Nuclear factor-κB in pancreatitis: Jack-of-all-trades, but which one is more important?

Gastroenterology. 2013 Jan;144(1):26-9. doi: 10.1053/j.gastro.2012.11.016. Epub 2012 Nov 16.

Abstract

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.

Publication types

  • Editorial
  • Comment

MeSH terms

  • Acinar Cells / metabolism*
  • Animals
  • I-kappa B Kinase / metabolism*
  • I-kappa B Proteins / genetics*
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism*
  • Pancreatitis / genetics*
  • Pancreatitis / metabolism*
  • Pancreatitis / pathology*
  • Serpins / genetics*
  • Transcription Factor RelA / genetics*
  • Transcription Factor RelA / metabolism*
  • alpha 1-Antichymotrypsin / genetics*

Substances

  • I-kappa B Proteins
  • NF-kappa B
  • Nfkbia protein, mouse
  • Rela protein, mouse
  • Serpina3k protein, mouse
  • Serpins
  • Transcription Factor RelA
  • alpha 1-Antichymotrypsin
  • NF-KappaB Inhibitor alpha
  • I-kappa B Kinase
  • Ikbkb protein, mouse