Missorting of cathepsin B into the secretory compartment of CI-MPR/IGFII-deficient mice does not induce spontaneous trypsinogen activation but leads to enhanced trypsin activity during experimental pancreatitis--without affecting disease severity. [electronic resource]
Producer: 20110621Description: 565-75 p. digitalISSN:- 1899-1505
- Amylases -- blood
- Animals
- Cathepsin B -- metabolism
- Ceruletide -- metabolism
- Disease Progression
- Insulin-Like Growth Factor II -- metabolism
- Lysosomes -- metabolism
- Mice
- Mice, Knockout
- Pancreas -- metabolism
- Pancreatitis -- chemically induced
- Peptide Hydrolases -- metabolism
- Receptor, IGF Type 2 -- metabolism
- Secretory Vesicles -- metabolism
- Trypsin -- metabolism
- Trypsinogen -- metabolism
- Vacuoles -- metabolism
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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