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1 ations suggest that R0=1.6 in the absence of virus integration.
2 la188 contact analogous tDNA bases to effect virus integration.
3 esent in the adjacent intron or generated by virus integration.
4 nces, as is characteristic for avian sarcoma virus integration.
5 and anonymous cDNAs disrupted as a result of virus integration.
6 e investigate potential oncogenic impacts of virus integration.
7 e leukemia virus, and avian sarcoma/leukosis virus integrations.
8 hat the transcription factor Friend leukemia virus integration 1 (Fli-1) is a target of miR-145a and
9 vious data demonstrated that friend leukemia virus integration 1 (Fli-1), an erythroblast transformat
14 how similarities with human immunodeficiency virus integration and provide a unifying mechanism for d
15 g cytokine regulators, that are disrupted by virus integration, and we determined mechanisms through
17 e findings reveal another mechanism in which virus integration can ignite tumorigenesis and a promisi
18 , and we determined mechanisms through which virus integration causes deregulation of cellular gene e
20 l cancers by whole-genome sequencing detects virus integration in 77%, revealing five statistically s
22 ction of RIG-I in suppressing DNA repair and virus integration into the host genome, and meanwhile en
25 p52, and Rep40) are pleiotropic effectors of virus integration, replication, transcription, and virio
26 including wingless-type murine mammary tumor virus integration site (WNT) pathway subtype, Sonic Hedg
28 To address the cellular origin of ecotropic virus integration site 1 (EVI1)-expressing aggressive KM
29 tures of Rep68 bound to the adeno-associated virus integration site 1 in different nucleotide-bound s
30 into the safe-harbor locus adeno-associated virus integration site 1 in human embryonic stem cells.
31 i-1 (B-cell-specific Moloney murine leukemia virus integration site 1) as a regulator of human epider
33 MDS and EVI1 complex protein EVI1 [ecotropic virus integration site 1], in 5 patients) or PRDM16 (pos
34 ducible by wingless-type mouse mammary tumor virus integration site family member (WNT)/beta-catenin
35 nt refers to the wingless-type mammary tumor virus integration site family of proteins), that are reg
36 esenchymal Wingless-type Mouse Mammary Tumor Virus integration site family, member 10B (Wnt10b)/beta-
37 the cellular gene at the mouse mammary tumor virus integration site in the int-5 locus is aromatase.
38 Meis (named for a myeloid ecotropic leukemia virus integration site), respectively, are encoded by mu
40 f Wingless-related MMTV (mouse mammary tumor virus) integration site 3 (WNT3) by ingrowing axons from
42 ical wingless-type MMTV (mouse mammary tumor virus) integration site family (WNT) signaling pathway i