Sequence variation and the transcriptional activity of the upstream regulatory region in human papillomavirus 16 E7 variants in cervical cancer of Korean women.
Abstract: The other sequence variations, which were matched with the TFBS, were A7485C, G7489A, T7743G and G7842A.
Abstract: The sequence variations T7781C and C7786T were matched with YY1 binding sites, G7193T and C7689A were matched with TEF1 binding sites, and C7394T and C7395T were matched with GRE binding sites.
Abstract: Using PCR-directed sequencing, the presence of sequence variations in URRs were analyzed and the sites of sequence variation were matched with the known transcriptional factor binding site (TFBS) in 26 HPV 16 E7 variants, 21 case
Differential splicing of E6 within human papillomavirus type 18 variants and functional consequences.
PMID: 16099904
2005
The Journal of general virology
Abstract: Mutagenesis analysis of the reference clone showed that a C491A change reverts the phenotype.
Human papillomavirus 16 minor capsid protein L2 helps capsomeres assemble independently of intercapsomeric disulfide bonding.
Abstract: Similar particles were obtained from the Sf9 cells co-infected with baculoviruses expressing L2 and an L1 mutant that lacks a C-terminal cysteine (C428S) and can form capsomeres but no capsids when expressed alone.
[Investigation of human papillomavirus, its types and variants].
Abstract: HPV 16 (55.8% in squamous cell carcinoma patients and 35.3% in cervical adenocarcinoma patients) and its European HPV 16 L83V variant were detected more frequently in cervical cancer patients.
Abstract: In particular, we describe methods for the identification of variation within the HPV-16 E5 open reading frame and for the detection of the nt 131 A-->G mutation of the E6 ORF, using restriction fragment length polymorphism assays.
Human papillomavirus type 16 E6 and E7 genotypes in head-and-neck carcinomas.
Abstract: Sequence analysis of the E6-E7 segments revealed three different HPV16 E6-E7 genotypes: the HPV16 prototype (6 of 21 cases), the E6 variant T350G (8 of 21 cases), and the E6-E7 variant A131G/C712A (7 of 21 cases).
Abstract: The E6 variants T350G and A131G have been associated with increased oncogenic potential in cervical cancer patients depending on host genetic factors.
Induction of tetrasomy by human papillomavirus type 16 E7 protein is independent of pRb binding and disruption of differentiation.
Abstract: Of seven HPV-16 E7 mutants analysed (H2P, Delta6-10, Delta21-24, C24G, S31G/S32G, A50S and S71I), five were severely impaired in their ability to induce tetrasomy in monolayer and raft culture.
Abstract: Only mutant C24G induced tetrasomy to levels comparable with wild-type E7 in monolayer and raft culture.
Abstract: The casein kinase II phosphorylation defective mutant S31G/S32G induced tetrasomy to levels comparable with wild-type E7 in raft culture, but not in monolayer culture, and induction of tetrasomy did not correlate with raft morphology.
Result:
Human papillomavirus type 16 E6, E7, and L1 variants in cervical cancer in Indonesia, Suriname, and The Netherlands.
Abstract: RESULTS: A specific Javanese variant, with mutations 666A in E7 and 6826T in L1, was found in 73% of the Indonesian samples, 56% having an additional mutation in the E6 open reading frame (ORF; 276G), giving the predicted amino acid change N58S.
[Analysis of human papillomavirus 16 E6 oncogene mutation in Xinjiang Uygur women with cervical carcinoma].
Abstract: RESULTS: The result of PCR showed that the positive rate of HPV16E6 was 82.86%(29/35); 26 of these 29 PCR fragments were sequenced and analyzed, 15 of them maintained prototype (57.69%), 11 have L83V mutation (34.62%), and 2 have L83V/D63E mutation (7.69%).
E2 sequence variations of HPV 16 among patients with cervical neoplasia seen in the Indian subcontinent.
Abstract: Samples with digestion profiles III and IV revealed three variations in the hinge region (3516 C-A, 3538 A-C, 3566 T-G) and two in the DNA binding domain (3684 C-A, 3694 T-A) of the E2 sequence.
HPV mutation literature information.
PMID: 
2005
Oncology reports
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