{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sanz-Martinez P"],"funding":["Deutsche Forschungsgemeinschaft"],"pagination":["480-486"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11760280"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(2)"],"pubmed_abstract":["Selective macroautophagy/autophagy of the endoplasmic reticulum, known as reticulophagy/ER-phagy, is essential to maintain ER homeostasis. We recently showed that members of the autophagy receptor family RETREG/FAM134 are regulated by phosphorylation-dependent ubiquitination. In an unbiased screen we had identified several kinases downstream of MTOR with profound impact on reticulophagy flux, including ATR and CSNK2/CK2. Inhibition of CSNK2 by SGC-CK2-1 prevented regulatory ubiquitination of RETREG1/FAM134B and RETREG3/FAM134C upon autophagy activation as well as the formation of high-density RETREG1- and RETREG3-clusters. Here we report on additional resource data of global proteomics upon CSNK2 and ATR inhibition, respectively. Our data suggests that the function of CSNK2 is mainly limit"],"journal":["Autophagy"],"pubmed_title":["Function of CSNK2/CK2 selectively affects the endoplasmic reticulum and the Golgi apparatus in mtor-mediated autophagy induction."],"pmcid":["PMC11760280"],"funding_grant_id":["515275293","512574446","259130777 (SFB1177)","403765277"],"pubmed_authors":["Stolz A","Berkane R","Sanz-Martinez P"],"additional_accession":[]},"is_claimable":false,"name":"Function of CSNK2/CK2 selectively affects the endoplasmic reticulum and the Golgi apparatus in mtor-mediated autophagy induction.","description":"Selective macroautophagy/autophagy of the endoplasmic reticulum, known as reticulophagy/ER-phagy, is essential to maintain ER homeostasis. We recently showed that members of the autophagy receptor family RETREG/FAM134 are regulated by phosphorylation-dependent ubiquitination. In an unbiased screen we had identified several kinases downstream of MTOR with profound impact on reticulophagy flux, including ATR and CSNK2/CK2. Inhibition of CSNK2 by SGC-CK2-1 prevented regulatory ubiquitination of RETREG1/FAM134B and RETREG3/FAM134C upon autophagy activation as well as the formation of high-density RETREG1- and RETREG3-clusters. Here we report on additional resource data of global proteomics upon CSNK2 and ATR inhibition, respectively. Our data suggests that the function of CSNK2 is mainly limit","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-05-09T17:49:22.828Z","creation":"2026-04-08T01:08:30.429Z"},"accession":"S-EPMC11760280","cross_references":{"pubmed":["39178915"],"doi":["10.1080/15548627.2024.2395725"]}}