<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ye Y</submitter><funding>Flight Attendant Medical Research Institute</funding><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><pagination>1816-26</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4633763</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>212(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>We noted an interaction between Atg7 and p-IκBα, which was decreased in MH-S </pubmed_abstract><journal>The Journal of infectious diseases</journal><pubmed_title>Inhibition of p-IκBα Ubiquitylation by Autophagy-Related Gene 7 to Regulate Inflammatory Responses to Bacterial Infection.</pubmed_title><pmcid>PMC4633763</pmcid><funding_grant_id>R15 AI101973-01</funding_grant_id><funding_grant_id>R01 AI109317</funding_grant_id><funding_grant_id>R01 AI109317-01A1</funding_grant_id><funding_grant_id>R03 AI097532-01A1</funding_grant_id><funding_grant_id>R03 AI097532</funding_grant_id><funding_grant_id>103007</funding_grant_id><funding_grant_id>P30 GM103329</funding_grant_id><funding_grant_id>R15 AI101973</funding_grant_id><pubmed_authors>Dhasarathy A</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Lichter N</pubmed_authors><pubmed_authors>Wu M</pubmed_authors><pubmed_authors>Jundt MC</pubmed_authors><pubmed_authors>Tan S</pubmed_authors><pubmed_authors>Ye Y</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Hidebrand A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of p-IκBα Ubiquitylation by Autophagy-Related Gene 7 to Regulate Inflammatory Responses to Bacterial Infection.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>We noted an interaction between Atg7 and p-IκBα, which was decreased in MH-S </description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Dec</publication><modification>2025-05-31T22:54:31.239Z</modification><creation>2025-05-31T22:54:31.239Z</creation></dates><accession>S-EPMC4633763</accession><cross_references><pubmed>26022442</pubmed><doi>10.1093/infdis/jiv301</doi></cross_references></HashMap>