<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jiang M</submitter><funding>the health commission of Zhejiang Province of China</funding><funding>Natural Science Foundation of Zhejiang Province of China</funding><funding>National Natural Science Foundation of China</funding><pagination>31</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11765366</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>&lt;h4>Background/objectives&lt;/h4>UFMylation, a newly identified ubiquitin-like modification, modulates a variety of physiological processes, including endoplasmic reticulum homeostasis maintenance, DNA damage response, embryonic development, and tumor progression. Recent reports showed that UFMylation plays a protective role in preventing liver steatosis and fibrosis, serving as a defender of liver homeostasis in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the regulation of UFMylation in MASLD remains unclear. This study aimed to determine the expressed patterns of UFMylation components in multiple tissues of leptin-deficient &lt;i>ob/ob&lt;/i> mice and high-fat diet (HFD)-fed mice, which are mimicking the conditions of MASLD.&lt;h4>Methods&lt;/h4>The &lt;i></pubmed_abstract><journal>Genes</journal><pubmed_title>Systematic Analysis of UFMylation Family Genes in Tissues of Mice with Metabolic Dysfunction-Associated Steatotic Liver Disease.</pubmed_title><pmcid>PMC11765366</pmcid><funding_grant_id>32270751, 82371571</funding_grant_id><funding_grant_id>2024KY239</funding_grant_id><funding_grant_id>LQ24C070003, LY24H250002</funding_grant_id><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Zeng Q</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Jiang M</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Qi S</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Duan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Systematic Analysis of UFMylation Family Genes in Tissues of Mice with Metabolic Dysfunction-Associated Steatotic Liver Disease.</name><description>&lt;h4>Background/objectives&lt;/h4>UFMylation, a newly identified ubiquitin-like modification, modulates a variety of physiological processes, including endoplasmic reticulum homeostasis maintenance, DNA damage response, embryonic development, and tumor progression. Recent reports showed that UFMylation plays a protective role in preventing liver steatosis and fibrosis, serving as a defender of liver homeostasis in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the regulation of UFMylation in MASLD remains unclear. This study aimed to determine the expressed patterns of UFMylation components in multiple tissues of leptin-deficient &lt;i>ob/ob&lt;/i> mice and high-fat diet (HFD)-fed mice, which are mimicking the conditions of MASLD.&lt;h4>Methods&lt;/h4>The &lt;i></description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-04-18T03:26:57.931Z</modification><creation>2025-04-04T22:06:55.276Z</creation></dates><accession>S-EPMC11765366</accession><cross_references><pubmed>39858578</pubmed><doi>10.3390/genes16010031</doi></cross_references></HashMap>