{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(12)"],"submitter":["Kim EY"],"pubmed_abstract":["<h4>Background</h4>Activating transcription factor 3 (ATF3) is a negative regulator of proinflammatory cytokine expression in macrophages, and ATF3 deficient mice are more susceptible to endotoxic shock. This study addresses the role of ATF3 in the Kdo(2)-Lipid A-induced Toll-like receptor 4 (TLR4) signaling pathway in mouse embryonic fibroblasts (MEF). Kdo(2)-Lipid A upregulates ATF3 expression in wild type MEF cells and induces both nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) activation via the TLR4 signaling pathway, while neither of these pathways is activated in ATF3-/- MEF cells. Interestingly, in contrast to Kdo(2)-Lipid A, the activation of both NF-κB and JNK by TNF-α was normal in ATF3-/- MEF cells.<h4>Methodology/principal findings</h4>We found that several g"],"journal":["PloS one"],"pagination":["e14181"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2996292"],"repository":["biostudies-literature"],"pubmed_title":["ATF3 plays a key role in Kdo2-lipid A-induced TLR4-dependent gene expression via NF-κB activation."],"pmcid":["PMC2996292"],"pubmed_authors":["Kim EY","Shin HY","Choi YM","Choi S","Kim DG","Kim JY","Rhee DK","Kwon HK","Kim YS"],"additional_accession":[]},"is_claimable":false,"name":"ATF3 plays a key role in Kdo2-lipid A-induced TLR4-dependent gene expression via NF-κB activation.","description":"<h4>Background</h4>Activating transcription factor 3 (ATF3) is a negative regulator of proinflammatory cytokine expression in macrophages, and ATF3 deficient mice are more susceptible to endotoxic shock. This study addresses the role of ATF3 in the Kdo(2)-Lipid A-induced Toll-like receptor 4 (TLR4) signaling pathway in mouse embryonic fibroblasts (MEF). Kdo(2)-Lipid A upregulates ATF3 expression in wild type MEF cells and induces both nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) activation via the TLR4 signaling pathway, while neither of these pathways is activated in ATF3-/- MEF cells. Interestingly, in contrast to Kdo(2)-Lipid A, the activation of both NF-κB and JNK by TNF-α was normal in ATF3-/- MEF cells.<h4>Methodology/principal findings</h4>We found that several g","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Dec","modification":"2025-04-04T21:04:44.413Z","creation":"2019-03-26T23:09:10Z"},"accession":"S-EPMC2996292","cross_references":{"pubmed":["21152039"],"doi":["10.1371/journal.pone.0014181"]}}