Nuclear Factor-κB in Pancreatitis: Jack-of-All-Trades, But Which One Is More Important?

See “Deletion of IκBα activates RelA to reduce acute pancreatitis in mice through up-regulation of Spi2A,” by Neuhöfer P, Liang S, Einwächter H, et al, on page 192; and “Activation of nuclear factor-κB in acinar cells increases the severity of pancreatitis in mice,” by Huang H, Liu Y, Daniluk J, et...

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Veröffentlicht in:	Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2013-01, Vol.144 (1), p.26-29
Hauptverfasser:	Gukovsky, Ilya, Gukovskaya, Anna
Format:	Artikel
Sprache:	eng
Schlagworte:	Acinar Cells - metabolism alpha 1-Antichymotrypsin - genetics Animals Gastroenterology and Hepatology I-kappa B Kinase - metabolism I-kappa B Proteins - genetics NF-kappa B - metabolism NF-KappaB Inhibitor alpha Pancreatitis - genetics Pancreatitis - metabolism Pancreatitis - pathology Serpins - genetics Transcription Factor RelA - genetics Transcription Factor RelA - metabolism
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Beschreibung
Zusammenfassung:	See “Deletion of IκBα activates RelA to reduce acute pancreatitis in mice through up-regulation of Spi2A,” by Neuhöfer P, Liang S, Einwächter H, et al, on page 192; and “Activation of nuclear factor-κB in acinar cells increases the severity of pancreatitis in mice,” by Huang H, Liu Y, Daniluk J, et al, on page 202.
ISSN:	0016-5085 1528-0012
DOI:	10.1053/j.gastro.2012.11.016