<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Oh S</submitter><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pubmed_abstract>The term CASM describes a process in which LC3 and other Atg8 proteins are covalently ligated to lipids in damaged endomembranes. While CASM is commonly described as a cytoprotective response to multiple types of membrane damage, the ways in which CASM helps cells maintain homeostasis are still unclear. Here, we show that CASM contributes to the maintenance or repair of Golgi apparatus architecture following the loss of TRIM46, a ubiquitin ligase with roles in microtubule organization. TRIM46-deficient cells were notable for enhanced TFEB-driven lysosomal biogenesis and Golgi ribbon fragmentation, with colocalization between the &lt;i>trans&lt;/i>-Golgi marker TGN46 and the Atg8 proteins LC3B and GABARAP. Similar results were seen when Golgi architecture was disrupted by inhibitors of microtubul</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2025.09.04.674289</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12424704</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A role for CASM in the repair of damaged Golgi architecture.</pubmed_title><pmcid>PMC12424704</pmcid><funding_grant_id>T32 AI007538</funding_grant_id><funding_grant_id>P20 GM121176</funding_grant_id><funding_grant_id>R01 AI155746</funding_grant_id><funding_grant_id>P30 CA118100</funding_grant_id><pubmed_authors>Saha B</pubmed_authors><pubmed_authors>Ullah S</pubmed_authors><pubmed_authors>Oh S</pubmed_authors><pubmed_authors>Mandell MA</pubmed_authors></additional><is_claimable>false</is_claimable><name>A role for CASM in the repair of damaged Golgi architecture.</name><description>The term CASM describes a process in which LC3 and other Atg8 proteins are covalently ligated to lipids in damaged endomembranes. While CASM is commonly described as a cytoprotective response to multiple types of membrane damage, the ways in which CASM helps cells maintain homeostasis are still unclear. Here, we show that CASM contributes to the maintenance or repair of Golgi apparatus architecture following the loss of TRIM46, a ubiquitin ligase with roles in microtubule organization. TRIM46-deficient cells were notable for enhanced TFEB-driven lysosomal biogenesis and Golgi ribbon fragmentation, with colocalization between the &lt;i>trans&lt;/i>-Golgi marker TGN46 and the Atg8 proteins LC3B and GABARAP. Similar results were seen when Golgi architecture was disrupted by inhibitors of microtubul</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-04-16T03:21:16.872Z</modification><creation>2026-04-16T03:12:43.369Z</creation></dates><accession>S-EPMC12424704</accession><cross_references><pubmed>40950167</pubmed><doi>10.1101/2025.09.04.674289</doi></cross_references></HashMap>