A preclinical model of chronic pancreatitis driven by trypsinogen autoactivation
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry
Link
http://www.nature.com/articles/s41467-018-07347-y.pdf
Reference17 articles.
1. Yadav, D. & Lowenfels, A. B. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology 144, 1252–1261 (2013).
2. Hegyi, E. & Sahin-Tóth, M. Genetic risk in chronic pancreatitis: The trypsin-dependent pathway. Dig. Dis. Sci. 62, 1692–1701 (2017).
3. Szabó, A. & Sahin-Tóth, M. Increased activation of hereditary pancreatitis-associated human cationic trypsinogen mutants in presence of chymotrypsin C. J. Biol. Chem. 287, 20701–20710 (2012).
4. Geisz, A., Hegyi, P. & Sahin-Tóth, M. Robust autoactivation, chymotrypsin C independence and diminished secretion define a subset of hereditary pancreatitis-associated cationic trypsinogen mutants. Febs. J. 280, 2888–22899 (2013).
5. Athwal, T. et al. Expression of human cationic trypsinogen (PRSS1) in murine acinar cells promotes pancreatitis and apoptotic cell death. Cell Death Dis. 5, e1165 (2014).
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