Literature DB >> 20553529

Interaction of viral oncoproteins with cellular target molecules: infection with high-risk vs low-risk human papillomaviruses.

David Pim1, Lawrence Banks.   

Abstract

Persistent infection by a subgroup of so-called high-risk human papillomaviruses (HPVs) that have a tropism for mucosal epithelia has been defined as the cause of more than 98% of cervical carcinomas as well as a high proportion of other cancers of the anogenital region. Infection of squamous epithelial tissues in the head and neck region by these same high-risk HPVs is also associated with a subset of cancers. Despite the general conservation of genetic structure amongst all HPV types, infection by the low-risk types, whether in genital or head and neck sites, carries a negligible risk of malignant progression, and infections have a markedly different pathology. In this review, we will examine and discuss the interactions that the principal viral oncoproteins of the high-risk mucosotrophic HPVs and their counterparts from the low-risk group make with cellular target proteins, with a view to explaining the differences in their respective pathology.

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Year:  2010        PMID: 20553529     DOI: 10.1111/j.1600-0463.2010.02618.x

Source DB:  PubMed          Journal:  APMIS        ISSN: 0903-4641            Impact factor:   3.205


  50 in total

Review 1.  Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.

Authors:  Aloysius J Klingelhutz; Ann Roman
Journal:  Virology       Date:  2012-01-27       Impact factor: 3.616

2.  Immunologic responses to a novel DNA vaccine targeting human papillomavirus-11 E6E7.

Authors:  Julie Ahn; Shiwen Peng; Chien-Fu Hung; Richard B S Roden; Tzyy-Choou Wu; Simon R Best
Journal:  Laryngoscope       Date:  2017-07-17       Impact factor: 3.325

3.  Differential in vitro immortalization capacity of eleven (probable) [corrected] high-risk human papillomavirus types.

Authors:  Denise M Schütze; Peter J F Snijders; Leontien Bosch; Duco Kramer; Chris J L M Meijer; Renske D M Steenbergen
Journal:  J Virol       Date:  2013-11-20       Impact factor: 5.103

4.  Longitudinal assessment of DNA methylation changes during HPVE6E7-induced immortalization of primary keratinocytes.

Authors:  Denise M Schütze; Jan M Kooter; Saskia M Wilting; Chris J L M Meijer; Wim Quint; Peter J F Snijders; Renske D M Steenbergen
Journal:  Epigenetics       Date:  2015-01-23       Impact factor: 4.528

5.  The small splice variant of HPV16 E6, E6, reduces tumor formation in cervical carcinoma xenografts.

Authors:  Maria Filippova; Whitney Evans; Robert Aragon; Valery Filippov; Vonetta M Williams; Linda Hong; Mark E Reeves; Penelope Duerksen-Hughes
Journal:  Virology       Date:  2014-01-01       Impact factor: 3.616

6.  Human Papillomavirus 11 Early Protein E6 Activates Autophagy by Repressing AKT/mTOR and Erk/mTOR.

Authors:  Boya Zhang; Yinjing Song; Siyuan Sun; Rui Han; Chunting Hua; Stijn van der Veen; Hao Cheng
Journal:  J Virol       Date:  2019-05-29       Impact factor: 5.103

7.  The PTPN14 Tumor Suppressor Is a Degradation Target of Human Papillomavirus E7.

Authors:  Anita Szalmás; Vjekoslav Tomaić; Om Basukala; Paola Massimi; Suruchi Mittal; József Kónya; Lawrence Banks
Journal:  J Virol       Date:  2017-03-13       Impact factor: 5.103

8.  HPV type 16 E6 and NFX1-123 augment JNK signaling to mediate keratinocyte differentiation and L1 expression.

Authors:  Justine Levan; Portia A Vliet-Gregg; Kristin L Robinson; Lisa R Matsumoto; Rachel A Katzenellenbogen
Journal:  Virology       Date:  2019-03-16       Impact factor: 3.616

9.  Recombination-dependent oligomerization of human papillomavirus genomes upon transient DNA replication.

Authors:  Marit Orav; Liisi Henno; Helen Isok-Paas; Jelizaveta Geimanen; Mart Ustav; Ene Ustav
Journal:  J Virol       Date:  2013-08-28       Impact factor: 5.103

Review 10.  The papillomavirus E7 proteins.

Authors:  Ann Roman; Karl Munger
Journal:  Virology       Date:  2013-05-31       Impact factor: 3.616

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