Reduced expression of mutant trypsinogen delays disease onset in a spontaneous mouse model of pancreatitis

Objectives Premature intrapancreatic activation of trypsinogen has been implicated in pancreatic injury and chronic pancreatitis. Biochemical analyses of hereditary pancreatitis associated mutations in the trypsinogen activation peptide revealed that the common phenotypic change is a markedly increased propensity for autoactivation. We recently generated two different knock-in mice (T7D23A Cre and T7D23A Neo), carrying the same heterozygous D23A mutation in the activation peptide of mouse T7 trypsinogen.

Source: Pancreatology - June 1, 2018 Category: Gastroenterology Authors: Andrea Geisz, Anna Orekhova, Miklos Sahin-Toth Tags: Session 7. Progress in experimental pancreatitis - free papers Source Type: research