{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu A"],"funding":["Korea National Institute of Health","Bio-MAX Institute,  Seoul National University","Bio-MAX Institute, Seoul National University","Seoul National University"],"pagination":["8826"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11909186"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Exposure to diesel exhaust particles (DEPs), which are major constituents of urban air pollution, is associated with adverse health outcomes. Previous studies have shown that DEPs enhance the expression of pro-inflammatory cytokines and immune responses. However, few studies have focused on genomic variants that regulate DEP-induced signaling. Here, we identify a frequently found genomic variant, ACP5, in allergic diseases, and establish an ACP5 knock-out (KO) human bronchial epithelial cell line (BEAS-2B) using CRISPR/Cas9 editing to mimic the ACP5 mutation. DEP-induced apoptosis and intracellular reactive oxygen species (ROS) were significantly increased in the ACP5 KO cells compared with controls, suggesting that ACP5 KO cells were at increased risk from DEP exposure. A gene expression "],"journal":["Scientific reports"],"pubmed_title":["The regulatory role of ACP5 in the diesel exhaust particle-induced AHR inflammatory signaling pathway in a human bronchial epithelial cell line."],"pmcid":["PMC11909186"],"funding_grant_id":["2015-NI-67002-00","2023 Bio-Connect program (Bio-MAX - BMC)","2020-NG-010-02","0525-20220151"],"pubmed_authors":["Han MH","Yoo HM","Park JH","Chae DH","Heo HR","Kim HS","An HB","Oh MK","Park KS","Kang KS","Yu KR","Park HS","Cho K","Yoon D","Choi U","Yu A","Lim HJ","Heo J"],"additional_accession":[]},"is_claimable":false,"name":"The regulatory role of ACP5 in the diesel exhaust particle-induced AHR inflammatory signaling pathway in a human bronchial epithelial cell line.","description":"Exposure to diesel exhaust particles (DEPs), which are major constituents of urban air pollution, is associated with adverse health outcomes. Previous studies have shown that DEPs enhance the expression of pro-inflammatory cytokines and immune responses. However, few studies have focused on genomic variants that regulate DEP-induced signaling. Here, we identify a frequently found genomic variant, ACP5, in allergic diseases, and establish an ACP5 knock-out (KO) human bronchial epithelial cell line (BEAS-2B) using CRISPR/Cas9 editing to mimic the ACP5 mutation. DEP-induced apoptosis and intracellular reactive oxygen species (ROS) were significantly increased in the ACP5 KO cells compared with controls, suggesting that ACP5 KO cells were at increased risk from DEP exposure. A gene expression ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-20T00:08:51.549Z","creation":"2025-04-20T00:08:51.549Z"},"accession":"S-EPMC11909186","cross_references":{"pubmed":["40087344"],"doi":["10.1038/s41598-024-84280-9"]}}