FIGURE 7.

Current working model for arpin functions and Arp2/3 inhibition in intestinal epithelial cells. Under basal conditions, arpin localizes at cell junctions to maintain Arp2/3 activity low and prevent junction protein internalization. During inflammation, arpin is downregulated, allowing for Arp2/3 activation, junction protein internalization, stress fiber formation, and thus barrier dysfunction. On the other hand, CK666 strengthens the epithelial barrier and protects from inflammation-induced barrier dysfunction by preventing Arp2/3-dependent junction protein internalization. Question marks indicate that the exact mechanism of internalization is still unclear.