Meister, T <br/><br/>
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] 

 -  Journal of physiology and pharmacology : an official journal of the Polish Physiological Society  Oct 2010 
 - 565-75 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>1899-1505 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Amylases--blood<br/>Animals<br/>Cathepsin B--metabolism<br/>Ceruletide--metabolism<br/>Disease Progression<br/>Insulin-Like Growth Factor II--metabolism<br/>Lysosomes--metabolism<br/>Mice<br/>Mice, Knockout<br/>Pancreas--metabolism<br/>Pancreatitis--chemically induced<br/>Peptide Hydrolases--metabolism<br/>Receptor, IGF Type 2--metabolism<br/>Secretory Vesicles--metabolism<br/>Trypsin--metabolism<br/>Trypsinogen--metabolism<br/>Vacuoles--metabolism