The transcription factor Erg controls endothelial cell quiescence by repressing activity of nuclear factor (NF)-κB p65.

ABSTRACT: The interaction of transcription factors with specific DNA sequences is critical for activation of gene expression programs. In endothelial cells (EC), the transcription factor NF-κB is important in the switch from quiescence to activation, and is tightly controlled to avoid excessive inflammation and organ damage. Here we describe a novel mechanism that controls the activation of NF-κB in EC. The transcription factor Erg, the most highly expressed ETS member in resting EC, controls quiescence by repressing proinflammatory gene expression. Focusing on intercellular adhesion molecule 1(ICAM)-1 as a model, we identify two ETS binding sites (EBS -118 and -181) within the ICAM-1 promoter required for Erg-mediated repression. We show that Erg binds to both EBS -118 and EBS -181, the latter loca

SUBMITTER: Dryden NH 

PROVIDER: S-EPMC3320982 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature