FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1988032963> ?p ?o ?g. }

• W1988032963 endingPage "998.e4" @default.
• W1988032963 startingPage "989" @default.
• W1988032963 abstract "Background & AimsWomen with hepatitis B virus (HBV) infection usually have lower viral loads than men, reducing their risk of liver cancer. There are 2 androgen-responsive elements in the HBV enhancer I that contribute to higher viral titers in men. We investigated whether and how estrogen signaling affects progression of HBV infection.MethodsOvariectomy and estrogen supplementation were used to evaluate the effect of estrogen on HBV titers in transgenic mice with replicating HBV in hepatocytes. The effect of estrogen signaling on transcription of HBV genes, and the mechanisms of regulation, were studied in HepG2 cells.ResultsHBV titers increased in female mice after ovariectomy and decreased in male mice supplemented with estrogen. Hepatic expression of estrogen receptor (ER)–α was increased by estrogen exposure. In HepG2 cells, up-regulation of ER-α reduced HBV transcription, which required a specific region within enhancer I. Direct DNA binding of ER-α and histone deacetylase activity were not required for ER-α–mediated repression of HBV genes. Overexpression of hepatocyte nuclear factor (HNF)-4α, which binds to this region, overcame the repressive effect of ER-α. ER-α did not repress transcription of an HBV replicon with a mutant HNF-4α binding site within enhancer I. Coimmunoprecipitation assays showed an interaction between ER-α and HNF-4α; this interaction prevented HNF-4α binding to enhancer I and activation of HBV transcription.ConclusionsEstrogen can repress transcription of HBV genes by up-regulating ER-α, which interacts with and alters binding of HNF-4α to the HBV enhancer I. These findings might account for the lower viral load and reduced incidence of liver cancer in HBV-infected women than men. Women with hepatitis B virus (HBV) infection usually have lower viral loads than men, reducing their risk of liver cancer. There are 2 androgen-responsive elements in the HBV enhancer I that contribute to higher viral titers in men. We investigated whether and how estrogen signaling affects progression of HBV infection. Ovariectomy and estrogen supplementation were used to evaluate the effect of estrogen on HBV titers in transgenic mice with replicating HBV in hepatocytes. The effect of estrogen signaling on transcription of HBV genes, and the mechanisms of regulation, were studied in HepG2 cells. HBV titers increased in female mice after ovariectomy and decreased in male mice supplemented with estrogen. Hepatic expression of estrogen receptor (ER)–α was increased by estrogen exposure. In HepG2 cells, up-regulation of ER-α reduced HBV transcription, which required a specific region within enhancer I. Direct DNA binding of ER-α and histone deacetylase activity were not required for ER-α–mediated repression of HBV genes. Overexpression of hepatocyte nuclear factor (HNF)-4α, which binds to this region, overcame the repressive effect of ER-α. ER-α did not repress transcription of an HBV replicon with a mutant HNF-4α binding site within enhancer I. Coimmunoprecipitation assays showed an interaction between ER-α and HNF-4α; this interaction prevented HNF-4α binding to enhancer I and activation of HBV transcription. Estrogen can repress transcription of HBV genes by up-regulating ER-α, which interacts with and alters binding of HNF-4α to the HBV enhancer I. These findings might account for the lower viral load and reduced incidence of liver cancer in HBV-infected women than men." @default.
• W1988032963 created "2016-06-24" @default.
• W1988032963 creator A5013662606 @default.
• W1988032963 creator A5037531063 @default.
• W1988032963 creator A5061524286 @default.
• W1988032963 creator A5070257043 @default.
• W1988032963 creator A5070823441 @default.
• W1988032963 creator A5086740134 @default.
• W1988032963 creator A5088393966 @default.
• W1988032963 creator A5090280328 @default.
• W1988032963 date "2012-04-01" @default.
• W1988032963 modified "2023-10-18" @default.
• W1988032963 title "Estrogen Receptor α Represses Transcription of HBV Genes via Interaction With Hepatocyte Nuclear Factor 4α" @default.
• W1988032963 cites W1965874843 @default.
• W1988032963 cites W1970254730 @default.
• W1988032963 cites W1981708899 @default.
• W1988032963 cites W1983020857 @default.
• W1988032963 cites W1984655196 @default.
• W1988032963 cites W1988825643 @default.
• W1988032963 cites W1992349567 @default.
• W1988032963 cites W1996711919 @default.
• W1988032963 cites W1997860146 @default.
• W1988032963 cites W2003137401 @default.
• W1988032963 cites W2007705662 @default.
• W1988032963 cites W2015824057 @default.
• W1988032963 cites W2025658404 @default.
• W1988032963 cites W2029683589 @default.
• W1988032963 cites W2039845199 @default.
• W1988032963 cites W2039972354 @default.
• W1988032963 cites W2045496667 @default.
• W1988032963 cites W2069181588 @default.
• W1988032963 cites W2081540673 @default.
• W1988032963 cites W2082711035 @default.
• W1988032963 cites W2083589028 @default.
• W1988032963 cites W2083643651 @default.
• W1988032963 cites W2085785933 @default.
• W1988032963 cites W2099467939 @default.
• W1988032963 cites W2099866336 @default.
• W1988032963 cites W2100866222 @default.
• W1988032963 cites W2102349447 @default.
• W1988032963 cites W2110617523 @default.
• W1988032963 cites W2122496801 @default.
• W1988032963 cites W2125069527 @default.
• W1988032963 cites W2125840593 @default.
• W1988032963 cites W2139025111 @default.
• W1988032963 cites W2153619533 @default.
• W1988032963 cites W2156008071 @default.
• W1988032963 cites W2158228456 @default.
• W1988032963 cites W2159674010 @default.
• W1988032963 cites W2161152775 @default.
• W1988032963 cites W2161352669 @default.
• W1988032963 cites W2165241118 @default.
• W1988032963 cites W2216094174 @default.
• W1988032963 doi "https://doi.org/10.1053/j.gastro.2011.12.045" @default.
• W1988032963 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22240483" @default.
• W1988032963 hasPublicationYear "2012" @default.
• W1988032963 type Work @default.
• W1988032963 sameAs 1988032963 @default.
• W1988032963 citedByCount "102" @default.
• W1988032963 countsByYear W19880329632012 @default.
• W1988032963 countsByYear W19880329632013 @default.
• W1988032963 countsByYear W19880329632014 @default.
• W1988032963 countsByYear W19880329632015 @default.
• W1988032963 countsByYear W19880329632016 @default.
• W1988032963 countsByYear W19880329632017 @default.
• W1988032963 countsByYear W19880329632018 @default.
• W1988032963 countsByYear W19880329632019 @default.
• W1988032963 countsByYear W19880329632020 @default.
• W1988032963 countsByYear W19880329632021 @default.
• W1988032963 countsByYear W19880329632022 @default.
• W1988032963 countsByYear W19880329632023 @default.
• W1988032963 crossrefType "journal-article" @default.
• W1988032963 hasAuthorship W1988032963A5013662606 @default.
• W1988032963 hasAuthorship W1988032963A5037531063 @default.
• W1988032963 hasAuthorship W1988032963A5061524286 @default.
• W1988032963 hasAuthorship W1988032963A5070257043 @default.
• W1988032963 hasAuthorship W1988032963A5070823441 @default.
• W1988032963 hasAuthorship W1988032963A5086740134 @default.
• W1988032963 hasAuthorship W1988032963A5088393966 @default.
• W1988032963 hasAuthorship W1988032963A5090280328 @default.
• W1988032963 hasBestOaLocation W19880329631 @default.
• W1988032963 hasConcept C101762097 @default.
• W1988032963 hasConcept C104317684 @default.
• W1988032963 hasConcept C111936080 @default.
• W1988032963 hasConcept C121608353 @default.
• W1988032963 hasConcept C134018914 @default.
• W1988032963 hasConcept C134320426 @default.
• W1988032963 hasConcept C150194340 @default.
• W1988032963 hasConcept C153911025 @default.
• W1988032963 hasConcept C154456304 @default.
• W1988032963 hasConcept C159047783 @default.
• W1988032963 hasConcept C172313692 @default.
• W1988032963 hasConcept C2522874641 @default.
• W1988032963 hasConcept C2777164284 @default.
• W1988032963 hasConcept C2780593183 @default.
• W1988032963 hasConcept C502942594 @default.
• W1988032963 hasConcept C530470458 @default.
• W1988032963 hasConcept C54355233 @default.

• next