{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ye Y"],"funding":["Flight Attendant Medical Research Institute","NIAID NIH HHS","National Institutes of Health","NIGMS NIH HHS"],"pagination":["1816-26"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4633763"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["212(11)"],"pubmed_abstract":["<h4>Background</h4>Klebsiella pneumoniae causes serious infections and healthcare burdens in humans. We have previously reported that the deficiency of autophagy-related gene (Atg) 7 in macrophages (murine alveolar macrophage cell line [MH-S]) induced irregular host immunity against K. pneumoniae and worsened pathologic effects in the lung. In the current study, we investigated the molecular mechanism by which Atg7 influenced K. pneumoniae-induced inflammatory responses.<h4>Methods</h4>Expression levels of Atg7, ubiquitin (Ub), and tumor necrosis factor (TNF) α and phosphorylation of IκBα (p-IκBα) were determined with immunoblotting. Ubiquitylation of p-IκBα was determined with immunoprecipitation.<h4>Results</h4>We noted an interaction between Atg7 and p-IκBα, which was decreased in MH-S "],"journal":["The Journal of infectious diseases"],"pubmed_title":["Inhibition of p-IκBα Ubiquitylation by Autophagy-Related Gene 7 to Regulate Inflammatory Responses to Bacterial Infection."],"pmcid":["PMC4633763"],"funding_grant_id":["R15 AI101973-01","R01 AI109317","R01 AI109317-01A1","R03 AI097532-01A1","R03 AI097532","103007","P30 GM103329","R15 AI101973"],"pubmed_authors":["Dhasarathy A","Li X","Lichter N","Wu M","Jundt MC","Tan S","Ye Y","Zhou X","Hidebrand A"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of p-IκBα Ubiquitylation by Autophagy-Related Gene 7 to Regulate Inflammatory Responses to Bacterial Infection.","description":"<h4>Background</h4>Klebsiella pneumoniae causes serious infections and healthcare burdens in humans. We have previously reported that the deficiency of autophagy-related gene (Atg) 7 in macrophages (murine alveolar macrophage cell line [MH-S]) induced irregular host immunity against K. pneumoniae and worsened pathologic effects in the lung. In the current study, we investigated the molecular mechanism by which Atg7 influenced K. pneumoniae-induced inflammatory responses.<h4>Methods</h4>Expression levels of Atg7, ubiquitin (Ub), and tumor necrosis factor (TNF) α and phosphorylation of IκBα (p-IκBα) were determined with immunoblotting. Ubiquitylation of p-IκBα was determined with immunoprecipitation.<h4>Results</h4>We noted an interaction between Atg7 and p-IκBα, which was decreased in MH-S ","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Dec","modification":"2025-05-31T22:54:31.239Z","creation":"2025-05-31T22:54:31.239Z"},"accession":"S-EPMC4633763","cross_references":{"pubmed":["26022442"],"doi":["10.1093/infdis/jiv301"]}}