Efficient production and optimization of E7 oncoprotein from Iranian human papillomavirus type 16 in Lactococcus lactis using nisin-controlled gene expression (NICE) system

2017 ◽  
Vol 110 ◽  
pp. 554-560 ◽  
Author(s):  
Amir Hossein Mohseni ◽  
Vadood Razavilar ◽  
Hossein Keyvani ◽  
Mohammad Reza Razavi ◽  
Ramazan Ali Khavari-Nejad
1992 ◽  
Vol 66 (4) ◽  
pp. 2418-2427 ◽  
Author(s):  
W C Phelps ◽  
K Münger ◽  
C L Yee ◽  
J A Barnes ◽  
P M Howley

2012 ◽  
Vol 72 (16) ◽  
pp. 4008-4016 ◽  
Author(s):  
Sean F. Jabbar ◽  
Soyeong Park ◽  
Johannes Schweizer ◽  
Marthe Berard-Bergery ◽  
Henry C. Pitot ◽  
...  

2000 ◽  
Vol 20 (17) ◽  
pp. 6483-6495
Author(s):  
Boris Mannhardt ◽  
Stuart A. Weinzimer ◽  
Mechthild Wagner ◽  
Marc Fiedler ◽  
Pinchas Cohen ◽  
...  

2008 ◽  
Vol 82 (7) ◽  
pp. 3665-3678 ◽  
Author(s):  
Monika Somberg ◽  
Xiaomin Zhao ◽  
Monika Fröhlich ◽  
Magnus Evander ◽  
Stefan Schwartz

ABSTRACT We have initiated a screen for cellular factors that can induce human papillomavirus type 16 (HPV-16) late gene expression in human cancer cells. We report that the overexpression of polypyrimidine tract binding protein (PTB), also known as heterologous nuclear ribonucleoprotein I (hnRNP I), induces HPV-16 late gene expression in cells transfected with subgenomic HPV-16 plasmids or with full-length HPV-16 genomes and in persistently HPV-16-infected cells. In contrast, other hnRNPs such as hnRNP B1/A2, hnRNP F, and hnRNP Q do not induce HPV-16 late gene expression. PTB activates SD3632, the only 5′ splice site on the HPV-16 genome that is used exclusively by late mRNAs. PTB interferes with splicing inhibitory sequences located immediately upstream and downstream of SD3632, thereby activating late gene expression. One AU-rich PTB-responsive element was mapped to a 198-nucleotide sequence located downstream of SD3632. The deletion of this element induced HPV-16 late gene expression in the absence of PTB. Our results suggest that the overexpression of PTB interferes with cellular factors that interact with the inhibitory sequences. One may speculate that an increase in PTB levels or a reduction in the concentration of a PTB antagonist is required for the activation of HPV-16 late gene expression during the viral life cycle.


Virology ◽  
2002 ◽  
Vol 295 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Alexandra Eichten ◽  
Matthew Westfall ◽  
Jennifer A. Pietenpol ◽  
Karl Münger

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