scholarly journals A20 and ABIN-1 team up against intestinal epithelial cell death

2018 ◽  
Vol 215 (7) ◽  
pp. 1771-1773
Author(s):  
Ken Cadwell

A20 and its binding partner ABIN-1 are genetically linked to inflammatory diseases. In this issue of JEM, Kattah et al. (https://doi.org/10.1084/jem.20180198) demonstrate that simultaneous deletion in a mouse model leads to instantaneous cell death in the intestinal epithelium and mortality.

2014 ◽  
Vol 219 (3) ◽  
pp. S14-S15
Author(s):  
Anne S. Roberts ◽  
Stephanie C. Papillon ◽  
Avafia Y. Roberts ◽  
Mark R. Frey ◽  
Henri R. Ford ◽  
...  

2014 ◽  
Vol 94 (12) ◽  
pp. 1419-1430 ◽  
Author(s):  
Debby Laukens ◽  
Lindsey Devisscher ◽  
Lien Van den Bossche ◽  
Pieter Hindryckx ◽  
Roosmarijn E Vandenbroucke ◽  
...  

2002 ◽  
Vol 169 (11) ◽  
pp. 6187-6192 ◽  
Author(s):  
Naotoshi Kinoshita ◽  
Takachika Hiroi ◽  
Noriyuki Ohta ◽  
Satoshi Fukuyama ◽  
Eun Jeong Park ◽  
...  

2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Minyi Xu ◽  
Jin Tao ◽  
Yidong Yang ◽  
Siwei Tan ◽  
Huiling Liu ◽  
...  

Author(s):  
Iris Stolzer ◽  
Laura Schickedanz ◽  
Mircea T. Chiriac ◽  
Rocío López-Posadas ◽  
Guntram A. Grassl ◽  
...  

AbstractIntestinal homeostasis and the maintenance of the intestinal epithelial barrier are essential components of host defense during gastrointestinal Salmonella Typhimurium infection. Both require a strict regulation of cell death. However, the molecular pathways regulating epithelial cell death have not been completely understood. Here, we elucidated the contribution of central mechanisms of regulated cell death and upstream regulatory components during gastrointestinal infection. Mice lacking Caspase-8 in the intestinal epithelium are highly sensitive towards bacterial induced enteritis and intestinal inflammation, resulting in an enhanced lethality of these mice. This phenotype was associated with an increased STAT1 activation during Salmonella infection. Cell death, barrier breakdown and systemic infection were abrogated by an additional deletion of STAT1 in Casp8ΔIEC mice. In the absence of epithelial STAT1, loss of epithelial cells was abolished which was accompanied by a reduced Caspase-8 activation. Mechanistically, we demonstrate that epithelial STAT1 acts upstream of Caspase-8-dependent as well as -independent cell death and thus might play a major role at the crossroad of several central cell death pathways in the intestinal epithelium. In summary, we uncovered that transcriptional control of STAT1 is an essential host response mechanism that is required for the maintenance of intestinal barrier function and host survival.


2016 ◽  
Vol 150 (4) ◽  
pp. S59
Author(s):  
Ling Shao ◽  
Michael G. Kattah ◽  
Michael Whang ◽  
Bao Duong ◽  
Michio Onizawa ◽  
...  

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