Abstract:
:The enhancer of human papillomavirus type 16 (HPV-16) is considered to be specific for epithelial cells, in particular for cervical carcinoma-derived cell lines. We reexamined this hypothesis with the complete enhancer as well as nonoverlapping subclones and found all clones to be active in epithelial cell lines derived from the epidermis and from carcinomas of the cervix, mammary gland, and colon, but inactive in fibroblast, lymphoma, and embryonal carcinoma cells. Although the virus infects only human mucosal epithelia, enhancer activity was independent of the exact type or of the species of origin of the transfected epithelial cell. In spite of epithelial cell specificity, we found that the activity of the HPV-16 enhancer varied strongly from a cytomegalovirus enhancer and the simian virus 40 enhancer in a cell line-dependent manner. This suggests varying quantitative contributions of enhancer elements rather than regulation by an all-or-none switch. Cell type specificity was maintained by a 91-bp subclone of the 400-bp enhancer. Most of the enhancer activity of this fragment was eliminated by alternative mutations in binding sites for the ubiquitous factors AP-1, nuclear factor 1 (NF1), or TEF-2. These three types of factors bind this 91-bp enhancer without cooperation, although activation appears to be synergistic. Outside the 91-bp fragment, a motif typical for papillomavirus enhancers, namely an octamerlike sequence flanked by an NF1-binding site, contributes to enhancer function, as the activity was strongly reduced upon its deletion. In HPV-16, this motif is bound by the oct-1 factor as well as by a probably novel factor, NFA, whereas a related motif of HPV-11 is recognized only by NFA. On examination, none of the five types of transcription factors involved in HPV enhancer activation was restricted to epithelial cells, but NF1, AP-1, and oct-1 were present in higher concentration in HeLa cells than in fibroblasts. Only NF1 showed some qualitative cell type-specific differences. We propose that the epithelial specificity of the HPV-16 enhancer is brought about via binding sites for supposed ubiquitous transcription factors. The mechanism of this activation apparently involves synergism between factors that vary in concentration and may include cell-specific functional differences residing outside the DNA-binding domain of these factors.
journal_name
J Viroljournal_title
Journal of virologyauthors
Chong T,Apt D,Gloss B,Isa M,Bernard HUdoi
10.1128/JVI.65.11.5933-5943.1991subject
Has Abstractpub_date
1991-11-01 00:00:00pages
5933-43issue
11eissn
0022-538Xissn
1098-5514journal_volume
65pub_type
杂志文章abstract:UNLABELLED:A balance between the functions of the influenza virus surface proteins hemagglutinin (HA) and neuraminidase (NA) is thought to be important for the transmission of viruses between humans. Here we describe two pandemic H1N1 viruses, A/swine/Virginia/1814-1/2012 and A/swine/Virginia/1814-2/2012 (pH1N1low-1 an...
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pub_type: 杂志文章
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abstract::Human immunodeficiency virus type 1 (HIV-1) sequences were generated from blood and from brain tissue obtained by stereotactic biopsy from six patients undergoing a diagnostic neurosurgical procedure. Proviral DNA was directly amplified by nested PCR, and 8 to 36 clones from each sample were sequenced. Phylogenetic an...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.68.11.7467-7481.1994
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pub_type: 杂志文章
doi:10.1128/JVI.79.17.11547-11551.2005
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abstract::Kinetic analysis showed that the Ki values and the Ki/Km ratios for mutated, recombinant M184V human immunodeficiency virus type 1 reverse transcriptase (RT) for (-)2'-dideoxy-3'-thiacytidine triphosphate (3TCTP) were 35-fold higher than the equivalent values for wild-type RT but only about twice as high as the equiva...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.70.8.5642-5645.1996
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pub_type: 杂志文章
doi:10.1128/JVI.37.1.248-255.1981
更新日期:1981-01-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.52.3.777-783.1984
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.74.24.11977-11982.2000
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.75.4.1816-1823.2001
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.26.2.532-535.1978
更新日期:1978-05-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.00720-17
更新日期:2017-08-10 00:00:00
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.67.10.5749-5753.1993
更新日期:1993-10-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.69.5.2786-2793.1995
更新日期:1995-05-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.71.1.519-526.1997
更新日期:1997-01-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.69.3.1903-1906.1995
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:1996-06-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.59.3.764-767.1986
更新日期:1986-09-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2012-04-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.75.11.5090-5098.2001
更新日期:2001-06-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.69.12.7541-7547.1995
更新日期:1995-12-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.43.1.104-112.1982
更新日期:1982-07-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2011-08-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2010-02-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.00396-09
更新日期:2009-10-01 00:00:00