Post-ischemic brain damage: NF-κB dimer heterogeneity as a molecular determinant of neuron vulnerability

Marina Pizzi, Ilenia Sarnico, Annamaria Lanzillotta, Leontino Battistin, PierFranco Spano

Research output: Contribution to journalArticlepeer-review


Nuclear factor-kappaB (NF-κB) has been proposed to serve a dual function as a regulator of neuron survival in pathological conditions associated with neurodegeneration. NF-κB is a transcription family of factors comprising five different proteins, namely p50, RelA/p65, c-Rel, RelB and p52, which can combine differently to form active dimers in response to external stimuli. Recent research shows that diverse NF-κB dimers lead to cell death or cell survival in neurons exposed to ischemic injury. While the p50/p65 dimer participates in the pathogenesis of post-ischemic injury by inducing pro-apoptotic gene expression, c-Rel-containing dimers increase neuron resistance to ischemia by inducing anti-apoptotic gene transcription. We present, in this report, the latest findings and consider the therapeutic potential of targeting different NF-κB dimers to limit ischemia-associated neurodegeneration.

Original languageEnglish
Pages (from-to)27-35
Number of pages9
JournalFEBS Journal
Issue number1
Publication statusPublished - Jan 2009


  • Bcl-xL
  • Bim
  • Brain ischemia
  • c-Rel
  • Cell death
  • Leptin
  • Neurodegeneration
  • Nuclear factor-kappaB
  • Oxygen glucose deprivation
  • p65

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology


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