1. Nuclear Factor-κB in Pancreatitis: Jack-of-All-Trades, But Which One Is More Important? 
Ilya Gukovsky, Anna Gukovskaya 
Gastroenterology 
Volume 144, Issue 1, Pages (January 2013)
DOI: /j.gastro
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2. Figure 1
Pathways through which acinar cell NF-κB activation regulates inflammation in pancreatitis. A major proinflammatory mechanism is the induction of cytokines and other mediators, as emphasized by Huang et al.21 In contrast, Neuhöfer et al20 emphasize the protective effect of NF-κB against acinar cell necroptosis, limiting pancreatic inflammation. The mechanisms underlying this prosurvival effect of NF-κB are not clear but may involve PAP1,19 Spi2A,20 Bcl-xL,35 and other proteins. One mechanism whereby acinar cell necrosis may promote pancreatic inflammation is through activation of the inflammasome.22,23 The protective effect of NF-κB activation could also be through limiting IL-1β processing and secretion.24
Gastroenterology  , 26-29DOI: ( /j.gastro )
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