ライフサイエンスコーパス: viral integration

1 ociation with both spcDNAs and hot-spots for viral integration.

2 understanding of the molecular mechanisms of viral integration.

3 a translocation had occurred at the site of viral integration.

4 ional activation, cancer, viral latency, and viral integration.

5 enomic 'safe harbor' site rather than random viral integration.

6 ase of the tethered p12 post mitosis, before viral integration.

7 t virus-induced cell killing is triggered by viral integration.

8 chromosomal rearrangements in cancer and of viral integration.

9 T antigen that provides indirect evidence of viral integration.

10 ce-inducing substitutions were defective for viral integration.

11 nses and possible gene alterations following viral integration.

12 ll specific, and inhibition occurs following viral integration.

13 s, both genes are highly expressed following viral integration.

14 ty of leukemias and lymphomas as a result of viral integration.

15 on surrounding c-myc is indeed a hot spot of viral integration.

16 lular sequence was not linked to the site of viral integration.

17 luding homeobox A9 (Hoxa9)/myeloid ecotropic viral integration 1 (Meis1)/pre-B-cell leukemia homeobox

18 A was found in primary infection, whereas in viral integration, 4 patients had HHV-6A and 17 patients

19 We addressed this question for viral integration, a fundamental mechanism of horizontal

20 t genetic rearrangement in processes such as viral integration and excision and chromosomal segregati

21 terial chromosome dimers to adeno-associated viral integration and is a versatile tool for mammalian

22 chromosome remodelling, viral replication or viral integration and may account for the local hypermet

23 th host chromatin and significantly impaired viral integration and replication in HIV-1-susceptible c

24 such, are important models for the study of viral integration and target site selection.

25 s study, we set out to identify the sites of viral integration and to assess the efficiency of the ov

26 t structural intermediates in recombination, viral integration, and DNA repair.

27 splantation showed sustained Btk expression, viral integration, and partial functional responses, con

28 53) in viral entry, a karyopherin (TNPO3) in viral integration, and the Mediator complex (Med28) in v

29 s the hypothesis that the sites of oncogenic viral integration are nonrandom and that genes at the si

30 Viral integrations are important in human biology, yet g

31 l limitations (for example, mutation through viral integration) are eliminated.

32 hat spans the Evi5 locus and is disrupted by viral integration at Evi5.

33 ression of the same genes in tumours without viral integration at the same site.

34 Unexpectedly, about half of the viral integrations at Nf1 represented a previously undis

35 l polymorphisms INS119G and INR231G retarget viral integration away from gene-dense regions.

36 itself is weak without hormonal stimulation, viral integration can position the 5' LTR elements to ef

37 rtant for basic cellular functions including viral integration, control of gene expression, productio

38 vitro integration junctions suggest that the viral integration event itself is mediated by terminal r

39 rst molecular characterization of an in vivo viral integration event within a confirmed fragile site

40 xperimental evidence that the high number of viral integration events (>90%) found in actively expres

41 tool called seeksv to detect somatic SVs and viral integration events.

42 r of DNA damage sites dramatically increases viral integration frequency.

43 However, when the inhibitor was added after viral integration had occurred, no inhibition of HIV inf

44 We propose that activation of DNA-PK during viral integration has a central role in CD4(+) T-cell de

45 However, viral integration has associated risks, such as the unin

46 The cellular genes disrupted by viral integration have been identified in four of these

47 A number of viral integrations have been shown to occur within the v

48 ppears to be the most common site of somatic viral integration in BXH-2 mice.

49 entified by viral tagging as common sites of viral integration in BXH2 leukemias.

50 teosarcomas, positive for SV40 by PCR, found viral integration in half of these.

51 omain and was identified as a common site of viral integration in myeloid leukemias arising in BXH-2

52 was originally isolated as a common site of viral integration in myeloid tumors of the BXH-2 recombi

53 , the Hoxa-9 gene is frequently activated by viral integration in the same BXH-2 leukemias, suggestin

54 To study the role of viral integration in tumorigenesis, we analyzed the posi

55 rexpression of TERT mRNA in tumors harboring viral integrations in the TERT promoter.

56 We show that viral integrations in tumor cells lie near cellular sequ

57 , and have all of the hallmarks of authentic viral integration, including the removal of a terminal T

58 hed adjacent normal samples, indicating that viral integration induced host driver genetic alteration

59 Viral integration into a host genome is defined by two c

60 LEDGF/p75, which promotes viral integration into active genes, stabilizes Tpr at t

61 of early cervical lesions revealed frequent viral integration into gene-poor regions of the host gen

62 Evidence from several studies indicates that viral integration into genic regions is accompanied by l

63 lignant progression is often associated with viral integration into host cell chromatin.

64 xpansion of latently infected T cells due to viral integration into specific genes contribute to this

65 rus (HIV) replication and, in particular, to viral integration into the host chromatin.

66 both human and HPV38 genomes, indicative of viral integration into the host DNA, something not previ

67 Viral integration into the host genome is an important a

68 ection from infection reflects prevention of viral integration into the host genome.

69 blocking steps in reverse transcription and viral integration into the host genome.

70 an DeltaLR-9 of short-latency lymphomas with viral integrations into c-myb.

71 The mechanism of killing during viral integration involved the activation of DNA-depende

72 pies/hair follicle cell), demonstrating that viral integration is not confined to blood cells.

73 are nonrandom and that genes at the sites of viral integration may play important roles in carcinogen

74 s of these patterns can provide insight into viral integration mechanisms, pathology and genome evolu

75 Similarly, reported examples of viral integration near microRNAs suggest that altered ex

76 0% of TBLV-induced lymphomas have detectable viral integrations near c-myc by Southern blotting, wher

77 Viral integration of HPV into the host genome is not req

78 verified experiments show that more than 90% viral integration sequences detected by seeksv are true.

79 eukemia homeobox (PBX) and myeloid ecotropic viral integration site (MEIS) proteins control cell fate

80 homeobox (KNOX) and animal Myeloid ecotropic viral integration site (MEIS) proteins share a TALE home

81 The gene ectopic viral integration site 1 (EVI) and its variant myelodysp

82 Enhanced expression of ecotropic viral integration site 1 (EVI-1) occurs in approximately

83 In addition, aberrant expression of ectopic viral integration site 1 (EVI1) has also been found in s

84 Ecotropic viral integration site 1 (EVI1) is an oncogenic dual dom

85 the transforming potential of the ecotropic viral integration site 1 (Evi1) oncogene is thought to b

86 Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zi

87 Ecotropic viral integration site 1 (EVI1), required for normal emb

88 Myeloid ecotropic viral integration site 1 (Meis1) forms a heterodimer wit

89 operative interaction with myeloid ecotropic viral integration site 1 homolog (MEIS1).

90 Meis1 (Myeloid Ecotropic viral Integration Site 1) is a homeobox gene that was or

91 transcriptional signature of EVI1 (ecotropic viral integration site 1)-rearranged (EVI1-r) acute myel

92 iptional repressor, ETS variant 6, ecotropic viral integration site 1, and homeobox A11.

93 It is highly related to ecotropic viral integration site 3 (EVI3), a protein that, like EB

94 nd 4, a major fragile region that includes a viral integration site between exons 4 and 5, and cancer

95 Clone Lists describe the viral integration site clones along with the tumor model

96 transfer strategy to show the importance of viral integration site in cellular immortalization.

97 some (BAC) clone, RP364B14, corresponding to viral integration site in CRL2504 cells, reverted their

98 andmarks, five cancer cell break points, one viral integration site, and one aphidicolin break cluste

99 proximately 18 kb upstream of another common viral integration site, Gfi1, on mouse chromosome 5.

100 Ecotropic viral integration site-1 (EVI1) and myelodysplastic synd

101 Ecotropic viral integration site-1 (EVI1) is an oncogenic zinc fin

102 tumor suppressor, whereas myeloid ecotropic viral integration site-1 (Meis1) is an oncogene.

103 The proto-oncogene EVI1 (ecotropic viral integration site-1), located on chromosome band 3q

104 cell lines located in the middle of an HPV16 viral integration site.

105 ng previous cytogenetic observations linking viral integration sites and fragile sites.

106 NC tumors and keratinocyte clones identified viral integration sites in a variety of chromosomes, wit

107 tagging through the identification of common viral integration sites in BXH-2 leukaemia.

108 fication of genes located in the vicinity of viral integration sites in human cancers may be helpful

109 rom the regenerated myocardium showed common viral integration sites in the human genome.

110 is, we carried out a genome-wide analysis of viral integration sites in the prostate cell line DU145

111 Cancer SVs and viral integration sites must be discovered in a genome-w

112 The viral integration sites occur throughout the genome, lea

113 engage nucleosomes in vitro and redistribute viral integration sites on the genomic scale.

114 model to identify both CIS genes and unique viral integration sites or compare the integration sites

115 Viral integration sites that contribute to oncogenesis a

116 tumor-associated DNA viruses and identifying viral integration sites that may unravel novel mechanism

117 Viral integration sites were also detected in expressed

118 By using inverse PCR, 28 unique viral integration sites were identified in rapid-onset t

119 various sizes as well as translocations and viral integration sites with high sensitivity and low fa

120 rse collection of genomic perturbations near viral integration sites, including direct gene disruptio

121 l perturbations of cellular genes at or near viral integration sites.

122 n of HPV, cannot be reliably used to predict viral integration status.

123 y, we describe two quantitative cell culture viral integration systems.

124 ue to the lack of reproducible and efficient viral integration systems.

125 te significantly to the observed increase in viral integrations that specify a Switching phenotype, p

126 rus (AAV) is unique in its ability to target viral integration to a specific site on chromosome 19 (c

127 sure of cells to zidovudine, indicating that viral integration was not required to induce secretion.

128 Notably, viral integrations were found in many genes, including n

129 Understanding viral integration will help improve the safety of retrov

130 Such widespread random viral integration will likely increase carcinogenic oppo

131 bitors, which could block one of the ends of viral integration, would lead to similar aberrant integr