<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>3(6)</volume><submitter>Faure-Dupuy S</submitter><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Immune-mediated induction of cytidine deaminase APOBEC3B (A3B) expression leads to HBV covalently closed circular DNA (cccDNA) decay. Here, we aimed to decipher the signalling pathway(s) and regulatory mechanism(s) involved in A3B induction and related HBV control.&lt;h4>Methods&lt;/h4>Differentiated HepaRG cells (dHepaRG) knocked-down for NF-κB signalling components, transfected with siRNA or micro RNAs (miRNA), and primary human hepatocytes ± HBV or HBVΔX or HBV-RFP, were treated with lymphotoxin beta receptor (LTβR)-agonist (BS1). The biological outcomes were analysed by reverse transcriptase-qPCR, immunoblotting, luciferase activity, chromatin immune precipitation, electrophoretic mobility-shift assay, targeted-bisulfite-, miRNA-, RNA-, genome-sequencing, and mass-s</pubmed_abstract><journal>JHEP reports : innovation in hepatology</journal><pagination>100354</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8523871</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Control of APOBEC3B induction and cccDNA decay by NF-κB and miR-138-5p.</pubmed_title><pmcid>PMC8523871</pmcid><pubmed_authors>Riedl T</pubmed_authors><pubmed_authors>Rolland M</pubmed_authors><pubmed_authors>Lipka DB</pubmed_authors><pubmed_authors>Lucifora J</pubmed_authors><pubmed_authors>Farhat R</pubmed_authors><pubmed_authors>Schonung M</pubmed_authors><pubmed_authors>Schuster LC</pubmed_authors><pubmed_authors>Hizir Z</pubmed_authors><pubmed_authors>Prokosch S</pubmed_authors><pubmed_authors>Heikenwalder M</pubmed_authors><pubmed_authors>Gillet N</pubmed_authors><pubmed_authors>Rippe K</pubmed_authors><pubmed_authors>Ollinger R</pubmed_authors><pubmed_authors>Rad R</pubmed_authors><pubmed_authors>Stadler M</pubmed_authors><pubmed_authors>Parent R</pubmed_authors><pubmed_authors>Tscharahganeh D</pubmed_authors><pubmed_authors>Protzer U</pubmed_authors><pubmed_authors>Dejardin E</pubmed_authors><pubmed_authors>Wettengel J</pubmed_authors><pubmed_authors>Durantel D</pubmed_authors><pubmed_authors>Leuchtenberger C</pubmed_authors><pubmed_authors>Unger K</pubmed_authors><pubmed_authors>Reisinger F</pubmed_authors><pubmed_authors>Engleitner T</pubmed_authors><pubmed_authors>Neuhaus K</pubmed_authors><pubmed_authors>Schuehle S</pubmed_authors><pubmed_authors>Remouchamps C</pubmed_authors><pubmed_authors>Barnault R</pubmed_authors><pubmed_authors>Faure-Dupuy S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Control of APOBEC3B induction and cccDNA decay by NF-κB and miR-138-5p.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Immune-mediated induction of cytidine deaminase APOBEC3B (A3B) expression leads to HBV covalently closed circular DNA (cccDNA) decay. Here, we aimed to decipher the signalling pathway(s) and regulatory mechanism(s) involved in A3B induction and related HBV control.&lt;h4>Methods&lt;/h4>Differentiated HepaRG cells (dHepaRG) knocked-down for NF-κB signalling components, transfected with siRNA or micro RNAs (miRNA), and primary human hepatocytes ± HBV or HBVΔX or HBV-RFP, were treated with lymphotoxin beta receptor (LTβR)-agonist (BS1). The biological outcomes were analysed by reverse transcriptase-qPCR, immunoblotting, luciferase activity, chromatin immune precipitation, electrophoretic mobility-shift assay, targeted-bisulfite-, miRNA-, RNA-, genome-sequencing, and mass-s</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-03-27T17:06:22.565Z</modification><creation>2025-04-04T13:16:59.325Z</creation></dates><accession>S-EPMC8523871</accession><cross_references><pubmed>34704004</pubmed><doi>10.1016/j.jhepr.2021.100354</doi></cross_references></HashMap>