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- W2113180849 endingPage "8583" @default.
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- W2113180849 abstract "Transcriptional activation of myc family proto-oncogenes through the insertion of viral sequences is the predominant mechanism by which woodchuck hepatitis virus (WHV) induces liver tumors in chronically infected animals. The main target is N-myc2, a functional retroposon of the N-myc gene, but c-myc and N-myc are also marginally involved. Here we identify a major, liver-specific regulatory element in the WHV genome (We2) which efficiently activates the N-myc2 promoter in cultured hepatoma cells. In the context of the episomal viral genome, We2 governs the production of pregenomic RNA and thus plays a central role in the control of viral replication. We2 activity is primarily controlled by the liver-enriched HNF1 and HNF4 transcription factors, although NF1 and Oct proteins were also shown to bind in a central region. The expression of HNF1 and HNF4 appears to be maintained in woodchuck tumors. Thus, We2 is a prime candidate for controlling myc gene cis activation during WHV-induced hepatocarcinogenesis." @default.
- W2113180849 created "2016-06-24" @default.
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- W2113180849 creator A5087686339 @default.
- W2113180849 date "1996-12-01" @default.
- W2113180849 modified "2023-10-18" @default.
- W2113180849 title "The HNF1/HNF4-dependent We2 element of woodchuck hepatitis virus controls viral replication and can activate the N-myc2 promoter" @default.
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- W2113180849 doi "https://doi.org/10.1128/jvi.70.12.8571-8583.1996" @default.
- W2113180849 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/190950" @default.
- W2113180849 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8970982" @default.
- W2113180849 hasPublicationYear "1996" @default.
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