<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(9)</volume><submitter>Lai TY</submitter><pubmed_abstract>Macrophages play a pivotal role in the immune system through recognition and elimination of microbial pathogens. Toll-like receptors (TLRs) on macrophages interact with microbial substances and initiate signal transduction through intracellular adapters. TLR4, which recognizes the lipopolysaccharides (LPS) on Gram-positive and Gram-negative bacteria, triggers downstream signaling mediators and eventually activates IκB kinase (IKK) complex and mitogen-activated protein kinases (MAPKs) such as p38. Previous reports revealed that, in addition to NF-κB, a core transcription factor of the innate immune response, the induction of some LPS-induced genes in macrophages required another transcription factor whose activity depends on p38. However, these additional transcription factors remain to be </pubmed_abstract><journal>PloS one</journal><pagination>e73153</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3759409</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Transcription of Tnfaip3 is regulated by NF-κB and p38 via C/EBPβ in activated macrophages.</pubmed_title><pmcid>PMC3759409</pmcid><pubmed_authors>Lai LC</pubmed_authors><pubmed_authors>Chuang EY</pubmed_authors><pubmed_authors>Lai TY</pubmed_authors><pubmed_authors>Chuang LL</pubmed_authors><pubmed_authors>Hsu LC</pubmed_authors><pubmed_authors>Tsai MH</pubmed_authors><pubmed_authors>Wu SD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcription of Tnfaip3 is regulated by NF-κB and p38 via C/EBPβ in activated macrophages.</name><description>Macrophages play a pivotal role in the immune system through recognition and elimination of microbial pathogens. Toll-like receptors (TLRs) on macrophages interact with microbial substances and initiate signal transduction through intracellular adapters. TLR4, which recognizes the lipopolysaccharides (LPS) on Gram-positive and Gram-negative bacteria, triggers downstream signaling mediators and eventually activates IκB kinase (IKK) complex and mitogen-activated protein kinases (MAPKs) such as p38. Previous reports revealed that, in addition to NF-κB, a core transcription factor of the innate immune response, the induction of some LPS-induced genes in macrophages required another transcription factor whose activity depends on p38. However, these additional transcription factors remain to be </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2026-04-07T21:13:25.491Z</modification><creation>2026-04-07T18:00:31.552Z</creation></dates><accession>S-EPMC3759409</accession><cross_references><pubmed>24023826</pubmed><doi>10.1371/journal.pone.0073153</doi></cross_references></HashMap>