scholarly journals P059. Two new genetic mouse models for ulcerative colitis based on lateral tight junction disruption.

2016 ◽  
Vol 10 (suppl 1) ◽  
pp. S118.1-S118
2017 ◽  
Vol 11 (10) ◽  
pp. 1247-1257 ◽  
Author(s):  
Wolfgang Stremmel ◽  
Simone Staffer ◽  
Mathias Jochen Schneider ◽  
Hongying Gan-Schreier ◽  
Andreas Wannhoff ◽  
...  

2009 ◽  
Vol 390 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Achim Krüger

Abstract Knockout mice are the gold standard to probe for the role of a specific protease within the interacting network of proteases, substrates, and inhibitors. This proteolytic network, or protease web, determines cell signaling and organ homeostasis. Therefore, protease deficiency or inhibition is intrinsically tied to alterations within this network, always leading to new molecular phenotypes, which define susceptibility of an organ to disease. Furthermore, recent hints, mainly from research on matrix metalloproteinases, about the impact of the protease web on inter-organ signaling molecules suggest the existence of a proteolytic internet of communicating local organ- or molecular polymorphism-specific networks, thereby defining homeostasis and disease susceptibility in the whole organism.


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