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1 e cationic trypsinogen gene in patients with hereditary pancreatitis.
2 trypsinogen activation are not the cause of hereditary pancreatitis.
3 ce of patients with sporadic pancreatitis or hereditary pancreatitis.
4 e cationic trypsinogen (Tg) of patients with hereditary pancreatitis.
5 lack of association of PRSS2 mutations with hereditary pancreatitis.
6 s and one was proven by DNA analysis to have hereditary pancreatitis.
7 trypsinogen (Tg-1) has been associated with hereditary pancreatitis.
8 omechanism of the Asn-21 --> Ile mutation in hereditary pancreatitis.
9 apancreatic trypsinogen activation and cause hereditary pancreatitis.
10 trypsinogen (PRSS1) cause autosomal dominant hereditary pancreatitis.
11 might be of pathophysiological relevance in hereditary pancreatitis, a human inborn disorder associa
12 SS1 are frequently detected in patients with hereditary pancreatitis, a rare genetic disease of the p
14 f PRSS1 mutations as pathogenic mediators of hereditary pancreatitis and indicate that persistent pan
16 ibition can contribute to the development of hereditary pancreatitis associated with the Arg(117) -->
17 r hand, the results clearly demonstrate that hereditary pancreatitis-associated mutations do not lead
18 recombinant human cationic trypsinogen with hereditary pancreatitis-associated mutations N29I, N29T,
19 ine cationic trypsinogen or PRSS1 mutations (hereditary pancreatitis), BRCA2 mutations (usually in as
23 alization of the gene for autosomal dominant hereditary pancreatitis (HP) to a small region of the lo
26 trypsinogen mutants associated with classic hereditary pancreatitis (N29I, N29T, V39A, R122C, and R1
28 ivation, mutations in PRSS2 are not found in hereditary pancreatitis suggesting that activation of th
29 he disease-causing mutation in kindreds with hereditary pancreatitis that lack the previously identif
30 ations and the initiation and progression of hereditary pancreatitis, we have sought to generate a tr
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