Colitis-induced upregulation of tumor necrosis factor receptor-2 (TNFR2) terminates epithelial regenerative signaling to restore homeostasis.

Colonic epithelial repair is a key determinant of health. Repair involves changes in epithelial differentiation, an extensive proliferative response, and upregulation of regeneration-associated "fetal-like" transcripts, including (Sca-1), that represent Yap1 and interferon targets. However, little is known about how this regenerative program terminates and how homeostasis is restored during injury and inflammation.

Persistence of Lgr5+ colonic epithelial stem cells in mouse models of inflammatory bowel disease.

Intestinal mucosal healing is the primary therapeutic goal of medical treatments for inflammatory bowel disease (IBD). Epithelial stem cells are key players in the healing process. Lgr5+ stem cells maintain cellular turnover during homeostasis in the colonic crypt.

Overexpressed Gliotactin activates BMP signaling through interfering with the Tkv-Dad association.

Epithelial junctions ensure cell-cell adhesion and establish permeability barriers between cells. At the corners of epithelia, the tricellular junction (TCJ) is formed by three adjacent epithelial cells and generates a functional barrier. In , a key TCJ protein is Gliotactin (Gli) where loss of Gli disrupts barrier formation and function.

Scribble and Discs Large mediate tricellular junction formation.

Junctional complexes that mediate cell adhesion are key to epithelial integrity, cell division and permeability barrier formation. In , the scaffolding proteins Scribble (Scrib) and Discs Large (Dlg) are key regulators of epithelial polarity, proliferation, assembly of junctions and protein trafficking. We found that Scrib and Dlg are necessary for the formation of the tricellular junction (TCJ), a unique junction that forms in epithelia at the point of convergence of three neighboring cells.

The Drosophila tricellular junction protein Gliotactin regulates its own mRNA levels through BMP-mediated induction of miR-184.

Epithelial bicellular and tricellular junctions are essential for establishing and maintaining permeability barriers. Tricellular junctions are formed by the convergence of three bicellular junctions at the corners of neighbouring epithelia. Gliotactin, a member of the Neuroligin family, is located at theDrosophilatricellular junction, and is crucial for the formation of tricellular and septate junctions, as well as permeability barrier function.

Inhibitory Effect of Codeine on Sucrase Activity.

Codeine is a common drug widely used in some countries as a pain reliever. The effect of codeine on yeast sucrase activity was studied in this report. Non-competitive inhibition was observed using double reciprocal plot.