ライフサイエンスコーパス: BPV-1

1 BPV-1 E6 preferentially associated with membrane-bound A

2 BPV-1 E6 was further shown to be recruited to isolated G

3 BPV-1 E6 was introduced into C127 cells (PBE6) by retrov

4 BPV-1 E7 was observed in the cytoplasm of basal and lowe

5 BPV-1 efficiently induces anchorage-independent growth a

6 BPV-1 has served as the prototype for studies of the mol

7 BPV-1-induced papillomas show characteristics of repress

8 tyrosine (Y) in the bovine papillomavirus 1 (BPV-1) E2 protein at amino acid 102.

9 Bovine papillomavirus 1 (BPV-1) E6 has served as a model system for studies of E6

10 discovered that the bovine papillomavirus 1 (BPV-1) transcription and replication regulator E2 is pho

11 the hitchhiking of bovine papillomavirus-1 (BPV-1), and the viral protein E2 binds to both plasmids

12 lexes of the bovine papillomavirus strain 1 (BPV-1) E2 protein and DNA show that the protein does not

13 V-16) E2 and bovine papillomavirus strain 1 (BPV-1) E2 to discriminate among binding sites with diffe

14 structures of bovine papillomavirus type 1 (BPV-1) and human papillomavirus type 1 (HPV-1).

15 product of the bovine papillomavirus type 1 (BPV-1) E1 translational open reading frame is required f

16 tion domain of bovine papillomavirus type 1 (BPV-1) E2 alone or this binding domain plus the adjacent

17 Bovine papillomavirus type 1 (BPV-1) E2 binds cellular chromatin in complex with Brd4

18 For example, bovine papillomavirus type 1 (BPV-1) E2 binds to all chromosomes as small speckles in

19 shown that the bovine papillomavirus type 1 (BPV-1) E6 and E7 genes independently sensitize mouse cel

20 pillomaviruses Bovine Papillomavirus Type 1 (BPV-1) E6 and human papillomavirus (HPV) types 1 and 8 (

21 The bovine papillomavirus type 1 (BPV-1) E6 oncoprotein can transform fibroblasts and indu

22 The bovine papillomavirus type 1 (BPV-1) E7 does not bind pRB efficiently yet is required

23 e examined for bovine papillomavirus type 1 (BPV-1) E7 localization.

24 The bovine papillomavirus type 1 (BPV-1) E7 oncoprotein is required for the full transform

25 The bovine papillomavirus type 1 (BPV-1) exonic splicing suppressor (ESS) is juxtaposed im

26 regulation of bovine papillomavirus type 1 (BPV-1) gene expression during the virus life cycle.

27 regulation of bovine papillomavirus type 1 (BPV-1) gene expression during the virus life cycle.

28 regulation of bovine papillomavirus type 1 (BPV-1) gene expression.

29 containing the bovine papillomavirus type 1 (BPV-1) genome were reported to exhibit increased TNF sen

30 oncoprotein of bovine papillomavirus type 1 (BPV-1) has been shown to transform cells through a p53-i

31 Bovine papillomavirus type 1 (BPV-1) induces fibropapillomas in its natural host and c

32 Bovine papillomavirus type 1 (BPV-1) is a small DNA virus that causes fibropapillomas

33 E6 gene of the bovine papillomavirus type 1 (BPV-1) is expressed in fibropapillomas caused by BPV-1 a

34 oncoprotein of bovine papillomavirus type 1 (BPV-1) is required for the full transformation activity

35 Bovine papillomavirus type 1 (BPV-1) late gene expression is regulated at both transcr

36 Bovine papillomavirus type 1 (BPV-1) late pre-mRNAs are spliced in keratinocytes in a

37 selection of a bovine papillomavirus type 1 (BPV-1) late-specific splice site, and binding of SRp20 t

38 Bovine papillomavirus type 1 (BPV-1) requires viral proteins E1 and E2 for efficient D

39 Furthermore, bovine papillomavirus type 1 (BPV-1) transformation was also suppressed in cells co-tr

40 nital HPV, and bovine papillomavirus type 1 (BPV-1), a papillomavirus known to be transmitted via fom

41 In bovine papillomavirus type 1 (BPV-1), a switch in 3' splice site utilization from an e

42 Bovine papillomavirus, type 1 (BPV-1), E1, and E2 bind cooperatively as dimers to proxi

43 in, encoded by bovine papillomavirus type 1 (BPV-1), has been shown to interact with basal transcript

44 t from that of bovine papillomavirus type 1 (BPV-1).

45 8, HPV-11, and bovine papillomavirus type 1 (BPV-1).

46 A BPV-1 late pre-mRNA containing the nt 3225 3' splice sit

47 tion although this result also occurred in a BPV-1 E2 mutant lacking a previously identified phosphor

48 Deletion or mutation of either element in a BPV-1 late pre-mRNA switches splicing to the late-specif

49 of the ESS in the alternative splicing of a BPV-1 late pre-mRNA in vivo.

50 Much less is known about BPV-1 gene expression and replication in bovine epitheli

51 In addition BPV-1 E1 can inhibit activation of the viral P89 promote

52 Although BPV-1 E7 by itself is not sufficient to induce cellular

53 Our studies thus categorize HPV-18 E2 and BPV-1 E2 in the same protein family, a finding consisten

54 ific binding of the homologous HPV-16 E2 and BPV-1 E2 proteins is significantly different.

55 Like the H-ras and BPV-1 promoters, HPV-16 p97 was down-regulated in 3T3-ts

56 n between Saccharomyces cerevisiae TFIIB and BPV-1 E2, an observation that is consistent with the imp

57 effector of NOTCH-induced transcription, and BPV-1 E6 represses synthetic NOTCH-responsive promoters,

58 n human TFIIB (hTFIIB) required for VP16 and BPV-1 E2 indicates that these acidic activators interact

59 requirements for specific DNA recognition as BPV-1 and HPV-11 E1.

60 te in vitro and in vivo interactions between BPV-1 E6 and the focal adhesion protein paxillin.

61 uced transformation of cells expressing both BPV-1 E6 and E7, as well as E6 alone, suggesting that th

62 required for full transformation of C127 by BPV-1.

63 1) is expressed in fibropapillomas caused by BPV-1 and in tissue culture cells transformed by BPV-1.

64 kingly similar to a fibropapilloma caused by BPV-1 in the natural host.

65 d for full transformation of murine cells by BPV-1.

66 BPV-1 transformed cells, may be mediated by BPV-1 E6 through its interaction with paxillin.

67 The induction of cell proliferation by BPV-1 E7 can occur in the retinoblastoma gene (Rb)-null

68 1 and in tissue culture cells transformed by BPV-1.

69 Lastly, a chimeric BPV-1 E2C containing the spindle localization domain fro

70 bovine wart or were transfected with cloned BPV-1 DNA.

71 nocytes plated on a collagen raft containing BPV-1-transformed fibroblasts.

72 together, our results suggest that cytosolic BPV-1 E6 is first recruited to the TGN, where it is then

73 tively active mutant form of FGFR3 decreased BPV-1 and HPV-31 transient replication although this res

74 ins but classify together the more divergent BPV-1 and HPV-18 E2 proteins.

75 oth forms have star-shaped capsomeres, as do BPV-1 and HPV-1, but the open CRPV capsids are approxima

76 e importance of the E2-TFIIB interaction for BPV-1 E2 transactivation in both systems.

77 selection of the proximal 3' splice site for BPV-1 RNA splicing in DT40-ASF cells, a genetically engi

78 ion of MHC I in cells transformed by E5 from BPV-1 and BPV-4.

79 DNA-binding domains of the E2 proteins from BPV-1 and human papillomavirus strain 16 (HPV-16) to a s

80 Furthermore, BPV-1 E7 sensitizes Rb-null cells to TNF-induced apoptos

81 cteristic of many transformed cells, and, in BPV-1 transformed cells, may be mediated by BPV-1 E6 thr

82 ed the viral DNA from mitotic chromosomes in BPV-1 transformed cells.

83 ous residues required for E1 dimerization in BPV-1 and the low risk HPV-11 are also required for HPV-

84 We have recently identified in BPV-1 late pre-mRNAs two purine-rich exonic splicing enh

85 Significantly, c-Myc levels are increased in BPV-1 E7-expressing cells.

86 or the processing of most BPV-1 pre-mRNAs in BPV-1-transformed C127 cells and at early to intermediat

87 We created a series of missense mutations in BPV-1 E1 at codons 295, 344-345, 446, 464, 466, 497-498,

88 dies indicate an important role for c-Myc in BPV-1 E7-induced cell proliferation.

89 pression, we investigated the role of p53 in BPV-1 E6 and E7 modulation of Fas-mediated apoptosis.

90 ciated kinase activities are up-regulated in BPV-1 E7-expressing cells.

91 ereby papillomavirus oncoproteins, including BPV-1 E6, and the cancer-associated HPV-8 E6 repress NOT

92 the viral episomes with Brd4, and to inhibit BPV-1 DNA-mediated cellular transformation.

93 f a dominant negative c-Myc mutant inhibited BPV-1 E7-induced DNA synthesis.

94 ression of E7 and E5 in basal keratinocytes, BPV-1 E7 cooperated with E5 as well as E6 in an anchorag

95 d superficial differentiating keratinocytes, BPV-1 E7 is only observed in basal and lower spinous epi

96 Expression of late BPV-1 L1 or human papillomavirus (HPV) L1, the major cap

97 nt) 3225, is used for the processing of most BPV-1 pre-mRNAs in BPV-1-transformed C127 cells and at e

98 Consistent with this observation, BPV-1 E7 does not efficiently activate the transcription

99 The ability of BPV-1 E6 to complex with paxillin correlated with its ab

100 We investigated the biological activities of BPV-1 E7 in several assays.

101 Further analysis of BPV-1 late-pre-mRNA splicing in vitro revealed a 48-nt p

102 n integral part of the DNA-binding domain of BPV-1 E2.

103 thin the amino-terminal activation domain of BPV-1 E2.

104 hen located either upstream or downstream of BPV-1 SE1.

105 ESS) is juxtaposed immediately downstream of BPV-1 splicing enhancer 1 and negatively modulates selec

106 Our studies indicate that expression of BPV-1 E7 induces DNA synthesis and stimulates cells to e

107 Our results indicate that expression of BPV-1 E7 sensitizes cells to tumor necrosis factor alpha

108 ysiological conditions for the expression of BPV-1 late RNAs and for selection of the proximal 3' spl

109 ability to enhance anchorage independence of BPV-1 E6-expressing cells.

110 ability to enhance anchorage independence of BPV-1 E6-transformed cells.

111 sent study, we investigated the mechanism of BPV-1 E7-induced cell proliferation.

112 encodes one of the two major oncoproteins of BPV-1.

113 e actin fiber network, and overexpression of BPV-1 E6 led to disruption of actin fiber formation.

114 nhibit gene expression of the E6 promoter of BPV-1 (bovine papillomavirus type 1) and HPV types 16 an

115 The transforming properties of BPV-1 primarily reside in two genes, E5 and E6.

116 embranes, suggesting that the recruitment of BPV-1 E6 and AP-1 to Golgi membranes involves a common f

117 The recruitment of BPV-1 E6 to Golgi membranes was AP-1 independent, but th

118 the frequency of morphological reversion of BPV-1 transformed C127 cells resulting in the complete e

119 sion of spliceosome assembly and splicing of BPV-1 pre-mRNAs.

120 kles do not contain Brd4, and unlike that of BPV-1, the N-terminal Brd4-interacting domain of HPV-8 E

121 tion, it enhances the abilities of the other BPV-1 oncogenes to induce anchorage independence.

122 of the tumour viruses bovine papillomavirus (BPV-1) and Simian virus 40 (SV40) are the initiator prot

123 f the E2 protein from bovine papillomavirus (BPV-1).

124 ta indicate the utility of ts against H-ras, BPV-1 and HPV-16 promoters and their respective oncogene

125 ious studies of the mechanisms that regulate BPV-1 alternative splicing identified three cis-acting e

126 acts to identify cis elements which regulate BPV-1 3' splice site selection.

127 We also provide evidence that BPV-1 E6 mediated-sensitization of cells to TNF-induced

128 We report here that BPV-1 E6 and E7 can each independently inhibit anoikis,

129 These studies indicate that BPV-1 E7 can sensitize cells to apoptosis through mechan

130 Our data indicate that BPV-1 splicing regulation is very complex and is likely

131 We propose that BPV-1 E6, through its interaction with AP-1, can affect

132 The BPV-1 E2 DNA-binding domain is only moderately sensitive

133 The BPV-1 E6 oncoprotein induces tumorigenic transformation

134 The BPV-1 ESS was inserted downstream of the 3' splice site

135 The BPV-1 p89 and p2443 promoters were down-regulated in 3T3

136 6 E2 DNA binding domain (HPV16-E2/D) and the BPV-1 E2 DNA binding domain (BPV1-E2/D) to sites bearing

137 y, we demonstrate an interaction between the BPV-1 E6 protein and AP-1, the TGN (trans-Golgi network)

138 activation of the viral P89 promoter by the BPV-1 E2TA.

139 nstrated that suppression of splicing by the BPV-1 ESS requires an upstream suboptimal 3' splice site

140 rted downstream of the 3' splice site in the BPV-1 late pre-mRNA, Rous sarcoma virus src pre-mRNA, hu

141 us, these data suggest that selection of the BPV-1 nt 3225 3' splice site is regulated by both positi

142 SE2 are required for preferential use of the BPV-1 nucleotide (nt) 3225 3' splice site in nonpermissi

143 e cancer-related human papillomaviruses, the BPV-1 E7 protein does not associate efficiently with the

144 e-dependent DNA helicase, DNA binding to the BPV-1 origin of viral DNA replication, and association w

145 (HPV-16) p97 promoter has similarity to the BPV-1 p89 promoter, the ability of ts to suppress p97 wa

146 ptor 3 (FGFR3) coimmunoprecipitated with the BPV-1 E2 protein, as did human papillomavirus 31 (HPV-31

147 Therefore, BPV-1 E7 may serve to modulate the cellular response of

148 ly expressed in keratinocytes for binding to BPV-1 E2.

149 In contrast to BPV-1 E2, the HPV-8 E2 protein targets the short arms of

150 isingly, HPV-18 E2 behaves more similarly to BPV-1 E2 than HPV-16 E2 in its functional properties.

151 This study examines the mechanisms by which BPV-1 E6 association with the cellular focal adhesion ad

152 de mice, we have developed a system in which BPV-1 can replicate and produce infectious viral particl

153 urthermore, AP-1 proteins could compete with BPV-1 E6 for binding to Golgi membranes, suggesting that

154 also suppressed in cells co-transfected with BPV-1 plus ts and in ts expressing cell lines transfecte

155 in ts expressing cell lines transfected with BPV-1.

156 tructure of the core domain contained within BPV-1 E2 is similar to the corresponding regions of othe