ライフサイエンスコーパス: E7 protein

1 protein (pRb) by the papillomavirus type 16 E7 protein.

2 ulsed with cell lysates containing wild-type E7 protein.

3 wild-type E7 DNA vaccine expressing a stable E7 protein.

4 moting activity of the human papilloma virus E7 protein.

5 -binding motifs expressed a rapidly degraded E7 protein.

6 r suppressor protein (pRb) by transduced HPV E7 protein.

7 ombinant adenovirus that expresses the HPV16 E7 protein.

8 on or expression of the human papillomavirus E7 protein.

9 own enhances the ubiquitination of the HPV16 E7 protein.

10 an ferritin and human papillomavirus derived E7 protein.

11 eratinocytes in collaboration with the viral E7 protein.

12 enza hemagglutinin, and human papillomavirus E7 protein.

13 motif and the CR3 zinc binding domain of the E7 protein.

14 activity that is not shared by low-risk HPV E7 protein.

15 function is disrupted by the papillomavirus E7 protein.

16 uman cells is the inactivation of pRB by the E7 protein.

17 of the human papillomavirus type 18 (HPV-18) E7 protein.

18 express high-risk human papillomavirus (HPV) E7 proteins.

19 e seen in cells that express only HPV E6 and E7 proteins.

20 expressing the human papillomavirus16 E6 and E7 proteins.

21 oteins were also less stable than the LR HPV E7 proteins.

22 ays are shown to detect low levels of E6 and E7 proteins.

23 lls, a cell line that expresses HPV16 E6 and E7 proteins.

24 emonstrated for the low-risk HPV-6 or HPV-11 E7 proteins.

25 sm in the presence of high- and low-risk HPV E7 proteins.

26 high-risk human papillomavirus (HPV) E6 and E7 proteins.

27 thway components FANCA and FANCD2 stimulates E7 protein accumulation in human keratinocytes and cause

28 E7 proteins act by associating with members of the retin

29 high-risk human papillomavirus (HPV) E6 and E7 proteins act cooperatively to mediate multiple activi

30 Repression of the E7 protein activated the Rb pathway but not the p53 path

31 propose that the human papillomavirus E6 and E7 proteins actively prevent senescence from occurring i

32 elevated nuclear levels of the low-risk HPV E7 protein afforded by the inducible system account for

33 gen and human papillomavirus type 16 (HPV16) E7 protein also bind host regulatory factors, we investi

34 udies demonstrated that the high-risk E6 and E7 proteins also play roles in the productive life cycle

35 lex phenotype involving both the function of E7 protein and a cis element necessary for the activatio

36 n diameter) achieved efficient codelivery of E7 protein and STING agonists to the myeloid cell popula

37 stably transfected plasmids encoding E6 and E7 proteins and examined their transforming potential in

38 es encoding the human papilloma virus E6 and E7 proteins and is over-expressed in women with cervical

39 The impact of human papilloma virus (HPV16) E7 proteins and retinoblastoma (RB) antisense oligonucle

40 high-risk human papillomavirus (HPV) E6 and E7 proteins, and repression of HPV gene expression cause

41 The human papillomavirus (HPV) E7 protein appears to be a major determinant for this ac

42 16 (HPV16) and bovine papillomavirus (BPV1) E7 proteins are capable of partially substituting for SV

43 The HPV-16 E6 and E7 proteins are highly expressed in differentiating kera

44 However, E7 proteins are maintained at high levels in most HPV-po

45 ycle arrest, indicating that the majority of E7 proteins are the translational products of E6*I mRNAs

46 azobenzene linker as an adjuvant, and HPV16 E7 protein as an antigen.

47 Here, we show that low- and high-risk HPV E7 proteins, as well as simian virus 40 T antigen and ad

48 In vitro, the E6 and E7 proteins associate with the cellular p53 and Rb prote

49 VOPC cells harboring MUC16, SIRPA and HPV-16-E7 proteins augmented invasion and induced epithelial to

50 E6 and E7 proteins bind to and inactivate the cellular tumor su

51 novirus E1A and human papillomavirus type 16 E7 protein but exhibit wild-type binding to E2F or DP, a

52 We show that the HPV16 E7 protein but not SV40 T antigen can complement mutatio

53 the absence of UL97, expression of wild-type E7 protein, but not a mutant E7 unable to bind pRb famil

54 (MARCHF8) induced by HPV16 E6 stabilizes the E7 protein by degrading CUL1 and UBE2L3 and blocking E7

55 we report that MARCHF8 stabilizes the HPV16 E7 protein by degrading the components of the S-phase ki

56 We show that the HPV E7 protein can interact with p21(Cip1) and abrogate p21(

57 A number of E7 proteins can increase IL-18BP production, and a regio

58 ration of this combination adjuvant with HPV E7 protein caused tumor rejection in all tumor-bearing m

59 potency of DNA vaccines; and (3) accelerated E7 protein degradation leads to enhanced antigen present

60 plasmids targeting HPV-16 and HPV-18 E6 and E7 proteins, delivered by electroporation, would cause h

61 We have demonstrated previously that the E7 protein destabilizes p130, a pRb-related pocket prote

62 The HPV E7 protein destabilizes the p130/retinoblastoma suscepti

63 ut the truncated E6 variants and full-length E7 protein did not.

64 The low-risk HPV-6 E6 and E7 proteins did not cause any significant change in the

65 The low-risk HPV-6 E6 and E7 proteins did not induce such abnormalities.

66 on of high-risk, but not low-risk, HPV E6 or E7 proteins disrupts the p53-dependent G1 arrest that ce

67 er-related human papillomaviruses, the BPV-1 E7 protein does not associate efficiently with the retin

68 We show that the HPV E7 protein downregulates miR-203 expression upon differe

69 se observations prove unequivocally that the E7 protein drives S-phase reentry in postmitotic, differ

70 Our data suggest that HPV E7 proteins dysregulate hormone-dependent gene expressio

71 mor suppressor pathway is inactivated by the E7 protein, E6 repression activates p53 signaling, which

72 High-risk human papillomavirus (HPV) E7 proteins enable oncogenic transformation of HPV-infec

73 e expression of either the E6 protein or the E7 protein encoded by integrated HPV18 DNA in HeLa cervi

74 Our studies indicate that the HPV E7 protein enhances HIF-1 transcriptional activity where

75 human papillomavirus type 16 (HPV-16) E6 and E7 proteins exhibit deregulation of G2/M genes, allowing

76 ells pulsed with lysates containing ETA(dII)/E7 protein exhibited enhanced MHC class I presentation o

77 ecrete the human papilloma virus-16 (HPV-16) E7 protein expressed in HPV-16-associated cervical cance

78 the host cellular proteins that bind to the E7 proteins expressed from 17 different HPV types.

79 in normal and human papillomavirus 16 E6 and E7 protein-expressing human mammary epithelial cells.

80 The E7 protein forms a complex with the cellular tumor suppr

81 The E7 protein from high-risk HPV types alters cell cycle pr

82 We believe that the E7 protein from HPV-16 can modulate the cytoplasmic loca

83 e report a direct interaction between E6 and E7 proteins from carcinogenic HPV types 16 and 31.

84 mine the consequences of removing the E6 and E7 proteins from cervical cancer cells, we infected HeLa

85 emonstrate that this ability is shared among E7 proteins from different HPV types.

86 The E7 proteins from diverse HPVs bind to the host cellular

87 Unlike the E7 proteins from the cancer-related human papillomavirus

88 The E6 and E7 proteins from the high-risk human papillomaviruses (H

89 Interestingly, the E6 and E7 proteins from the low-risk HPV types also inhibited M

90 The E6 and E7 proteins from the low-risk virus HPV-6 were not able

91 l lines without the combined presence of the E7 protein, further exemplifying the independent roles o

92 e we tested the hypothesis that the low-risk E7 protein has an intrinsic ability to decrease expressi

93 The HPV-16 E7 protein has been reported to target pRB family member

94 ing the human papillomavirus (HPV)-16 E6 and E7 proteins have achieved limited success in HPV-positiv

95 ty of transcriptional changes are due to the E7 protein impairing pocket protein function.

96 by the high-risk human papillomavirus (HPV) E7 protein in a manner which is dependent upon retinobla

97 BP1 and significantly decreased the level of E7 protein in Caski cells, suggesting that phosphorylati

98 ethyl ketone (TLCK) modified the HPV type 18 E7 protein in cell extracts as well as in living cells a

99 lation machinery to maintain a high level of E7 protein in differentiated cells.

100 ARCHF8 prevents the degradation of the HPV16 E7 protein in HPV+ HNC cells by ubiquitinating and degra

101 try, we have confirmed the expression of HPV E7 protein in prostate tissues positive for HPV DNA.

102 ortant new functions for the low-risk E6 and E7 proteins in the episomal maintenance of low-risk HPV-

103 tumor suppressor for degradation, while the E7 protein inactivates the retinoblastoma susceptibility

104 high-risk human papillomavirus (HPV) E6 and E7 proteins, including binding and degradation of p53 as

105 RB antisense oligonucleotides and E7 proteins increased apoptosis in p21(+/+), but not p21

106 This study demonstrates that the E7 protein increases production of the anti-inflammatory

107 ssion of high-risk, but not low-risk, E6 and E7 proteins increases the frequency of foreign DNA integ

108 a grade 2/3 and murine skin displaying HPV16 E7 protein-induced epithelial hyperplasia, which closely

109 pitope from the human papillomavirus (HPV)16 E7 protein induces a specific CTL response that prevents

110 The E1A/E7 protein interacted with p300 and pRb and immortalized

111 Although E7 protein is best known for its ability to inactivate t

112 The human papillomavirus (HPV) E7 protein is one of only two viral proteins that remain

113 continuous expression of both the E6 and the E7 protein is required for optimal proliferation of cerv

114 uous neutralization of the Rb pathway by the E7 protein is required to maintain the proliferation of

115 In this study, we demonstrate that the HPV E7 protein is sufficient to increase levels of the MRN c

116 An alteration of the pRb pathways by the E7 proteins is one of the mechanisms that's account for

117 llomaviruses (HPVs), in combination with the E7 protein, is essential for the efficient immortalizati

118 V+ HNC cells drastically decreases the HPV16 E7 protein level while increasing the CUL1 and UBE2L3 pr

119 tores CUL1 and UBE2L3 expression, decreasing E7 protein levels and inhibiting the proliferation of HP

120 E7 in CaSki cervical carcinoma cells reduces E7 protein levels and inhibits cancer cell growth both i

121 , overexpression of CUL1 or UBE2L3 decreases E7 protein levels and suppresses in vivo tumor growth.

122 and UBE2L3 in HPV+ HNC cells decreases HPV16 E7 protein levels and suppresses tumor growth in vivo.

123 ur results suggest that HPV16 maintains high E7 protein levels in the host cell by inducing MARCHF8,

124 Similarly, decreased E7 protein levels were observed in the C3 cells that wer

125 protein constructs containing modified E6 or E7 proteins, novel adjuvants, fusion proteins such as im

126 The E7 protein of HPV-16 binds all retinoblastoma tumor supp

127 The E7 protein of HPV-16 was able to disrupt the response of

128 virus (VSV-G)-together with DNA encoding the E7 protein of human papillomavirus type 16, a model cerv

129 The E6 and E7 proteins of cancer-associated human papillomavirus (H

130 The E7 proteins of high-risk HPV genotypes efficiently inact

131 mbinant vaccinia virus expressing the E6 and E7 proteins of HPV 16 and 18 (TA-HPV).

132 The E6 and E7 proteins of HPV 16 immortalize human keratinocytes an

133 The E7 proteins of human papillomaviruses (HPVs) contribute

134 The E7 proteins of human papillomaviruses (HPVs) promote S-p

135 The E7 proteins of LR HPV-11 and -6b uniquely possess lysine

136 thus identify p600 as a shared target of the E7 proteins of multiple papillomaviruses.

137 However, the E6 and E7 proteins of the 'low risk' HPV-6b did not demonstrate

138 The E6 and E7 proteins of the high risk human papillomaviruses (HPV

139 We have examined the possibility that the E7 proteins of the high-risk human papillomavirus (HPV)

140 cultures of primary human keratinocytes, the E7 proteins of the high-risk mucosotrophic HPV-18, the b

141 ation frequency in NHOK expressing the E6 or E7 proteins of the non-oncogenic HPV-6b.

142 Moreover, the efficiencies of the E7 proteins of various HPV types or mutations to induce

143 human papillomavirus type 18 (HPV-18) E6 and E7 proteins on global patterns of host gene expression i

144 ease was not due to altered stability of the E7 protein or an increase in the steady-state level of t

145 c vaccination efforts have focused on E6 and E7 proteins; our results suggest that E2 and E5 should a

146 The HPV E7 protein plays an important role in the viral life cyc

147 Enforced expression of the wild-type HPV16 E7 protein prevented Rb activation in response to E2 exp

148 The human papillomavirus (HPV) E7 protein promotes S-phase reentry in a fraction of pos

149 The human papillomavirus type 18 (HPV-18) E7 protein promotes S-phase reentry in postmitotic, diff

150 e physiological roles of the low-risk E6 and E7 proteins remain unclear.

151 restingly, expression of the low-risk HPV 6b E7 protein resulted in an increase in MHC class I heavy

152 Thus, high level expression of the HPV-16 E7 protein sensitizes keratinocytes to apoptosis which r

153 HPV E7 proteins share structural and functional similarities

154 based vaccination against the E1, E2, E6, or E7 protein significantly reduced papilloma volumes relat

155 f HCvECs in the presence of high-risk HPV E6/E7 proteins, suggesting that the hyperactivated YAP1 syn

156 HPV E6 and E7 proteins suppress the levels of miR-424, and this is

157 After HPV infection, the E7 protein suppresses ubiquitin ligase FBW7 expression l

158 ed mutagenesis, we determined regions of the E7 protein that were essential for its antiapoptotic act

159 s were transformation deficient and included E7 proteins that bound retinoblastoma protein in vitro.

160 E7 proteins that bound the retinoblastoma protein (Rb) s

161 s itself but enhanced the capacity of mutant E7 protein to stimulate DNA synthesis to the same level

162 e tested the ability of wild-type and mutant E7 proteins to affect the activity of the Rb pathway and

163 impact the ability of several high-risk HPV E7 proteins to bind and degrade the retinoblastoma tumor

164 te correlation between the ability of mutant E7 proteins to inactivate the Rb pathway and to inhibit

165 the differential abilities of LR and HR HPV E7 proteins to promote unscheduled DNA replication in or

166 s that direct expression of the HPV16 E6 and E7 proteins to the head and neck tissues of mice to diss

167 s to human papillomavirus-16 (HPV-16) E6 and E7 proteins using a recombinant E6/E7 fusion protein and

168 Quantitation of the individual E6 and E7 proteins, using a newly developed immunoprecipitation

169 hanced expression of MUC16, SIRPA and HPV-16-E7 protein was detectable in the circulating exosomes of

170 The level of E7 protein was strongly induced in HPV-containing Caski,

171 The same set of mutated E7 proteins was able to abrogate all three growth arrest

172 all endpoints, seropositivity for the E6 and E7 proteins was significantly associated with enhanced a

173 requency in NHOK expressing the HPV-6b E6 or E7 proteins was the same as in NHOK.

174 cell line that inducibly expresses the HPV16 E7 protein, we show that an accumulation of E7 induces q

175 w VSV vectors expressing the CRPV E1, E2, or E7 protein were produced and compared to the previously

176 es encoding the wild-type CRPV E1-E2, E6, or E7 protein were tested alone and in all possible combina

177 regard, the biologically more potent HR HPV E7 proteins were also less stable than the LR HPV E7 pro

178 Both high- and low-risk HPV E7 proteins were found to bind to HIF-1alpha through a d

179 Metabolic labeling in vivo demonstrated that E7 proteins were indeed phosphorylated in a CKII motif-d

180 he human papillomavirus (HPV) type 16 E6 and E7 proteins were measured in 20 women with known HPV and

181 One, Lm-E7, expresses and secretes E7 protein, whereas a second, Lm-LLO-E7, secretes E7 as

182 Expression of the human papilloma virus 16 E7 protein (which inactivates all members of the retinob

183 e conserved region (CR) 1 and CR2 domains in E7 protein, which are involved in the inactivation of pR

184 The human papillomavirus type 16 E7 protein, which binds to both c-Jun and Rb, inhibits t

185 ted whether the human papillomavirus type 16 E7 protein, which inactivates pRb family proteins by dir

186 Thus the natural function of E7 protein, which inactivates pRB family proteins, is to

187 In this study, we demonstrated that the E7 protein, which induces S phase reentry in suprabasal

188 gh-risk human papillomaviruses (HPVs) E6 and E7 proteins, which neutralize cellular tumor suppressor

189 several new functions for the papillomavirus E7 proteins, which will contribute new insights into the

190 While all full-length E7 proteins with mutations outside of the LxCxE motif in