Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA414179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6220144.fastq.gz | Fastqsanger.gz | |||
| SRR6220145.fastq.gz | Fastqsanger.gz |
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Project description:The goals of this study are to check mRNA levels of genes and pathways regulated by RXRα knocking down, and figure out their influences to HBV infection. The mRNA profiles of wild-type (WT) and RXRα knockdown (RXRα-KD) HepG2-NTCP cells were generated by deep sequencing using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the gene level with TopHat followed by Cufflinks. Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the human genome. We find arachidonic acid synthesis, retinol metabolism pathways and serveral other genes are regulated by RXRα knockdown. We also revealed that reduced gene expression in arachidonic acid (AA)/eicosanoids biosynthesis pathways, in particular one of the AA synthases Phospholipase A2 Group IIA (PLA2G2A), is associated with increased HBV infection. Moreover, we also found exogenous treatment of AA inhibits HBV infection. These data implicate the participation of AA/eicosanoids biosynthesis pathways in the regulation of HBV infection, and point to a novel potential strategy for host-targeted therapies against HBV.
2017-12-21 | GSE108366 | GEO
Project description:Hepatitis B virus (HBV) infection leads tdevelopment of fatal liver complications. Due to a lack of effective measure to cure HBV infection, complete eradication of HBV is difficult. Thus, novel HBV therapeutic strategies are needed. Host proteins involved in the HBV infection processes are known to be regulated through phosphorylation. System level changes in phospho-signaling pathway in host during infection remains unclear. To this end, phosphoproteome profiling on HBV infected HepG2-NTCP cells was performed.
2022-06-09 | PXD015393 | Pride
Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acid-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acid uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acid metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection. Transcriptome profiling by DNA microarray of Huh7.5.1 cells transduced to express NTCP.
2016-10-25 | E-GEOD-79089 | biostudies-arrayexpress
Project description:Aim: Hepatitis B virus (HBV) infection is one of the most serious global health problems. Our previous study revealed that an increase in the miR-6126 serum level over one year of pegylated interferon therapy predicted a decrease in hepatitis B surface (HBs) antigens. We aimed to clarify whether miR-6126 downregulated the expression level of sodium taurocholate cotransporting polypeptide (NTCP), a host cell receptor required for HBV entry. Methods: HepG2-NTCP and PXB cells were utilized to evaluate the expression level of NTCP after transfection with miR-6126. The protein expression level of NTCP was evaluated using Western blot analysis and immunostaining. The expression profile of messenger RNAs was evaluated using next-generation sequencing to search for direct targets of miR-6126.
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Project description:Examination of interferon stimulated genes treated with different kind of interferon subtypes in HBV-infected HepG2-NTCP cells.
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Project description:Chronic hepatitis B virus (HBV) infections remain a health burden affecting ~250 million people worldwide. Thus far, available interferon-alpha (IFNα)-based therapies have shown unsatisfactory cure rates, and alternative therapeutic molecules are still required. However, their development has been hampered because accessible cell models supporting relevant HBV replication and appropriate antiviral activity are lacking. Strategies that reverse epigenetic alterations offer a unique opportunity for cell reprogramming, which is valuable for restoring altered cellular functions in human cell lines. This work aimed to investigate the feasibility of converting HepG2 cells that stably overexpress the HBV entry receptor (sodium/taurocholate cotransporting polypeptide, NTCP) toward IFNα-responsive cells using epigenetic reprogramming. Herein, we showed that an epigenetic regimen with non-cytotoxic doses of the demethylating compound 5-azacytidine restored the anti-HBV action of IFNα in epigenetically reprogrammed HepG2-NTCP-C4 cells, named REP-HepG2-NTCP cells. Thus, a significant inhibition in HBV DNA levels was measured in REP-HepG2-NTCP cells after IFNα treatment. This inhibitory effect was associated with the enhancement of IFNα-mediated induction of critical interferon-stimulated genes (ISGs), which was limited in non-reprogrammed cells. In particular, our data indicated that re-expression of 2’-5’-oligoadenylate synthetase 1 (OAS1) and interferon regulatory factor 9 (IRF9) was the result of an epigenetically driven unmasking of these genes in reprogrammed cells. At last, we evaluated the therapeutic potential of the IFN analog CDM-3008 in REP-HepG2-NTCP cells and demonstrated the efficiency of this chemical compound in triggering ISG induction and HBV inhibition. In summary, this study shows that epigenetic reprogramming promotes the IFNα response in HBV-infected cells and is potentially attractive for cell-based experimental screening of IFN-like compounds.
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Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acid-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acid uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acid metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection.
2016-10-25 | GSE79089 | GEO
Project description:Chronic hepatitis B, C and D virus (HBV, HCV, HDV) infections are leading causes of liver disease and cancer worldwide. Although these viruses differ markedly in their life cycle and genomic organization, they exclusively infect hepatocytes. Recently, the sodium taurocholate cotransporting polypeptide (NTCP) was identified as the first functional receptor for HBV and HDV. Here, we report that NTCP also facilitates HCV entry into human hepatocytes, by augmenting the bile acids-mediated repression of IFN-stimulated genes (ISGs), including IFITM2 and IFITM3, to increase the susceptibility of cells to HCV entry. Furthermore, an HBV-derived preS1 peptide, known to bind NTCP and to inhibit bile acids uptake and HBV infection, inhibits HCV entry by enhancing the expression of ISGs. Our study highlights NTCP as a novel player linking bile acids metabolism to the interferon response in hepatocytes and establishes a role for NTCP in the entry process of multiple hepatotropic viruses, via distinct mechanisms. Collectively, these findings enhance our understanding of hepatitis virus-host interactions and suggest NTCP as an attractive antiviral target for HBV/HCV co-infection.
2016-10-25 | GSE85091 | GEO
Project description:Microarray data to compare the gene expression in HepG2-NTCP and Huh-106 cell lines Knowledge of HBV virus-host interactions is still limited. Here, we performed a genome-wide gain-of-function screen using weakly permissive Huh-106 cells to uncover novel HBV host factors.
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Project description:In order to profile the transcriptomic change in NTCP-reconstituted HepG2 cells after the treatment with hepatocyte maintanace medium. HMM-pretreated HepG2/NTCP cells turned to be more susceptible to hepatitis B virus infection.
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