<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Frentzel S</submitter><funding>Deutsche Forschungsgemeinschaft</funding><pubmed_abstract>IκB proteins regulate the inhibition and activation of NF-κB transcription factor complexes. While classical IκB proteins keep NF-κB complexes inactive in the cytoplasm, atypical IκB proteins act on activated NF-κB complexes located in the nucleus. Most of the knowledge regarding the function of IκB proteins has been collected &lt;i>in vitro&lt;/i>, while far less is known regarding their impact on activation and regulation of immune responses during &lt;i>in vivo&lt;/i> infections. Combining &lt;i>in vivo Listeria monocytogenes&lt;/i> (Lm) infection with comparative &lt;i>ex vivo&lt;/i> transcriptional profiling of the hepatic response to the pathogen we observed that in contrast to wild type mice that mounted a robust inflammatory response, IκB&lt;sub>NS&lt;/sub>-deficiency was generally associated with a transcripti</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1028789</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9813228</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IκB&lt;sub>NS&lt;/sub>-deficiency protects mice from fatal &lt;i>Listeria monocytogenes&lt;/i> infection by blunting pro-inflammatory signature in Ly6C&lt;sup>high&lt;/sup> monocytes and preventing exaggerated innate immune responses.</pubmed_title><pmcid>PMC9813228</pmcid><pubmed_authors>Jeron A</pubmed_authors><pubmed_authors>Pausder A</pubmed_authors><pubmed_authors>Volckmar J</pubmed_authors><pubmed_authors>Schmitz I</pubmed_authors><pubmed_authors>Bruder D</pubmed_authors><pubmed_authors>Kershaw O</pubmed_authors><pubmed_authors>Frentzel S</pubmed_authors></additional><is_claimable>false</is_claimable><name>IκB&lt;sub>NS&lt;/sub>-deficiency protects mice from fatal &lt;i>Listeria monocytogenes&lt;/i> infection by blunting pro-inflammatory signature in Ly6C&lt;sup>high&lt;/sup> monocytes and preventing exaggerated innate immune responses.</name><description>IκB proteins regulate the inhibition and activation of NF-κB transcription factor complexes. While classical IκB proteins keep NF-κB complexes inactive in the cytoplasm, atypical IκB proteins act on activated NF-κB complexes located in the nucleus. Most of the knowledge regarding the function of IκB proteins has been collected &lt;i>in vitro&lt;/i>, while far less is known regarding their impact on activation and regulation of immune responses during &lt;i>in vivo&lt;/i> infections. Combining &lt;i>in vivo Listeria monocytogenes&lt;/i> (Lm) infection with comparative &lt;i>ex vivo&lt;/i> transcriptional profiling of the hepatic response to the pathogen we observed that in contrast to wild type mice that mounted a robust inflammatory response, IκB&lt;sub>NS&lt;/sub>-deficiency was generally associated with a transcripti</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-04-07T17:33:19.802Z</modification><creation>2025-04-06T00:52:50.606Z</creation></dates><accession>S-EPMC9813228</accession><cross_references><pubmed>36618344</pubmed><doi>10.3389/fimmu.2022.1028789</doi></cross_references></HashMap>