In this report, we present new findings that demonstrate LPS activation of the non-canonical pathway of NF-κB activation in human colonic epithelial cells, leading to increased nuclear RelB and p52. This cascade involves phosphorylations of …

RELA can either be phosphorylated in the RHD region or the TAD region, attracting different interaction partners. Triggered by lipopolysaccharide (LPS), protein kinase A (PKA) specifically phosphorylates serine 276 in the RHD domain in the cytoplasm, controlling NF-κB DNA-binding and oligomerization. [12]

Jul 31, 2023 · Here we used time-dependent multi-omics to investigate the selective functions of Rel and RelA, two closely related NF-κB proteins, in primary B lymphocytes activated via the B cell receptor.

Sep 11, 2014 · By intersecting the chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of the individual TFs in LPS-stimulated GM-BMDMs with gene expression data and histone methylation status data sets, we show that the IRF5 and RelA cistromes target inflammatory genes.

We find that RelA activation by LPS or TNF-α and activation of the IFN-γ pathway are both required for activation of key genes involved in adaptive immune responses. In contrast, RelA activation alone is sufficient for potent activation of genes involved in innate responses.

Lipopolysaccharide (LPS) modulates the transcription of the gene that codifies the enzyme arylalkylamine-N-acetyltransferase (AA-NAT) through nuclear translocation of the transcription factor nuclear factor-κ-light-chain-enhancer of activated B cells (NF-κB).

Feb 25, 2020 · We then dissected each gene’s regulatory strategy by testing RelA variants in a primary-cell genetic-complementation assay. All endogenous target genes require RelA to make DNA-base-specific contacts, and none are activatable by the DNA binding domain alone.

May 5, 2020 · Compared to the mock-treated group, the deamidated species of RelA was detectably reduced in LPS-treated or SeV-infected groups (Figure S6 C). Consistent with NF-κB activation, LPS treatment and SeV infection increased RelA phosphorylation of serine 536.

Feb 5, 2002 · Acute inflammation induced by intrapulmonary LPS requires nuclear factor (NF)-κB RelA. This study elucidates the effects of intrapulmonary LPS on IκB proteins, endogenous inhibitors of RelA, and th...

By binding the 3'-UTR of RELA, miR-138 negatively regulated p65 expression. The silencing of p65 also improved LPS-induced HTR-8/SVneo and JEG-3 cell dysfunction and TNF-α and IL-6 levels.