Kruppel-like factor 3 (KLF3) suppresses NF-κB-driven inflammation in mice.

ABSTRACT: Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. Less is known about direct transcriptional regulation of these responses, however. Here, using a combination of in vitro approaches and in vivo animal models, we show that endotoxin treat

SUBMITTER: Knights AJ 

PROVIDER: S-EPMC7196664 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature