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Methods:, Recombinant wild-type and mutant human cationic trypsinogens were expressed in Escherichia coli and purified to homogeneity, and trypsin autolysis and trypsinogen autoactivation were characterized. Results: Both mutations significantly enhanced the autoactivation of human cationic trypsinogen. In addition, the Arg117 --> His mutation inhibited autocatalytic inactivation of trypsin, while the Asn21 --> IIe mutation had no such effect. Conclusions: The findings support the notion that enhanced trypsinogen activation in the pancreas is the common: initiating step in hereditary pancreatitis, whereas trypsin stabilization plays a role in cases associated with the Arg117 --> His mutation. Copyright (C) 2001 S. 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