<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Saeed U</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Human parvulin peptidyl prolyl cis/trans isomerases PIN1 and PIN4 play important roles in cell cycle progression, DNA binding, protein folding and chromatin remodeling, ribosome biogenesis, and tubulin polymerization. In this article, we found that endogenous PIN1 and PIN4 were upregulated in selected hepatocellular carcinoma (HCC) cell lines.&lt;h4>Methods&lt;/h4>In this study, we inhibited PIN1 and PIN4 &lt;i>via&lt;/i> parvulin inhibitors (Juglone, PiB, ATRA, 6,7,4'-THIF, KPT6566, and EGCG). The native agarose gel electrophoresis (NAGE) immunoblotting analysis revealed that upon PIN1 and/ or PIN4 inhibition, the HBc protein expression and core particle or capsid synthesis reduced remarkably. The effects of PIN4 inhibition on hepatitis B virus (HBV) replication were more pronoun</pubmed_abstract><journal>Frontiers in microbiology</journal><pagination>921653</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9905731</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PIN1 and PIN4 inhibition &lt;i>via&lt;/i> parvulin impeders Juglone, PiB, ATRA, 6,7,4'-THIF, KPT6566, and EGCG thwarted hepatitis B virus replication.</pubmed_title><pmcid>PMC9905731</pmcid><pubmed_authors>Piracha ZZ</pubmed_authors><pubmed_authors>Saeed U</pubmed_authors></additional><is_claimable>false</is_claimable><name>PIN1 and PIN4 inhibition &lt;i>via&lt;/i> parvulin impeders Juglone, PiB, ATRA, 6,7,4'-THIF, KPT6566, and EGCG thwarted hepatitis B virus replication.</name><description>&lt;h4>Introduction&lt;/h4>Human parvulin peptidyl prolyl cis/trans isomerases PIN1 and PIN4 play important roles in cell cycle progression, DNA binding, protein folding and chromatin remodeling, ribosome biogenesis, and tubulin polymerization. In this article, we found that endogenous PIN1 and PIN4 were upregulated in selected hepatocellular carcinoma (HCC) cell lines.&lt;h4>Methods&lt;/h4>In this study, we inhibited PIN1 and PIN4 &lt;i>via&lt;/i> parvulin inhibitors (Juglone, PiB, ATRA, 6,7,4'-THIF, KPT6566, and EGCG). The native agarose gel electrophoresis (NAGE) immunoblotting analysis revealed that upon PIN1 and/ or PIN4 inhibition, the HBc protein expression and core particle or capsid synthesis reduced remarkably. The effects of PIN4 inhibition on hepatitis B virus (HBV) replication were more pronoun</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-19T20:49:02.038Z</modification><creation>2024-11-09T01:26:20.245Z</creation></dates><accession>S-EPMC9905731</accession><cross_references><pubmed>36760500</pubmed><doi>10.3389/fmicb.2023.921653</doi></cross_references></HashMap>