<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sanz-Martinez P</submitter><funding>Deutsche Forschungsgemeinschaft</funding><pagination>480-486</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11760280</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(2)</volume><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</pubmed_abstract><journal>Autophagy</journal><pubmed_title>Function of CSNK2/CK2 selectively affects the endoplasmic reticulum and the Golgi apparatus in mtor-mediated autophagy induction.</pubmed_title><pmcid>PMC11760280</pmcid><funding_grant_id>515275293</funding_grant_id><funding_grant_id>512574446</funding_grant_id><funding_grant_id>259130777 (SFB1177)</funding_grant_id><funding_grant_id>403765277</funding_grant_id><pubmed_authors>Stolz A</pubmed_authors><pubmed_authors>Berkane R</pubmed_authors><pubmed_authors>Sanz-Martinez P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Function of CSNK2/CK2 selectively affects the endoplasmic reticulum and the Golgi apparatus in mtor-mediated autophagy induction.</name><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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2026-05-09T17:49:22.828Z</modification><creation>2026-04-08T01:08:30.429Z</creation></dates><accession>S-EPMC11760280</accession><cross_references><pubmed>39178915</pubmed><doi>10.1080/15548627.2024.2395725</doi></cross_references></HashMap>