{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Gourisankar Ghosh Lab, Chemistry and Biochemistry, UCSD"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA172063"],"scientific_name":["Mus musculus"],"long_description":["By binding to specific DNA elements, known collectively as “κB sites”, contained within the promoters/enhancers of target genes, NF-κB regulates gene expression. We found that the identity of the central base pair (bp) of κB sites profoundly impacts the transcriptional activity of NF-κB dimers. RelA dimers prefer an A/T bp at this position for optimum transcriptional activation (A/T-centric) and discriminate against G/C-centric κB sites. The p52 homodimer, in contrast, activates transcription from G/C-centric κB sites in complex with Bcl3 but represses transcription from the A/T-centric sites. The p52:Bcl3 complex binds to these two classes of κB sites in distinct modes permitting recruitment of coactivator, corepressor, or both coactivator and corepressor complexes in promoters containing G/C, A/T or both G/C and A/T-centric sites. Therefore, through sensing of bp differences within κB sites, NF-κB dimers modulate biological programs by activating, repressing and altering expression of effector genes. Overall design: Total RNA extracted from bone marrow derived macrophages (BMDMs) with Bcl3 siRNA knockdown or mouse scramble siRNA knockdown were subjected to LPS stimulation."],"tag":["xref:PubMed:23063365"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Mus musculus","description":"Genome-wide analysis of macrophage gene expression upon Bcl3 knockdown","dates":{"last_updated":"2025-09-24","first_public":"2014-02-11"},"accession":"PRJNA172063","cross_references":{"GEO":["GSE39922"],"taxon":["10090"],"PubMed":["23063365"]}}