IκBα is required for full transcriptional induction of some NFκB-regulated genes in response to TNF in MCF-7 cells.

ABSTRACT: Inflammatory stimuli triggers the degradation of three inhibitory κB (IκB) proteins, allowing for nuclear translocation of nuclear factor-κB (NFκB) for transcriptional induction of its target genes. Of these three, IκBα is a well-known negative feedback regulator that limits the duration of NFκB activity. We sought to determine whether IκBα's role in enabling or limiting NFκB activation is important for tumor necrosis factor (TNF)-induced gene expression in human breast cancer cells (MCF-7). Contrary to our expectations, many more TNF-response genes showed reduced induction than enhanced induction in IκBα knockdown cells. Mathematical modeling was used to investigate the underlying mechanism. We found that the reduced activation of some NFκB target genes in IκBα-deficient cells could be ex

SUBMITTER: Ando M 

PROVIDER: S-EPMC8636565 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature