Fig. 8: Schematic diagram depicts that TRIM65 inhibiting intestine epithelial cells apoptosis is implicated in II/R injury via ubiquitination and degradation of TOX4.

Under normal physiological conditions, TRIM65 can directly bind to TOX4 and promote K48-linked ubiquitination and degradation of TOX4 in intestine epithelial cells. The CC and SPRY domain of TRIM65 and the N-terminal (residues 1-223) of TOX4 may be the key site of their interactions. In TRIM65-/- mouse, II/R induced TOX4 mediates intestine apoptosis, leading to an increase in BAX and a decrease in Bcl2, ultimately exacerbating intestinal damage.