ライフサイエンスコーパス: human papillomavirus 16

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 ed viral strains bovine papillomavirus-1 and human papillomavirus-16 discriminate between DNA targets

7 viously demonstrated replication defect of a human papillomavirus 16 E1 protein that was also unable

8 The human papillomavirus 16 E2 protein binds to four specifi

9 protein was degraded by transfection of the human papillomavirus 16 E6 (HPV-16 E6) gene and H460 cel

10 was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two

11 cinoma cell lines expressing a TAP-dependent human papillomavirus 16 E6 Ag epitope resulted in their

12 yndrome fibroblasts as well as in normal and human papillomavirus 16 E6 and E7 protein-expressing hum

13 man fibroblasts created by expression of the human papillomavirus 16 E6 gene.

14 Consistent with these findings, the human papillomavirus 16 E6 mutant Y54D, which selectivel

15 Expression of the human papillomavirus 16 E6 oncogene interferes with seve

16 Fibroblasts expressing human papillomavirus 16 E6 oncoprotein had impaired repa

17 sed in LCLs retrovirally transduced with the Human Papillomavirus 16 E6 oncoprotein, consistent with

18 al cells, as well as in cells expressing the human papillomavirus 16 E6 oncoprotein, on exposure of t

19 s region prevents the degradation induced by human papillomavirus 16 E6 protein.

20 sion of p53 and Rb through the regulation of human papillomavirus 16 E6/E7 genes.

21 s in ER-'poor' HMECs acutely transduced with human papillomavirus-16 E6 (HMEC-E6) through a rapid mit

22 Human papillomavirus-16 E6 and E7 inactivate the tumor s

23 d-type p53 protein in NSCLC cells expressing human papillomavirus-16 E6 oncoprotein blocked CD437-ind

24 found that, whereas UVB induces apoptosis in human papillomavirus-16 E6/7-immortalized keratinocytes,

25 Human papillomavirus-16 E6/E7 expression is common in SC

26 Although human papillomavirus-16 E6/E7 expression was detected in

27 Human papillomavirus 16 E7 (HPV16 E7) and adenovirus 5 E

28 uman cancer risk, transgenic mice expressing human papillomavirus 16 E7 oncogene (K14-HPV16-E7), show

29 Conjugate vaccines containing human papillomavirus 16 E7 oncoprotein or survivin as a

30 delta activity in vitro and interacted with human papillomavirus 16 E7 oncoprotein, suggesting that

31 ed with those of HPECs immortalized with the human Papillomavirus 16 E7 oncoprotein.

32 cence in HUCs, including HUCs transformed by human papillomavirus 16 E7 or E6, whose oncoprotein prod

33 hese studies, we crossed mice transgenic for human papillomavirus 16 E7 to knock-in mice genetically

34 nd E2F was blocked by enforced expression of human papillomavirus 16 E7.

35 Using human papillomavirus-16 E7 as a model antigen, we evalua

36 , whether naked or encapsidated by MusPV1 or human papillomavirus 16 (HPV 16) capsids, efficiently in

37 ed tetracycline-inducible vector system, and human papillomavirus 16 (HPV 16) E6 and E7 gene-immortal

38 Human Papillomavirus 16 (HPV-16) has been identified as

39 Recent studies have reported evidence of human papillomavirus 16 (HPV-16) in a very high proporti

40 induce CD8+ T-lymphocyte (CTL) responses to human papillomavirus-16 (HPV-16) E6 and E7 proteins usin

41 eratinocytes (NHOK) immortalized with cloned human papillomavirus-16 (HPV-16) genome than in primary

42 Human papillomavirus-16 (HPV-16) is associated etiologic

43 The 3'-untranslated regions (UTRs) of human papillomavirus 16 (HPV16) and bovine papillomaviru

44 Both human papillomavirus 16 (HPV16) and bovine papillomaviru

45 In agreement with previous studies, we found human papillomavirus 16 (HPV16) and HPV18 in oropharynge

46 nserved L2 residues 17 to 36 and neutralizes human papillomavirus 16 (HPV16) and HPV18.

47 The structure of human papillomavirus 16 (HPV16) complexed with H16.U4 fr

48 To replicate the double-stranded human papillomavirus 16 (HPV16) DNA genome, viral protei

49 The association between oral human papillomavirus 16 (HPV16) DNA load and infection c

50 mmary epithelial cells (MEC) immortalized by human papillomavirus 16 (HPV16) E6, the p53 degradation-

51 d on a sequence motif of 21 nucleotides from human papillomavirus 16 (HPV16) E6E7 bicistronic RNA was

52 Human papillomavirus 16 (HPV16) E6E7 pre-mRNA is bicistr

53 roepithelial cell (HUC) lines transformed by Human Papillomavirus 16 (HPV16) E7.

54 Human papillomavirus 16 (HPV16) enters its host cells by

55 Vulnerability of younger women to human papillomavirus 16 (HPV16) infection has been attri

56 rect cleavage of capsid-associated L2 during human papillomavirus 16 (HPV16) infection remains poorly

57 Human papillomavirus 16 (HPV16) is a worldwide health th

58 Human papillomavirus 16 (HPV16) is causative in many hum

59 Human papillomavirus 16 (HPV16) is the most prevalent HR

60 Human papillomavirus 16 (HPV16) is the most prevalent on

61 eatment, dramatically decreased infection of human papillomavirus 16 (HPV16) pseudovirus (PsV).

62 tudy, we utilized the oncogenes of high-risk human papillomavirus 16 (HPV16) to overcome the resistan

63 ed a novel interaction between Rint1 and the human papillomavirus 16 (HPV16) transcription and replic

64 s, including bovine papillomavirus (BPV) and human papillomavirus 16 (HPV16), associate with the cell

65 and that this combined therapy can eradicate human papillomavirus 16 (HPV16)-induced tumors.

66 A human papillomavirus 16 (HPV16)-targeted version of the

67 oblast growth factor modulate penetration of human papillomavirus 16-immortalized keratinocytes throu

68 of selected growth factors on penetration of human papillomavirus 16-immortalized keratinocytes throu

69 resulted in near-doubling of penetration of human papillomavirus 16-immortalized keratinocytes, wher

70 e found to be markedly increased compared to human papillomavirus-16-immortalized human oral keratino

71 Gaps also occur in intron 4, where a human papillomavirus 16 integration site has been locali

72 d of intron 3, a region known to encompass a human papillomavirus-16 integration site and two cluster

73 Human papillomavirus 16 is a causative agent of most cas

74 epithelial carcinogenesis [i.e., keratin 14-human papillomavirus 16 (K14-HPV16) transgenic mice].

75 The full-length human papillomavirus 16 major capsid protein L1 is expre

76 To study intracellular pathways by which the human papillomavirus 16 oncogene E7 participates in carc

77 However, yeast-expressed human papillomavirus 16 particles are irregular in shape

78 Virgin female keratin 14-human papillomavirus 16 transgenic mice were fed control