E6 and E7 Oncoproteins from Human Papillomavirus Type 16 Induce Activation of Human Transforming Growth Factorβ1Promoter throughout Sp1 Recognition Sequence

2006 ◽  
Vol 19 (3) ◽  
pp. 468-480 ◽  
Author(s):  
Oscar Peralta-Zaragoza ◽  
Víctor Bermúdez-Morales ◽  
Lourdes Gutiérrez-Xicotencatl ◽  
Juan Alcocer-González ◽  
Félix Recillas-Targa ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Recognition Sequence ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

Studies on in Vivo Induction of Cytotoxic T Lymphocyte Responses by Synthetic Peptides from E6 and E7 Oncoproteins of Human Papillomavirus Type 16

1995 ◽  
Vol 8 (3) ◽  
pp. 165-174 ◽  
Author(s):  
ASIS K. SARKAR ◽  
GUILLERMO TORTOLERO-LUNA ◽  
PRAMOD N. NEHETE ◽  
RALPH B. ARLINGHAUS ◽  
MICHELE FOLLEN MITCHELL ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
T Lymphocyte ◽  
Synthetic Peptides ◽  
Cytotoxic T Lymphocyte ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7 ◽  
Lymphocyte Responses ◽  
In Vivo Induction

scholarly journals Human papillomavirus type 16 E6 and E7 oncoproteins act synergistically to cause head and neck cancer in mice

Virology ◽  
2010 ◽  
Vol 407 (1) ◽  
pp. 60-67 ◽  
Author(s):  
Sean Jabbar ◽  
Katerina Strati ◽  
Myeong Kyun Shin ◽  
Henry C. Pitot ◽  
Paul F. Lambert
Keyword(s):  
Head And Neck Cancer ◽  
Human Papillomavirus ◽  
Head And Neck ◽  
Neck Cancer ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals Human papillomavirus type 16 E6 and E7 oncoproteins upregulate c-IAP2 gene expression and confer resistance to apoptosis

Oncogene ◽  
2005 ◽  
Vol 24 (32) ◽  
pp. 5069-5078 ◽  
Author(s):  
Huidong Yuan ◽  
Fenghua Fu ◽  
Jiaying Zhuo ◽  
Wei Wang ◽  
Junko Nishitani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Papillomavirus ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals Functional Interaction between Human Papillomavirus Type 16 E6 and E7 Oncoproteins and Cigarette Smoke Components in Lung Epithelial Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e38178 ◽  
Author(s):  
Juan Pablo Muñoz ◽  
Carolina González ◽  
Bárbara Parra ◽  
Alejandro H. Corvalán ◽  
Maria Lina Tornesello ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Lung Epithelial Cells ◽  
Functional Interaction ◽  
Human Papillomavirus Type 16 ◽  
Lung Epithelial ◽  
E6 And E7 Oncoproteins ◽  
E6 And E7

scholarly journals Multiple ASF/SF2 Sites in the Human Papillomavirus Type 16 (HPV-16) E4-Coding Region Promote Splicing to the Most Commonly Used 3′-Splice Site on the HPV-16 Genome

2010 ◽  
Vol 84 (16) ◽  
pp. 8219-8230 ◽  
Author(s):  
Monika Somberg ◽  
Stefan Schwartz
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Splice Site ◽  
Binding Sites ◽  
Mrna Levels ◽  
Coding Region ◽  
Cervical Lesions ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7

ABSTRACT Our results presented here demonstrate that the most abundant human papillomavirus type 16 (HPV-16) mRNAs expressing the viral oncogenes E6 and E7 are regulated by cellular ASF/SF2, itself defined as a proto-oncogene and overexpressed in cervical cancer cells. We show that the most frequently used 3′-splice site on the HPV-16 genome, site SA3358, which is used to produce primarily E4, E6, and E7 mRNAs, is regulated by ASF/SF2. Splice site SA3358 is immediately followed by 15 potential binding sites for the splicing factor ASF/SF2. Recombinant ASF/SF2 binds to the cluster of ASF/SF2 sites. Mutational inactivation of all 15 sites abolished splicing to SA3358 and redirected splicing to the downstream-located, late 3′-splice site SA5639. Overexpression of a mutant ASF/SF2 protein that lacks the RS domain, also totally inhibited the usage of SA3358 and redirected splicing to the late 3′-splice site SA5639. The 15 ASF/SF2 binding sites could be replaced by an ASF/SF2-dependent, HIV-1-derived splicing enhancer named GAR. This enhancer was also inhibited by the mutant ASF/SF2 protein that lacks the RS domain. Finally, silencer RNA (siRNA)-mediated knockdown of ASF/SF2 caused a reduction in spliced HPV-16 mRNA levels. Taken together, our results demonstrate that the major HPV-16 3′-splice site SA3358 is dependent on ASF/SF2. SA3358 is used by the most abundantly expressed HPV-16 mRNAs, including those encoding E6 and E7. High levels of ASF/SF2 may therefore be a requirement for progression to cervical cancer. This is supported by our earlier findings that ASF/SF2 is overexpressed in high-grade cervical lesions and cervical cancer.

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