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1 l structure of the complete E2NT module from human papillomavirus 16.
2  papillomavirus types ('high risk, including human papillomaviruses 16, 18, 31, 33, 45 and 56), furth
3 iority 1 month after the last dose of 2-dose human papillomavirus 16/18 AS04-adjuvanted (AS04-HPV-16/
4                                              Human papillomavirus 16/18 clearance rates at 12 months
5                        Conversely, oncogenic human papillomavirus-16/18 E6 protein significantly enha
6 he strongest HSIL determinants were baseline human papillomavirus 16 (adjusted odds ratio, 8.2; 95% c
7                                              Human papillomavirus-16 and HPV-18 incidence were simila
8                                              Human papillomavirus-16 cleared significantly slower tha
9 ed viral strains bovine papillomavirus-1 and human papillomavirus-16 discriminate between DNA targets
10 viously demonstrated replication defect of a human papillomavirus 16 E1 protein that was also unable
11                                          The human papillomavirus 16 E2 protein binds to four specifi
12  protein was degraded by transfection of the human papillomavirus 16 E6 (HPV-16 E6) gene and H460 cel
13  was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two
14 cinoma cell lines expressing a TAP-dependent human papillomavirus 16 E6 Ag epitope resulted in their
15 yndrome fibroblasts as well as in normal and human papillomavirus 16 E6 and E7 protein-expressing hum
16 man fibroblasts created by expression of the human papillomavirus 16 E6 gene.
17          Consistent with these findings, the human papillomavirus 16 E6 mutant Y54D, which selectivel
18                            Expression of the human papillomavirus 16 E6 oncogene interferes with seve
19                       Fibroblasts expressing human papillomavirus 16 E6 oncoprotein had impaired repa
20 sed in LCLs retrovirally transduced with the Human Papillomavirus 16 E6 oncoprotein, consistent with
21 al cells, as well as in cells expressing the human papillomavirus 16 E6 oncoprotein, on exposure of t
22 s region prevents the degradation induced by human papillomavirus 16 E6 protein.
23 sion of p53 and Rb through the regulation of human papillomavirus 16 E6/E7 genes.
24 s in ER-'poor' HMECs acutely transduced with human papillomavirus-16 E6 (HMEC-E6) through a rapid mit
25                                              Human papillomavirus-16 E6 and E7 inactivate the tumor s
26 d-type p53 protein in NSCLC cells expressing human papillomavirus-16 E6 oncoprotein blocked CD437-ind
27 found that, whereas UVB induces apoptosis in human papillomavirus-16 E6/7-immortalized keratinocytes,
28                                              Human papillomavirus-16 E6/E7 expression is common in SC
29                                     Although human papillomavirus-16 E6/E7 expression was detected in
30                                              Human papillomavirus 16 E7 (HPV16 E7) and adenovirus 5 E
31 uman cancer risk, transgenic mice expressing human papillomavirus 16 E7 oncogene (K14-HPV16-E7), show
32                Conjugate vaccines containing human papillomavirus 16 E7 oncoprotein or survivin as a
33  delta activity in vitro and interacted with human papillomavirus 16 E7 oncoprotein, suggesting that
34 ed with those of HPECs immortalized with the human Papillomavirus 16 E7 oncoprotein.
35 cence in HUCs, including HUCs transformed by human papillomavirus 16 E7 or E6, whose oncoprotein prod
36 hese studies, we crossed mice transgenic for human papillomavirus 16 E7 to knock-in mice genetically
37 nd E2F was blocked by enforced expression of human papillomavirus 16 E7.
38                                        Using human papillomavirus-16 E7 as a model antigen, we evalua
39 nt peptide binders against two oncoproteins, human papillomavirus 16 early protein 6 (HPV16 E6) and p
40 , whether naked or encapsidated by MusPV1 or human papillomavirus 16 (HPV 16) capsids, efficiently in
41 ed tetracycline-inducible vector system, and human papillomavirus 16 (HPV 16) E6 and E7 gene-immortal
42 sed to detect viral nucleic acids, including human papillomavirus 16 (HPV-16) and parvovirus B19 (PB-
43                                              Human Papillomavirus 16 (HPV-16) has been identified as
44     Recent studies have reported evidence of human papillomavirus 16 (HPV-16) in a very high proporti
45                                      We used human papillomavirus-16 (HPV-16) DNA as a model to evalu
46  induce CD8+ T-lymphocyte (CTL) responses to human papillomavirus-16 (HPV-16) E6 and E7 proteins usin
47 eratinocytes (NHOK) immortalized with cloned human papillomavirus-16 (HPV-16) genome than in primary
48                                              Human papillomavirus-16 (HPV-16) is associated etiologic
49                                         Both human papillomavirus 16 (HPV16) and bovine papillomaviru
50        The 3'-untranslated regions (UTRs) of human papillomavirus 16 (HPV16) and bovine papillomaviru
51 In agreement with previous studies, we found human papillomavirus 16 (HPV16) and HPV18 in oropharynge
52 nserved L2 residues 17 to 36 and neutralizes human papillomavirus 16 (HPV16) and HPV18.
53                             The structure of human papillomavirus 16 (HPV16) complexed with H16.U4 fr
54             To replicate the double-stranded human papillomavirus 16 (HPV16) DNA genome, viral protei
55                 The association between oral human papillomavirus 16 (HPV16) DNA load and infection c
56                                              Human papillomavirus 16 (HPV16) drives precursor cervica
57                                              Human papillomavirus 16 (HPV16) E2 is a DNA-binding prot
58  and wildtype p53 (p53WT) inactivated by the human papillomavirus 16 (HPV16) E6 oncogene.
59 mmary epithelial cells (MEC) immortalized by human papillomavirus 16 (HPV16) E6, the p53 degradation-
60 d on a sequence motif of 21 nucleotides from human papillomavirus 16 (HPV16) E6E7 bicistronic RNA was
61                                              Human papillomavirus 16 (HPV16) E6E7 pre-mRNA is bicistr
62                                              Human papillomavirus 16 (HPV16) E7 has long been known t
63 roepithelial cell (HUC) lines transformed by Human Papillomavirus 16 (HPV16) E7.
64                                              Human papillomavirus 16 (HPV16) enters its host cells by
65            Vulnerability of younger women to human papillomavirus 16 (HPV16) infection has been attri
66 rect cleavage of capsid-associated L2 during human papillomavirus 16 (HPV16) infection remains poorly
67                                              Human papillomavirus 16 (HPV16) is a causative agent in
68                                              Human papillomavirus 16 (HPV16) is a worldwide health th
69                                              Human papillomavirus 16 (HPV16) is causative in many hum
70                                              Human papillomavirus 16 (HPV16) is the most prevalent HR
71                                              Human papillomavirus 16 (HPV16) is the most prevalent on
72                                   Infectious human papillomavirus 16 (HPV16) L1/L2 pseudovirions were
73 g protein 1) is a restriction factor for the human papillomavirus 16 (HPV16) life cycle.
74                                    Using the human papillomavirus 16 (HPV16) murine model, TC-1, we d
75 eatment, dramatically decreased infection of human papillomavirus 16 (HPV16) pseudovirus (PsV).
76 tudy, we utilized the oncogenes of high-risk human papillomavirus 16 (HPV16) to overcome the resistan
77 ed a novel interaction between Rint1 and the human papillomavirus 16 (HPV16) transcription and replic
78 s, including bovine papillomavirus (BPV) and human papillomavirus 16 (HPV16), associate with the cell
79 and that this combined therapy can eradicate human papillomavirus 16 (HPV16)-induced tumors.
80 confirm a much higher incidence of high-risk human papillomavirus 16 (HPV16)-mediated carcinogenesis
81 e loss of E2 host gene regulation.IMPORTANCE Human papillomavirus 16 (HPV16)-positive tumors that ret
82                                            A human papillomavirus 16 (HPV16)-targeted version of the
83                                              Human papillomaviruses 16 (HPV16) is the primary causati
84 oblast growth factor modulate penetration of human papillomavirus 16-immortalized keratinocytes throu
85 of selected growth factors on penetration of human papillomavirus 16-immortalized keratinocytes throu
86  resulted in near-doubling of penetration of human papillomavirus 16-immortalized keratinocytes, wher
87 e found to be markedly increased compared to human papillomavirus-16-immortalized human oral keratino
88                                              Human papillomavirus-16 incidence was higher among high-
89 rogression.IMPORTANCE Although the high-risk human papillomavirus 16 infects anogenital and oropharyn
90         Gaps also occur in intron 4, where a human papillomavirus 16 integration site has been locali
91 d of intron 3, a region known to encompass a human papillomavirus-16 integration site and two cluster
92                                              Human papillomavirus 16 is a causative agent of most cas
93  epithelial carcinogenesis [i.e., keratin 14-human papillomavirus 16 (K14-HPV16) transgenic mice].
94                              The full-length human papillomavirus 16 major capsid protein L1 is expre
95 To study intracellular pathways by which the human papillomavirus 16 oncogene E7 participates in carc
96                     However, yeast-expressed human papillomavirus 16 particles are irregular in shape
97 zing additional mRNA antigens, including the human papillomavirus 16 proteins E6 and E7 and the varic
98 EBV) EBNA1 antibodies) and disease outcomes (human papillomavirus-16 seropositivity with cervical int
99                     Virgin female keratin 14-human papillomavirus 16 transgenic mice were fed control