FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2191036287> ?p ?o ?g. }

• W2191036287 endingPage "1740" @default.
• W2191036287 startingPage "1729" @default.
• W2191036287 abstract "ABSTRACT Hepatitis B virus (HBV) has been implicated as a potential trigger of hepatic steatosis although molecular mechanisms involved in the pathogenesis of HBV-associated hepatic steatosis still remain elusive. Our prior work has revealed that the expression level of liver fatty acid binding protein 1 (FABP1), a key regulator of hepatic lipid metabolism, was elevated in HBV-producing hepatoma cells. In this study, the effects of HBV X protein (HBx) mediated FABP1 regulation on hepatic steatosis and the underlying mechanism were determined. mRNA and protein levels of FABP1 were measured by quantitative RT-PCR (qPCR) and Western blotting. HBx-mediated FABP1 regulation was evaluated by luciferase assay, coimmunoprecipitation, and chromatin immunoprecipitation. Hepatic lipid accumulation was measured by using Oil-Red-O staining and the triglyceride level. It was found that expression of FABP1 was increased in HBV-producing hepatoma cells, the sera of HBV-infected patients, and the sera and liver tissues of HBV-transgenic mice. Ectopic overexpression of HBx resulted in upregulation of FABP1 in HBx-expressing hepatoma cells, whereas HBx abolishment reduced FABP1 expression. Mechanistically, HBx activated the FABP1 promoter in an HNF3β-, C/EBPα-, and PPARα-dependent manner, in which HBx increased the gene expression of HNF3β and physically interacted with C/EBPα and PPARα. On the other hand, knockdown of FABP1 remarkably blocked lipid accumulation both in long-chain free fatty acids treated HBx-expressing HepG2 cells and in a high-fat diet-fed HBx-transgenic mice. Therefore, FABP1 is a key driver gene in HBx-induced hepatic lipid accumulation via regulation of HNF3β, C/EBPα, and PPARα. FABP1 may represent a novel target for treatment of HBV-associated hepatic steatosis. IMPORTANCE Accumulating evidence from epidemiological and experimental studies has indicated that chronic HBV infection is associated with hepatic steatosis. However, the molecular mechanism underlying HBV-induced pathogenesis of hepatic steatosis still remains to be elucidated. In this study, we found that expression of liver fatty acid binding protein (FABP1) was dramatically increased in the sera of HBV-infected patients and in both sera and liver tissues of HBV-transgenic mice. Forced expression of HBx led to FABP1 upregulation, whereas knockdown of FABP1 remarkably diminished lipid accumulation in both in vitro and in vivo models. It is possible that HBx promotes hepatic lipid accumulation through upregulating FABP1 in the development of HBV-induced nonalcoholic fatty liver disease. Therefore, inhibition of FABP1 might have therapeutic value in steatosis-associated chronic HBV infection." @default.
• W2191036287 created "2016-06-24" @default.
• W2191036287 creator A5001523166 @default.
• W2191036287 creator A5030521131 @default.
• W2191036287 creator A5059099209 @default.
• W2191036287 creator A5059854137 @default.
• W2191036287 creator A5070879677 @default.
• W2191036287 creator A5076266323 @default.
• W2191036287 date "2016-02-15" @default.
• W2191036287 modified "2023-10-14" @default.
• W2191036287 title "Hepatitis B Virus X Protein Induces Hepatic Steatosis by Enhancing the Expression of Liver Fatty Acid Binding Protein" @default.
• W2191036287 cites W1496973986 @default.
• W2191036287 cites W1553141492 @default.
• W2191036287 cites W1965501203 @default.
• W2191036287 cites W1967705712 @default.
• W2191036287 cites W1972709924 @default.
• W2191036287 cites W1979354705 @default.
• W2191036287 cites W1980964148 @default.
• W2191036287 cites W1987229672 @default.
• W2191036287 cites W1988706402 @default.
• W2191036287 cites W1994056355 @default.
• W2191036287 cites W1995490785 @default.
• W2191036287 cites W1996446469 @default.
• W2191036287 cites W1996476188 @default.
• W2191036287 cites W1997901667 @default.
• W2191036287 cites W2005317793 @default.
• W2191036287 cites W2009092266 @default.
• W2191036287 cites W2009664127 @default.
• W2191036287 cites W2010338556 @default.
• W2191036287 cites W2010349866 @default.
• W2191036287 cites W2020814081 @default.
• W2191036287 cites W2026004488 @default.
• W2191036287 cites W2034937725 @default.
• W2191036287 cites W2035288512 @default.
• W2191036287 cites W2037396389 @default.
• W2191036287 cites W2041196096 @default.
• W2191036287 cites W2047438155 @default.
• W2191036287 cites W2052378749 @default.
• W2191036287 cites W2054648069 @default.
• W2191036287 cites W2056851249 @default.
• W2191036287 cites W2059549567 @default.
• W2191036287 cites W2066342925 @default.
• W2191036287 cites W2071997319 @default.
• W2191036287 cites W2074134609 @default.
• W2191036287 cites W2087106096 @default.
• W2191036287 cites W2089525503 @default.
• W2191036287 cites W2099356672 @default.
• W2191036287 cites W2102612565 @default.
• W2191036287 cites W2103116278 @default.
• W2191036287 cites W2124501164 @default.
• W2191036287 cites W2127163321 @default.
• W2191036287 cites W2131575050 @default.
• W2191036287 cites W2137052325 @default.
• W2191036287 cites W2140576094 @default.
• W2191036287 cites W2140788887 @default.
• W2191036287 cites W2147073885 @default.
• W2191036287 cites W2151106782 @default.
• W2191036287 cites W2158706540 @default.
• W2191036287 cites W2164778116 @default.
• W2191036287 cites W2171381764 @default.
• W2191036287 cites W2171902445 @default.
• W2191036287 cites W4230280576 @default.
• W2191036287 cites W4300705053 @default.
• W2191036287 doi "https://doi.org/10.1128/jvi.02604-15" @default.
• W2191036287 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4733992" @default.
• W2191036287 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26637457" @default.
• W2191036287 hasPublicationYear "2016" @default.
• W2191036287 type Work @default.
• W2191036287 sameAs 2191036287 @default.
• W2191036287 citedByCount "72" @default.
• W2191036287 countsByYear W21910362872016 @default.
• W2191036287 countsByYear W21910362872017 @default.
• W2191036287 countsByYear W21910362872018 @default.
• W2191036287 countsByYear W21910362872019 @default.
• W2191036287 countsByYear W21910362872020 @default.
• W2191036287 countsByYear W21910362872021 @default.
• W2191036287 countsByYear W21910362872022 @default.
• W2191036287 countsByYear W21910362872023 @default.
• W2191036287 crossrefType "journal-article" @default.
• W2191036287 hasAuthorship W2191036287A5001523166 @default.
• W2191036287 hasAuthorship W2191036287A5030521131 @default.
• W2191036287 hasAuthorship W2191036287A5059099209 @default.
• W2191036287 hasAuthorship W2191036287A5059854137 @default.
• W2191036287 hasAuthorship W2191036287A5070879677 @default.
• W2191036287 hasAuthorship W2191036287A5076266323 @default.
• W2191036287 hasBestOaLocation W21910362871 @default.
• W2191036287 hasConcept C101762097 @default.
• W2191036287 hasConcept C104317684 @default.
• W2191036287 hasConcept C126322002 @default.
• W2191036287 hasConcept C127561419 @default.
• W2191036287 hasConcept C134018914 @default.
• W2191036287 hasConcept C134320426 @default.
• W2191036287 hasConcept C150194340 @default.
• W2191036287 hasConcept C153911025 @default.
• W2191036287 hasConcept C159047783 @default.
• W2191036287 hasConcept C173396325 @default.
• W2191036287 hasConcept C2522874641 @default.
• W2191036287 hasConcept C2776175330 @default.

• next