[HTML][HTML] Increased activation of hereditary pancreatitis-associated human cationic trypsinogen mutants in presence of chymotrypsin C
A Szabó, M Sahin-Tóth - Journal of Biological Chemistry, 2012 - ASBMB
Mutations in human cationic trypsinogen (PRSS1) cause autosomal dominant hereditary
pancreatitis. Increased intrapancreatic autoactivation of trypsinogen mutants has been
hypothesized to initiate the disease. Autoactivation of cationic trypsinogen is proteolytically
regulated by chymotrypsin C (CTRC), which mitigates the development of trypsin activity by
promoting degradation of both trypsinogen and trypsin. Paradoxically, CTRC also increases
the rate of autoactivation by processing the trypsinogen activation peptide to a shorter form …
pancreatitis. Increased intrapancreatic autoactivation of trypsinogen mutants has been
hypothesized to initiate the disease. Autoactivation of cationic trypsinogen is proteolytically
regulated by chymotrypsin C (CTRC), which mitigates the development of trypsin activity by
promoting degradation of both trypsinogen and trypsin. Paradoxically, CTRC also increases
the rate of autoactivation by processing the trypsinogen activation peptide to a shorter form …