1 the notion that pancreatitis is a disease of autodigestion.

2 indirectly as a coprotease to stimulate LexA autodigestion.

3  of acinar cells, become activated and cause autodigestion.

4 disorganization leading to pancreatitis-like autodigestion.

5  to inhibit acinar-cell secretion leading to autodigestion and repress proliferation causing repair d

6  enzyme from products, elimination of enzyme autodigestion, and increased enzyme stability and activi

7 inR protein undergoes general base-catalyzed autodigestion as well as RecA-mediated cleavage at the p

8 a new class of lexA mutants, lexA (Adg-; for autodigestion-defective) mutants, termed Adg- for brevit

9 provision of energy and nutrients by cytosol autodigestion during starvation, and removal of defunct

10 e achieved after including reaction terms of autodigestion, inactivation, cannibalism, and distractio

11 lytic triad of protease IV, demonstrate that autodigestion is essential for the processing of proteas

12        Retinoic acid, an agent which induces autodigestion of cartilage in vitro, stimulated only the

13          Since the RecA protein mediates the autodigestion of UnmD to UmuD', this finding supports th

14  loci, and similarly undergoes a facilitated autodigestion on interaction with the RecA/single-strand

15                            Protease-mediated autodigestion provides a mechanistic link between the pa

16 ted; loss of this cleavage site would permit autodigestion resulting in pancreatitis.

17 ts role in mutagenesis by a RecA-facilitated autodigestion that removes the N-terminal 24 amino acids