FIG. 2.

Nuclear factor-kappa B (NF-κB) proinflammatory signaling pathway and regulation by miR-181. NF-κB, a dimer often consisting of p50/p65 subunits, is normally resident in the cytosol and is maintained in an inactive form by its inhibitor IκB. Stroke stimulates mitochondria to release ROS that activate the IκB kinase (IKK) complex. The activated IKK complex phosphorylates IκB and initiates its ubiquitination and degradation, freeing NF-κB to translocate to the nucleus, and binds the promoters of genes expressing proinflammatory cytokines, IκB, and other targets. miR-181 interacts with this pathway at multiple points. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars