<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16(8)</volume><submitter>Huang S</submitter><pubmed_abstract>&lt;h4>Aim&lt;/h4>In 2019, to examine the functions of METTL3 in liver and underlying mechanisms, we generated mice with hepatocyte-specific METTL3 homozygous knockout (METTL3Δhep) by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT) or Alb-Cre mice (JAX), respectively. In this study, we explored the potential reasons why hepatocyte-specific METTL3 homozygous disruption by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and then postnatal lethality.&lt;h4>Main methods&lt;/h4>Mice with hepatocyte-specific METTL3 knockout were generated by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT; Strain No. T003814) purchased from the GemPharmatech Co., Ltd., (Nanjing, China) or with Alb-Cre mice (JAX; Strain No. 003574) obtained from The</pubmed_abstract><journal>Aging</journal><pagination>7217-7248</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11087113</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Hepatocyte-specific METTL3 ablation by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and postnatal lethality.</pubmed_title><pmcid>PMC11087113</pmcid><pubmed_authors>Shen L</pubmed_authors><pubmed_authors>He D</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Han L</pubmed_authors><pubmed_authors>Lin T</pubmed_authors><pubmed_authors>Zhao W</pubmed_authors><pubmed_authors>Lin X</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Cong J</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Shen H</pubmed_authors><pubmed_authors>Zhou Z</pubmed_authors><pubmed_authors>Jia J</pubmed_authors><pubmed_authors>Huang S</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Xia J</pubmed_authors><pubmed_authors>Wu A</pubmed_authors><pubmed_authors>Dai G</pubmed_authors><pubmed_authors>Xiang X</pubmed_authors><pubmed_authors>Xiao D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hepatocyte-specific METTL3 ablation by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and postnatal lethality.</name><description>&lt;h4>Aim&lt;/h4>In 2019, to examine the functions of METTL3 in liver and underlying mechanisms, we generated mice with hepatocyte-specific METTL3 homozygous knockout (METTL3Δhep) by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT) or Alb-Cre mice (JAX), respectively. In this study, we explored the potential reasons why hepatocyte-specific METTL3 homozygous disruption by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and then postnatal lethality.&lt;h4>Main methods&lt;/h4>Mice with hepatocyte-specific METTL3 knockout were generated by simultaneously crossing METTL3fl/fl mice with Alb-iCre mice (GPT; Strain No. T003814) purchased from the GemPharmatech Co., Ltd., (Nanjing, China) or with Alb-Cre mice (JAX; Strain No. 003574) obtained from The</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-06-02T11:24:45.363Z</modification><creation>2026-05-27T03:07:30.91Z</creation></dates><accession>S-EPMC11087113</accession><cross_references><pubmed>38656880</pubmed><doi>10.18632/aging.205753</doi></cross_references></HashMap>