{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo X"],"funding":["Shanghai Committee of Science and Technology","National Natural Science Foundation of China","China Postdoctoral Science Foundation","Shanghai Shenkang Three Years Action Project"],"pagination":["e2118285119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8931368"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(11)"],"pubmed_abstract":["SignificanceUnderstanding autophagy regulation is instrumental in developing therapeutic interventions for autophagy-associated disease. Here, we identified SNAI2 as a regulator of autophagy from a genome-wide screen in HeLa cells. Upon energy stress, SNAI2 is transcriptionally activated by FOXO3 and interacts with FOXO3 to form a feed-forward regulatory loop to reinforce the expression of autophagy genes. Of note, SNAI2-increased FOXO3-DNA binding abrogates CRM1-dependent FOXO3 nuclear export, illuminating a pivotal role of DNA in the nuclear retention of nucleocytoplasmic shuttling proteins. Moreover, a dFoxO-Snail feed-forward loop regulates both autophagy and cell size in <i>Drosophila</i>, suggesting this evolutionarily conserved regulatory loop is engaged in more physiological activities."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["A coherent FOXO3-SNAI2 feed-forward loop in autophagy."],"pmcid":["PMC8931368"],"funding_grant_id":["32000547","2000229071","09DZ2260100","81771957","SHDC2020CR2054B","31970536"],"pubmed_authors":["Li W","Lv Z","Lu L","Ding X","Li Z","Zhan M","Guo X","Wu C","Ma X","Zhu X","Xue L","Peng K"],"additional_accession":[]},"is_claimable":false,"name":"A coherent FOXO3-SNAI2 feed-forward loop in autophagy.","description":"SignificanceUnderstanding autophagy regulation is instrumental in developing therapeutic interventions for autophagy-associated disease. Here, we identified SNAI2 as a regulator of autophagy from a genome-wide screen in HeLa cells. Upon energy stress, SNAI2 is transcriptionally activated by FOXO3 and interacts with FOXO3 to form a feed-forward regulatory loop to reinforce the expression of autophagy genes. Of note, SNAI2-increased FOXO3-DNA binding abrogates CRM1-dependent FOXO3 nuclear export, illuminating a pivotal role of DNA in the nuclear retention of nucleocytoplasmic shuttling proteins. Moreover, a dFoxO-Snail feed-forward loop regulates both autophagy and cell size in <i>Drosophila</i>, suggesting this evolutionarily conserved regulatory loop is engaged in more physiological activities.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2025-04-21T23:18:53.029Z","creation":"2025-04-05T19:06:03.56Z"},"accession":"S-EPMC8931368","cross_references":{"pubmed":["35271390"],"doi":["10.1073/pnas.2118285119"]}}