Intestinal deletion of Pofut1 in the mouse inactivates notch signaling and causes enterocolitis.

ABSTRACT:

Background & aims

Notch downstream targets are fundamental to intestinal cell lineage commitment and are suggested as therapeutic targets for colon cancer cells. However, the role of endogenous Notch signaling through receptor-ligand interaction, and effects of its longer term down-regulation on intestinal homeostasis, are unclear.

Methods

To address these issues, the gene encoding protein O-fucosyltransferase 1, an enzyme required for Notch ligand binding and thus activation of all Notch receptors, was deleted in the mouse intestinal and colonic epithelium, through Villin-Cre-mediated recombination.

Results

Pofut1 deletion inactivated Notch signaling, giving rise to smaller but viable mice. These mice exhibited a large increase in all intestinal secretory cell lineag

SUBMITTER: Guilmeau S 

PROVIDER: S-EPMC3207497 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature