Relative enhancer activity and transforming potential of authentic human papillomavirus type 6 genomes from benign and malignant lesions

Farr, Abigail; Wang, He; Kasher, M S; Roman, Ann

doi:10.1099/0022-1317-72-3-519

Cited by 27 publications

(33 citation statements)

References 49 publications

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“…O, ACTGT sequences (an arrow indicates the ACTGT sequence previously suggested to be important in silencer activity; Wu & Mounts, 1988). (a) 94 bp insertion relative to HPV-6b at nt 7350; (b) 24 bp insertion at nt 7323; (c) 58 bp insertion at nt 7350; (d) 49 bp deletion at nt 7350 (Kasher & Roman, 1988;Farr et al, 1991). Note that 57 nt of the 58 bp insertion (c) in HPV6-T70 are identical to the first 58 bp of the 94 bp insertion (a) of HPV6-W50.…”

Section: I Imentioning

confidence: 82%

“…The plasmids pW50acat and pT70acat were described previously (Farr et al, 1991) and contain the LCRs of the HPV6-W50 and HPV6-T70 genomes (GenBank accession numbers L22693 and L22694, respectively) inserted into the NdeI site of the enhancerless plasmid pSVEcat . pW50acat and pT70acat were used to generate the subclones of the LCRs (Fig.…”

Section: Methodsmentioning

confidence: 99%

“…The numbering system is that of HPV-6b (Schwarz et al, 1983). Nuclear factor binding sites C/EBP, AP1, CK, E2, SphI, AP3, GRE, NFI and NFIII were identified by computer search (Farr et al, 1991). O, ACTGT sequences (an arrow indicates the ACTGT sequence previously suggested to be important in silencer activity; Wu & Mounts, 1988).…”

Section: I Imentioning

confidence: 99%

“…When the entire LCRs of HPV6-W50 and HPV6-T70 were analysed for their influence on expression from a downstream promoter they were found to act similarly. Both acted as enhancers in epithelial cells (HeLa cells) and neither had enhancer activity in fibroblasts (Vero cells) (Farr et al, 1991). However, it was possible that the effect of the sequence differences was masked in the background of the entire LCR.…”

Section: Introductionmentioning

confidence: 99%

“…Fax +1 317 274 4090. e-mail aroman @indycms.iupui.edu Dollard et al, 1993;Kyo et al, 1993;Kyo et al, 1994;May et al, 1994). We have recently cloned and characterized an HPV-6 from a benign lesion, HPV6-W50, and one from a malignant lesion, HPV6-T70, in an effort to understand the relationship of the viral genomes to the type of lesion from which they were isolated (Kasher & Roman, 1988;Farr et al, 1991). The two viruses are identical in the genes implicated in oncogenesis (E5, E6 and E7), but differ in sequences in the 5' half of the LCR, upstream of the L1 polyadenylation signal.…”

Section: Introductionmentioning

confidence: 99%

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Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Farr

Pattison

Youn

et al. 1995

Journal of General Virology

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Human papillomavirus type 6 (HPV-6) DNA is the predominant HPV type found in condyloma acuminata: it is rarely found in carcinomas. We have previously reported cloning and characterizing an HPV-6 from a vulvar condyloma (HPV6-W50) and an HPV-6 from a vulvar carcinoma (HPV6-T70). The E5, E6 and E7 proteins encoded by the two genomes were identical, however, the two genomes differed in the long control region (LCR). Cloning of the entire LCR into the enhancerless plasmid pSVEcat showed that the two LCRs had comparable enhancer activity. Since the major differences between the two LCRs resided in the 5' end of the LCR, upstream of the L1 polyadenylation signal, we subcloned the two LCRs to analyse more closely their effect on cat gene expression. The data indicated that LCR subclones of the two genomes had comparable chloramphenicol acetyltransferase (CAT) activity. A negative regulatory region was detectable when the test plasmids were transfected into HeLa and C33A cells and in primary keratinocytes. A decrease in CAT activity was also detected when the SV40 early promoter was replaced with the putative HPV-6 E6 promoter. The negative regulatory region functioned in a position-and orientation-independent manner, thus fulfilling the definition of a silencer.

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Section: I Imentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Section: I Imentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Farr

Pattison

Youn

et al. 1995

Journal of General Virology

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Human papillomavirus type 16 variants isolated from vulvar Bowenoid papulosis

Fang

Guedes

Muñoz

et al. 1993

Journal of Medical Virology

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Tissues from two cases of Bowenoid papulosis of the vulva were found to contain human papillomavirus (HPV) 16 DNA by Southern blot hybridization. Analysis of the hybridization pattern revealed differences in a restriction fragment of one specimen as compared to the HPV 16 DNA prototype. To investigate if these differences could interfere with the expression of such oncogenic viral genomes, the corresponding DNA fragments were cloned and further analyzed. After amplification by PCR and DNA sequencing, a 213 base pairs duplication was mapped in the long control region (LCR) of this HPV 16 variant. One single PCR fragment was obtained from the other Bowenoid papulosis, which is identical in size with the same region in the HPV-16 prototype. The duplication in the HPV-16 LCR analyzed in this study maps upstream of a region containing several regulatory elements.

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The Relative Ability of Human Papillomavirus Type 6 and Human Papillomavirus Type 16 E7 Proteins to Transactivate E2F-Responsive Elements Is Promoter- and Cell-Dependent

Armstrong

Roman

1997

Virology

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The human papillomavirus 16 E7 protein (HPV 16 E7) transactivates the adenovirus E2 promoter (AdE2) by altering interactions between retinoblastoma (pRb) family members and the transcription factor E2F. To understand factors limiting the oncogenic potential of HPV 6, the relative ability of HPV 6 E7 as compared to HPV 16 E7 to transactivate the AdE2 promoter was determined. In primary baby rat kidney cells and human foreskin keratinocytes, HPV 16 E7 transactivated the AdE2 promoter to a greater extent than HPV 6 E7, consistent with the observation that HPV 16 E7 binds pRb with greater affinity. HPV 6 E7 gain of function correlated with increasing the affinity of the HPV 6 E7 pRb binding site of conserved region 2 (CR2). In keratinocytes, in contrast to the AdE2 promoter, the abilities of the two E7 proteins to transactivate the B-myb promoter, a promoter regulated by E2F bound to p107/p130, were comparable. Introducing a negative charge into the N-terminus (CR1) and a high affinity pRb binding site into CR2 of HPV 6 E7 resulted in a transactivator with greater activity than HPV 16 E7 for both the AdE2 and B-myb promoters. Both of the promoters were negatively regulated by E2F and transactivation by the E7 proteins required an intact E2F site. In C33-A cells, which contain a mutated pRb, the two E7 proteins had comparable transactivating activity on both the AdE2 and B-myb promoters. The data are consistent with the interpretation that HPV 16 E7 affects interactions of pRb and p107/p130 with the E2F transcription factor, whereas HPV 6 E7 only affects interactions of p107/p130.

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Relative enhancer activity and transforming potential of authentic human papillomavirus type 6 genomes from benign and malignant lesions

Cited by 27 publications

References 49 publications

Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Detection of silencer activity in the long control regions of human papillomavirus type 6 isolated from both benign and malignant lesions

Human papillomavirus type 16 variants isolated from vulvar Bowenoid papulosis

The Relative Ability of Human Papillomavirus Type 6 and Human Papillomavirus Type 16 E7 Proteins to Transactivate E2F-Responsive Elements Is Promoter- and Cell-Dependent

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