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1 ic integration mechanisms and the impacts of viral integration.
2 s, both genes are highly expressed following viral integration.
3 ty of leukemias and lymphomas as a result of viral integration.
4 on surrounding c-myc is indeed a hot spot of viral integration.
5 lular sequence was not linked to the site of viral integration.
6 ociation with both spcDNAs and hot-spots for viral integration.
7 understanding of the molecular mechanisms of viral integration.
8  a translocation had occurred at the site of viral integration.
9 tandard deviations away from samples without viral integration.
10 ional activation, cancer, viral latency, and viral integration.
11 enomic 'safe harbor' site rather than random viral integration.
12 ase of the tethered p12 post mitosis, before viral integration.
13 t virus-induced cell killing is triggered by viral integration.
14  chromosomal rearrangements in cancer and of viral integration.
15 T antigen that provides indirect evidence of viral integration.
16 ce-inducing substitutions were defective for viral integration.
17 nses and possible gene alterations following viral integration.
18 ll specific, and inhibition occurs following viral integration.
19  captured to quantify the number of distinct viral integrations.
20  virome-wide screening of early-stage clonal viral integrations.
21  existing methods and software for detecting viral integrations.
22 luding homeobox A9 (Hoxa9)/myeloid ecotropic viral integration 1 (Meis1)/pre-B-cell leukemia homeobox
23 A was found in primary infection, whereas in viral integration, 4 patients had HHV-6A and 17 patients
24               We addressed this question for viral integration, a fundamental mechanism of horizontal
25 t genetic rearrangement in processes such as viral integration and excision and chromosomal segregati
26 terial chromosome dimers to adeno-associated viral integration and is a versatile tool for mammalian
27 chromosome remodelling, viral replication or viral integration and may account for the local hypermet
28 th host chromatin and significantly impaired viral integration and replication in HIV-1-susceptible c
29 ween viral integrase and LEDGF/p75, reducing viral integration and retargeting the provirus to region
30  such, are important models for the study of viral integration and target site selection.
31 s study, we set out to identify the sites of viral integration and to assess the efficiency of the ov
32  a cytolytic effect on infected cells before viral integration, and a direct, non-cytolytic effect by
33 ciated with activating PIK3CA alterations or viral integration, and also expressed higher levels of H
34 t structural intermediates in recombination, viral integration, and DNA repair.
35 splantation showed sustained Btk expression, viral integration, and partial functional responses, con
36 53) in viral entry, a karyopherin (TNPO3) in viral integration, and the Mediator complex (Med28) in v
37 s the hypothesis that the sites of oncogenic viral integration are nonrandom and that genes at the si
38                                              Viral integrations are important in human biology, yet g
39 l limitations (for example, mutation through viral integration) are eliminated.
40 hat spans the Evi5 locus and is disrupted by viral integration at Evi5.
41 and FGFR3, enrichment of APOBEC mutagenesis, viral integration at known hotspots, and frequent epigen
42 ression of the same genes in tumours without viral integration at the same site.
43              Unexpectedly, about half of the viral integrations at Nf1 represented a previously undis
44 l polymorphisms INS119G and INR231G retarget viral integration away from gene-dense regions.
45 itself is weak without hormonal stimulation, viral integration can position the 5' LTR elements to ef
46                                              Viral integrations can be considered genetic markers for
47 rtant for basic cellular functions including viral integration, control of gene expression, productio
48 tage or metastatic potential, as a result of viral integration either affecting the cellular genes wh
49 Strikingly, our analysis revealed non-clonal viral integrations even in individuals without cancer.
50 vitro integration junctions suggest that the viral integration event itself is mediated by terminal r
51 rst molecular characterization of an in vivo viral integration event within a confirmed fragile site
52 xperimental evidence that the high number of viral integration events (>90%) found in actively expres
53 tool called seeksv to detect somatic SVs and viral integration events.
54 r of DNA damage sites dramatically increases viral integration frequency.
55  However, when the inhibitor was added after viral integration had occurred, no inhibition of HIV inf
56  We propose that activation of DNA-PK during viral integration has a central role in CD4(+) T-cell de
57                                     However, viral integration has associated risks, such as the unin
58              The cellular genes disrupted by viral integration have been identified in four of these
59                                  A number of viral integrations have been shown to occur within the v
60 ppears to be the most common site of somatic viral integration in BXH-2 mice.
61 entified by viral tagging as common sites of viral integration in BXH2 leukemias.
62 teosarcomas, positive for SV40 by PCR, found viral integration in half of these.
63 omain and was identified as a common site of viral integration in myeloid leukemias arising in BXH-2
64  was originally isolated as a common site of viral integration in myeloid tumors of the BXH-2 recombi
65 mechanism driven by immunity and centered on viral integration in the carcinogenesis of BKPyV.
66 nd interpreted these findings as evidence of viral integration in the human genome as a potential pat
67 , the Hoxa-9 gene is frequently activated by viral integration in the same BXH-2 leukemias, suggestin
68                         To study the role of viral integration in tumorigenesis, we analyzed the posi
69  binds R-loops and their resolution enhances viral integration in vitro.
70 nologies have been widely used to screen for viral integrations in cancer genomes, and a number of bi
71 ults provide evidence for some of the oldest viral integrations in the human genome and insights into
72 rexpression of TERT mRNA in tumors harboring viral integrations in the TERT promoter.
73                                 We show that viral integrations in tumor cells lie near cellular sequ
74 , and have all of the hallmarks of authentic viral integration, including the removal of a terminal T
75 hed adjacent normal samples, indicating that viral integration induced host driver genetic alteration
76                                              Viral integration into a host genome is defined by two c
77                    LEDGF/p75, which promotes viral integration into active genes, stabilizes Tpr at t
78  of early cervical lesions revealed frequent viral integration into gene-poor regions of the host gen
79 Evidence from several studies indicates that viral integration into genic regions is accompanied by l
80 lignant progression is often associated with viral integration into host cell chromatin.
81 xpansion of latently infected T cells due to viral integration into specific genes contribute to this
82 rus (HIV) replication and, in particular, to viral integration into the host chromatin.
83  both human and HPV38 genomes, indicative of viral integration into the host DNA, something not previ
84                                              Viral integration into the host genome is an important a
85 ection from infection reflects prevention of viral integration into the host genome.
86  blocking steps in reverse transcription and viral integration into the host genome.
87 an DeltaLR-9 of short-latency lymphomas with viral integrations into c-myb.
88              The mechanism of killing during viral integration involved the activation of DNA-depende
89 pies/hair follicle cell), demonstrating that viral integration is not confined to blood cells.
90                                 We find that viral integration may bring genome fragility, particular
91 are nonrandom and that genes at the sites of viral integration may play important roles in carcinogen
92 s of these patterns can provide insight into viral integration mechanisms, pathology and genome evolu
93              Similarly, reported examples of viral integration near microRNAs suggest that altered ex
94 0% of TBLV-induced lymphomas have detectable viral integrations near c-myc by Southern blotting, wher
95                                              Viral integration of HPV into the host genome is not req
96                   In conclusion, the dynamic viral integration patterns actively participate in the p
97 BV) infection are urgently needed because of viral integration, persistence of viral antigen expressi
98 verified experiments show that more than 90% viral integration sequences detected by seeksv are true.
99 ed to block IN-LEDGF/p75 interactions during viral integration, several of these compounds have been
100                       The number of distinct viral integrations significantly correlated with circula
101                                     Besides, viral integrations significantly correlated with host ge
102 nd administration of relational databases of viral integration site (IS) data.
103 on, we identified a potent myeloid ecotropic viral integration site (MEIS) inhibitor, MEISi-1, to ind
104 eukemia homeobox (PBX) and myeloid ecotropic viral integration site (MEIS) proteins control cell fate
105 homeobox (KNOX) and animal Myeloid ecotropic viral integration site (MEIS) proteins share a TALE home
106                             The gene ectopic viral integration site 1 (EVI) and its variant myelodysp
107             Enhanced expression of ecotropic viral integration site 1 (EVI-1) occurs in approximately
108  In addition, aberrant expression of ectopic viral integration site 1 (EVI1) has also been found in s
109                                    Ecotropic viral integration site 1 (EVI1) is an oncogenic dual dom
110  the transforming potential of the ecotropic viral integration site 1 (Evi1) oncogene is thought to b
111 ular and cellular functions of the ecotropic viral integration site 1 (EVI1) oncogene.
112                                    Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zi
113                                    Ecotropic viral integration site 1 (EVI1), required for normal emb
114                                    Ecotropic viral integration site 1 (EVI1/MECOM) is frequently upre
115                            Myeloid ecotropic viral integration site 1 (Meis1) forms a heterodimer wit
116                            Myeloid ecotropic viral integration site 1 (MEIS1) is a transcription fact
117    The pivotal role of the myeloid ecotropic viral integration site 1 (MEIS1) transcriptional factor
118 operative interaction with myeloid ecotropic viral integration site 1 homolog (MEIS1).
119 ption factor 1) and MEIS1 (myeloid ecotropic viral integration site 1 homolog), and remain so until t
120                     Meis1 (Myeloid Ecotropic viral Integration Site 1) is a homeobox gene that was or
121 transcriptional signature of EVI1 (ecotropic viral integration site 1)-rearranged (EVI1-r) acute myel
122 iptional repressor, ETS variant 6, ecotropic viral integration site 1, and homeobox A11.
123            It is highly related to ecotropic viral integration site 3 (EVI3), a protein that, like EB
124                                              Viral integration site analysis indicated a reduction in
125 nd 4, a major fragile region that includes a viral integration site between exons 4 and 5, and cancer
126                     Clone Lists describe the viral integration site clones along with the tumor model
127  transfer strategy to show the importance of viral integration site in cellular immortalization.
128 some (BAC) clone, RP364B14, corresponding to viral integration site in CRL2504 cells, reverted their
129 ecific chromosomal conformation mapping, and viral integration site sequencing (IS-seq) to frontal co
130 motifs corresponded to MEIS (myeloid ectopic viral integration site) transcription factors, suggestin
131 andmarks, five cancer cell break points, one viral integration site, and one aphidicolin break cluste
132 proximately 18 kb upstream of another common viral integration site, Gfi1, on mouse chromosome 5.
133                                    Ecotropic viral integration site-1 (EVI1) and myelodysplastic synd
134                                    Ecotropic viral integration site-1 (EVI1) is an oncogenic zinc fin
135  tumor suppressor, whereas myeloid ecotropic viral integration site-1 (Meis1) is an oncogene.
136          The overexpression of the ecotropic viral integration site-1 gene (EVI1/MECOM) marks the mos
137           The proto-oncogene EVI1 (ecotropic viral integration site-1), located on chromosome band 3q
138 cell lines located in the middle of an HPV16 viral integration site.
139                   Many studies have reported viral integration sites (VISs) proximal to structural or
140 ng previous cytogenetic observations linking viral integration sites and fragile sites.
141 NC tumors and keratinocyte clones identified viral integration sites in a variety of chromosomes, wit
142 tagging through the identification of common viral integration sites in BXH-2 leukaemia.
143 fication of genes located in the vicinity of viral integration sites in human cancers may be helpful
144 lyclonal proliferation of CD4(+) T cells and viral integration sites in the human genome.
145 rom the regenerated myocardium showed common viral integration sites in the human genome.
146 is, we carried out a genome-wide analysis of viral integration sites in the prostate cell line DU145
147                               Cancer SVs and viral integration sites must be discovered in a genome-w
148                                          The viral integration sites occur throughout the genome, lea
149 engage nucleosomes in vitro and redistribute viral integration sites on the genomic scale.
150  model to identify both CIS genes and unique viral integration sites or compare the integration sites
151                                              Viral integration sites that contribute to oncogenesis a
152 tumor-associated DNA viruses and identifying viral integration sites that may unravel novel mechanism
153 is, decreased infectivity, and redistributed viral integration sites to markers associated with late
154                                              Viral integration sites were also detected in expressed
155              By using inverse PCR, 28 unique viral integration sites were identified in rapid-onset t
156                  As a result, a total of 332 viral integration sites were identified in the six tumor
157  various sizes as well as translocations and viral integration sites with high sensitivity and low fa
158 rse collection of genomic perturbations near viral integration sites, including direct gene disruptio
159 l perturbations of cellular genes at or near viral integration sites.
160 nhibition of nuclear entry and alteration of viral integration sites.
161 n of HPV, cannot be reliably used to predict viral integration status.
162            Given the mutagenic potentials of viral integrations, such treatment effects should be con
163 ue to the lack of reproducible and efficient viral integration systems.
164 y, we describe two quantitative cell culture viral integration systems.
165 d VIcaller, a novel platform for identifying viral integrations that are derived from any characteriz
166 te significantly to the observed increase in viral integrations that specify a Switching phenotype, p
167 rus (AAV) is unique in its ability to target viral integration to a specific site on chromosome 19 (c
168 ormatics tools have been developed to detect viral integrations using NGS data.
169 , HPV18 and adeno-associated virus-2 (AAV2), viral integration was associated with local variations i
170    Dysregulation of a host gene disrupted by viral integration was defined by aberrant expression >2
171 sure of cells to zidovudine, indicating that viral integration was not required to induce secretion.
172                                    Expressed viral integrations were detected in all pre- and posttre
173                                     Notably, viral integrations were found in many genes, including n
174                                Understanding viral integration will help improve the safety of retrov
175                       Such widespread random viral integration will likely increase carcinogenic oppo
176 ration events and explore the correlation of viral integrations with host gene dysregulation.
177                             Searching clonal viral integrations with our platform has the capacity to
178  significantly greater reduction in distinct viral integrations, with 3.28-fold and 1.81-fold decreas
179 bitors, which could block one of the ends of viral integration, would lead to similar aberrant integr

 
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