戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
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 Y102E was unable to bind E1 and did not replicate
8                                              BPV-1-induced papillomas show characteristics of repress
9 tyrosine (Y) in the bovine papillomavirus 1 (BPV-1) E2 protein at amino acid 102.
10                     Bovine papillomavirus 1 (BPV-1) E6 has served as a model system for studies of E6
11 e on the HPV-16 and bovine papillomavirus 1 (BPV-1) L2 proteins.
12 discovered that the bovine papillomavirus 1 (BPV-1) transcription and replication regulator E2 is pho
13  the hitchhiking of bovine papillomavirus-1 (BPV-1), and the viral protein E2 binds to both plasmids
14 lexes of the bovine papillomavirus strain 1 (BPV-1) E2 protein and DNA show that the protein does not
15 V-16) E2 and bovine papillomavirus strain 1 (BPV-1) E2 to discriminate among binding sites with diffe
16  structures of bovine papillomavirus type 1 (BPV-1) and human papillomavirus type 1 (HPV-1).
17 product of the bovine papillomavirus type 1 (BPV-1) E1 translational open reading frame is required f
18 tion domain of bovine papillomavirus type 1 (BPV-1) E2 alone or this binding domain plus the adjacent
19                Bovine papillomavirus type 1 (BPV-1) E2 binds cellular chromatin in complex with Brd4
20   For example, bovine papillomavirus type 1 (BPV-1) E2 binds to all chromosomes as small speckles in
21 shown that the bovine papillomavirus type 1 (BPV-1) E6 and E7 genes independently sensitize mouse cel
22 pillomaviruses Bovine Papillomavirus Type 1 (BPV-1) E6 and human papillomavirus (HPV) types 1 and 8 (
23            The bovine papillomavirus type 1 (BPV-1) E6 oncoprotein can transform fibroblasts and indu
24            The bovine papillomavirus type 1 (BPV-1) E7 does not bind pRB efficiently yet is required
25 e examined for bovine papillomavirus type 1 (BPV-1) E7 localization.
26            The bovine papillomavirus type 1 (BPV-1) E7 oncoprotein is required for the full transform
27            The bovine papillomavirus type 1 (BPV-1) exonic splicing suppressor (ESS) is juxtaposed im
28  regulation of bovine papillomavirus type 1 (BPV-1) gene expression during the virus life cycle.
29  regulation of bovine papillomavirus type 1 (BPV-1) gene expression.
30 containing the bovine papillomavirus type 1 (BPV-1) genome were reported to exhibit increased TNF sen
31 oncoprotein of bovine papillomavirus type 1 (BPV-1) has been shown to transform cells through a p53-i
32                Bovine papillomavirus type 1 (BPV-1) induces fibropapillomas in its natural host and c
33                Bovine papillomavirus type 1 (BPV-1) is a small DNA virus that causes fibropapillomas
34 E6 gene of the bovine papillomavirus type 1 (BPV-1) is expressed in fibropapillomas caused by BPV-1 a
35 oncoprotein of bovine papillomavirus type 1 (BPV-1) is required for the full transformation activity
36                Bovine papillomavirus type 1 (BPV-1) late gene expression is regulated at both transcr
37                Bovine papillomavirus type 1 (BPV-1) late pre-mRNAs are spliced in keratinocytes in a
38 selection of a bovine papillomavirus type 1 (BPV-1) late-specific splice site, and binding of SRp20 t
39                Bovine papillomavirus type 1 (BPV-1) requires viral proteins E1 and E2 for efficient D
40   Furthermore, bovine papillomavirus type 1 (BPV-1) transformation was also suppressed in cells co-tr
41 nital HPV, and bovine papillomavirus type 1 (BPV-1), a papillomavirus known to be transmitted via fom
42             In bovine papillomavirus type 1 (BPV-1), a switch in 3' splice site utilization from an e
43               Bovine papillomavirus, type 1 (BPV-1), E1, and E2 bind cooperatively as dimers to proxi
44 in, encoded by bovine papillomavirus type 1 (BPV-1), has been shown to interact with basal transcript
45 t from that of bovine papillomavirus type 1 (BPV-1).
46 8, HPV-11, and bovine papillomavirus type 1 (BPV-1).
47                                            A BPV-1 late pre-mRNA containing the nt 3225 3' splice sit
48 tion although this result also occurred in a BPV-1 E2 mutant lacking a previously identified phosphor
49  Deletion or mutation of either element in a BPV-1 late pre-mRNA switches splicing to the late-specif
50  of the ESS in the alternative splicing of a BPV-1 late pre-mRNA in vivo.
51                     Much less is known about BPV-1 gene expression and replication in bovine epitheli
52                                  In addition BPV-1 E1 can inhibit activation of the viral P89 promote
53                                     Although BPV-1 E7 by itself is not sufficient to induce cellular
54 he phospho-acceptor sites of both HPV-16 and BPV-1 L2 resulted in the production of infectious virus
55    Our studies thus categorize HPV-18 E2 and BPV-1 E2 in the same protein family, a finding consisten
56 ific binding of the homologous HPV-16 E2 and BPV-1 E2 proteins is significantly different.
57                           Like the H-ras and BPV-1 promoters, HPV-16 p97 was down-regulated in 3T3-ts
58 n between Saccharomyces cerevisiae TFIIB and BPV-1 E2, an observation that is consistent with the imp
59 effector of NOTCH-induced transcription, and BPV-1 E6 represses synthetic NOTCH-responsive promoters,
60 n human TFIIB (hTFIIB) required for VP16 and BPV-1 E2 indicates that these acidic activators interact
61 requirements for specific DNA recognition as BPV-1 and HPV-11 E1.
62                                      Between BPV-1 and HPV-31 E2, 8 of the 11 tyrosines are conserved
63 te in vitro and in vivo interactions between BPV-1 E6 and the focal adhesion protein paxillin.
64                                         Both BPV-1 and HPV-31 Y102E are similar in that neither binds
65 uced transformation of cells expressing both BPV-1 E6 and E7, as well as E6 alone, suggesting that th
66  required for full transformation of C127 by BPV-1.
67 1) is expressed in fibropapillomas caused by BPV-1 and in tissue culture cells transformed by BPV-1.
68 kingly similar to a fibropapilloma caused by BPV-1 in the natural host.
69 d for full transformation of murine cells by BPV-1.
70  BPV-1 transformed cells, may be mediated by BPV-1 E6 through its interaction with paxillin.
71       The induction of cell proliferation by BPV-1 E7 can occur in the retinoblastoma gene (Rb)-null
72 1 and in tissue culture cells transformed by BPV-1.
73                           Lastly, a chimeric BPV-1 E2C containing the spindle localization domain fro
74  bovine wart or were transfected with cloned BPV-1 DNA.
75 nocytes plated on a collagen raft containing BPV-1-transformed fibroblasts.
76 together, our results suggest that cytosolic BPV-1 E6 is first recruited to the TGN, where it is then
77 tively active mutant form of FGFR3 decreased BPV-1 and HPV-31 transient replication although this res
78 ins but classify together the more divergent BPV-1 and HPV-18 E2 proteins.
79 oth forms have star-shaped capsomeres, as do BPV-1 and HPV-1, but the open CRPV capsids are approxima
80 e importance of the E2-TFIIB interaction for BPV-1 E2 transactivation in both systems.
81 selection of the proximal 3' splice site for BPV-1 RNA splicing in DT40-ASF cells, a genetically engi
82 ion of MHC I in cells transformed by E5 from BPV-1 and BPV-4.
83  DNA-binding domains of the E2 proteins from BPV-1 and human papillomavirus strain 16 (HPV-16) to a s
84                                 Furthermore, BPV-1 E7 sensitizes Rb-null cells to TNF-induced apoptos
85 cteristic of many transformed cells, and, in BPV-1 transformed cells, may be mediated by BPV-1 E6 thr
86 ed the viral DNA from mitotic chromosomes in BPV-1 transformed cells.
87 ous residues required for E1 dimerization in BPV-1 and the low risk HPV-11 are also required for HPV-
88               We have recently identified in BPV-1 late pre-mRNAs two purine-rich exonic splicing enh
89 Significantly, c-Myc levels are increased in BPV-1 E7-expressing cells.
90 or the processing of most BPV-1 pre-mRNAs in BPV-1-transformed C127 cells and at early to intermediat
91 We created a series of missense mutations in BPV-1 E1 at codons 295, 344-345, 446, 464, 466, 497-498,
92 dies indicate an important role for c-Myc in BPV-1 E7-induced cell proliferation.
93 pression, we investigated the role of p53 in BPV-1 E6 and E7 modulation of Fas-mediated apoptosis.
94 ciated kinase activities are up-regulated in BPV-1 E7-expressing cells.
95 only one E2 tyrosine phosphorylation site in BPV-1 (tyrosine 102) and one in HPV-16/31 (tyrosine 138)
96 ereby papillomavirus oncoproteins, including BPV-1 E6, and the cancer-associated HPV-8 E6 repress NOT
97 the viral episomes with Brd4, and to inhibit BPV-1 DNA-mediated cellular transformation.
98 f a dominant negative c-Myc mutant inhibited BPV-1 E7-induced DNA synthesis.
99 ression of E7 and E5 in basal keratinocytes, BPV-1 E7 cooperated with E5 as well as E6 in an anchorag
100 d superficial differentiating keratinocytes, BPV-1 E7 is only observed in basal and lower spinous epi
101                           Expression of late BPV-1 L1 or human papillomavirus (HPV) L1, the major cap
102 nt) 3225, is used for the processing of most BPV-1 pre-mRNAs in BPV-1-transformed C127 cells and at e
103            Consistent with this observation, BPV-1 E7 does not efficiently activate the transcription
104                               The ability of BPV-1 E6 to complex with paxillin correlated with its ab
105 We investigated the biological activities of BPV-1 E7 in several assays.
106                          Further analysis of BPV-1 late-pre-mRNA splicing in vitro revealed a 48-nt p
107 n integral part of the DNA-binding domain of BPV-1 E2.
108 thin the amino-terminal activation domain of BPV-1 E2.
109 hen located either upstream or downstream of BPV-1 SE1.
110 ESS) is juxtaposed immediately downstream of BPV-1 splicing enhancer 1 and negatively modulates selec
111      Our studies indicate that expression of BPV-1 E7 induces DNA synthesis and stimulates cells to e
112      Our results indicate that expression of BPV-1 E7 sensitizes cells to tumor necrosis factor alpha
113 ysiological conditions for the expression of BPV-1 late RNAs and for selection of the proximal 3' spl
114 ability to enhance anchorage independence of BPV-1 E6-expressing cells.
115 ability to enhance anchorage independence of BPV-1 E6-transformed cells.
116 sent study, we investigated the mechanism of BPV-1 E7-induced cell proliferation.
117 encodes one of the two major oncoproteins of BPV-1.
118 e actin fiber network, and overexpression of BPV-1 E6 led to disruption of actin fiber formation.
119 nhibit gene expression of the E6 promoter of BPV-1 (bovine papillomavirus type 1) and HPV types 16 an
120               The transforming properties of BPV-1 primarily reside in two genes, E5 and E6.
121 embranes, suggesting that the recruitment of BPV-1 E6 and AP-1 to Golgi membranes involves a common f
122                           The recruitment of BPV-1 E6 to Golgi membranes was AP-1 independent, but th
123  the frequency of morphological reversion of BPV-1 transformed C127 cells resulting in the complete e
124 sion of spliceosome assembly and splicing of BPV-1 pre-mRNAs.
125 kles do not contain Brd4, and unlike that of BPV-1, the N-terminal Brd4-interacting domain of HPV-8 E
126 tion, it enhances the abilities of the other BPV-1 oncogenes to induce anchorage independence.
127 02 is conserved between delta papillomavirus BPV-1 and alpha papillomavirus HPV-31 E2.
128 of the tumour viruses bovine papillomavirus (BPV-1) and Simian virus 40 (SV40) are the initiator prot
129 f the E2 protein from bovine papillomavirus (BPV-1).
130 ta indicate the utility of ts against H-ras, BPV-1 and HPV-16 promoters and their respective oncogene
131 ious studies of the mechanisms that regulate BPV-1 alternative splicing identified three cis-acting e
132 acts to identify cis elements which regulate BPV-1 3' splice site selection.
133                We also provide evidence that BPV-1 E6 mediated-sensitization of cells to TNF-induced
134                          We report here that BPV-1 E6 and E7 can each independently inhibit anoikis,
135                  These studies indicate that BPV-1 E7 can sensitize cells to apoptosis through mechan
136                       Our data indicate that BPV-1 splicing regulation is very complex and is likely
137                              We propose that BPV-1 E6, through its interaction with AP-1, can affect
138                                          The BPV-1 E2 DNA-binding domain is only moderately sensitive
139                                          The BPV-1 E6 oncoprotein induces tumorigenic transformation
140                                          The BPV-1 ESS was inserted downstream of the 3' splice site
141                                          The BPV-1 p89 and p2443 promoters were down-regulated in 3T3
142 6 E2 DNA binding domain (HPV16-E2/D) and the BPV-1 E2 DNA binding domain (BPV1-E2/D) to sites bearing
143 y, we demonstrate an interaction between the BPV-1 E6 protein and AP-1, the TGN (trans-Golgi network)
144  activation of the viral P89 promoter by the BPV-1 E2TA.
145 nstrated that suppression of splicing by the BPV-1 ESS requires an upstream suboptimal 3' splice site
146 rted downstream of the 3' splice site in the BPV-1 late pre-mRNA, Rous sarcoma virus src pre-mRNA, hu
147 e first phospho-specific modification of the BPV-1 and HPV-16 L2 capsid proteins.
148 us, these data suggest that selection of the BPV-1 nt 3225 3' splice site is regulated by both positi
149 SE2 are required for preferential use of the BPV-1 nucleotide (nt) 3225 3' splice site in nonpermissi
150 e cancer-related human papillomaviruses, the BPV-1 E7 protein does not associate efficiently with the
151 e-dependent DNA helicase, DNA binding to the BPV-1 origin of viral DNA replication, and association w
152  (HPV-16) p97 promoter has similarity to the BPV-1 p89 promoter, the ability of ts to suppress p97 wa
153 ptor 3 (FGFR3) coimmunoprecipitated with the BPV-1 E2 protein, as did human papillomavirus 31 (HPV-31
154                                   Therefore, BPV-1 E7 may serve to modulate the cellular response of
155 ly expressed in keratinocytes for binding to BPV-1 E2.
156                               In contrast to BPV-1 E2, the HPV-8 E2 protein targets the short arms of
157 isingly, HPV-18 E2 behaves more similarly to BPV-1 E2 than HPV-16 E2 in its functional properties.
158  This study examines the mechanisms by which BPV-1 E6 association with the cellular focal adhesion ad
159 de mice, we have developed a system in which BPV-1 can replicate and produce infectious viral particl
160 urthermore, AP-1 proteins could compete with BPV-1 E6 for binding to Golgi membranes, suggesting that
161 also suppressed in cells co-transfected with BPV-1 plus ts and in ts expressing cell lines transfecte
162 in ts expressing cell lines transfected with BPV-1.
163 tructure of the core domain contained within BPV-1 E2 is similar to the corresponding regions of othe

 
Page Top