Impaired regulation of nuclear factor-kappaB results in apoptosis induced by gamma radiation

Radiat Res. 1998 Jun;149(6):596-601.


Recent studies have shown that activation of nuclear factor-kappaB (NF-kappaB) is critical for cell survival. Cells from patients with ataxia telangiectasia (AT) have an impaired NF-kappaB response to ionizing radiation. AT cells also exhibit inappropriate regulation of apoptosis. We report here that expression of a dominant negative form of IkappaB-alpha, an inhibitor of NF-kappaB, protects AT fibroblasts from apoptosis induced by gamma radiation, but it enhances apoptosis in normal fibroblasts. Furthermore, the process leading to apoptosis may involve caspase 3-mediated cleavage of IkappaB-alpha. These data suggest that regulation of NF-kappaB may play an important role in programmed cell death induced by DNA damage in AT cells.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apoptosis / radiation effects*
  • Ataxia Telangiectasia / genetics
  • DNA Damage
  • DNA-Binding Proteins / metabolism
  • Gamma Rays
  • Humans
  • I-kappa B Proteins*
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / physiology*


  • DNA-Binding Proteins
  • I-kappa B Proteins
  • NF-kappa B
  • NFKBIA protein, human
  • NF-KappaB Inhibitor alpha