JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dollard, S C
Right arrow Articles by Chow, L T
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dollard, S C
Right arrow Articles by Chow, L T

 Previous Article  |  Next Article 

J Virol. 1993 March; 67(3): 1721-1726

Regulation of the human papillomavirus type 11 E6 promoter by viral and host transcription factors in primary human keratinocytes.

S C Dollard, T R Broker and L T Chow

Department of Biochemistry, University of Rochester School of Medicine and Dentistry, New York 14642.

ABSTRACT

Human papillomavirus (HPV) type 11 is strictly trophic for epithelial cells and induces benign condylomata of the external genitalia and also causes laryngeal papillomas. Primary keratinocytes are the appropriate hosts for studies of HPV gene regulation, but they are not frequently used, owing to difficulties in culturing and low transfection efficiencies. By modifying a Polybrene transfection procedure, we achieved consistently high transfection efficiencies in primary human foreskin keratinocytes and characterized the HPV type 11 enhancer in the context of the homologous E6 promoter. Contrary to previous studies with immortalized human cervical carcinoma C-33A cells, constitutive enhancer element II in the upstream regulatory region conferred no enhancer activity and did not abrogate repression by the homologous E2 protein. Rather, repression was strong, ranging from 5.6- to 20-fold for the various enhancer deletion mutations. By deletion analysis, a strong enhancer that included three nuclear factor 1 sites and one nuclear factor 1-associated factor-binding site was localized to a 45-bp region within constitutive enhancer element I, and it showed some degree of tissue specificity.


J Virol. 1993 March; 67(3): 1721-1726




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 1993 by the American Society for Microbiology. All rights reserved.