16/18-related disease burden using archival clinical samples.

Authors:  Naureen Ehsan Ilahi; Shoaib Naiyar Hashmi; Sobia Anwar; Sheeba Murad
Journal:  J Cancer Res Clin Oncol       Date:  2016-08-30       Impact factor: 4.553

7.  In vitro biological activities of the E6 and E7 genes vary among human papillomaviruses of different oncogenic potential.

Authors:  M S Barbosa; W C Vass; D R Lowy; J T Schiller
Journal:  J Virol       Date:  1991-01       Impact factor: 5.103

8.  Progression of human papillomavirus type 18-immortalized human keratinocytes to a malignant phenotype.

Authors:  P J Hurlin; P Kaur; P P Smith; N Perez-Reyes; R A Blanton; J K McDougall
Journal:  Proc Natl Acad Sci U S A       Date:  1991-01-15       Impact factor: 11.205

9.  The full-length E6 protein of human papillomavirus type 16 has transforming and trans-activating activities and cooperates with E7 to immortalize keratinocytes in culture.

Authors:  S A Sedman; M S Barbosa; W C Vass; N L Hubbert; J A Haas; D R Lowy; J T Schiller
Journal:  J Virol       Date:  1991-09       Impact factor: 5.103

10.  Single amino acid substitutions in "low-risk" human papillomavirus (HPV) type 6 E7 protein enhance features characteristic of the "high-risk" HPV E7 oncoproteins.

Authors:  B C Sang; M S Barbosa
Journal:  Proc Natl Acad Sci U S A       Date:  1992-09-01       Impact factor: 11.205

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