Selective suppression of a subset of Bax-dependent neuronal death by a cell permeable peptide inhibitor of Bax, BIP

Soo Young Kim, Hyun Kim, Woong Sun

Research output: Contribution to journalArticle


Bax, a pro-apoptotic member of Bcl-2 family proteins, plays a central role in the mitochondria-dependent apoptosis. Apoptotic signals induce the translocation of Bax from cytosol into the mitochondria, which triggers the release of apoptogenic molecules such as cytochrome C and apoptosis-inducing factor, AIF. Bax-inhibiting peptide (BIP) is a cell permeable peptide comprised of five amino acids designed from the Bax-interaction domain of Ku70. Because BIP inhibits Bax translocation and Bax-mediated release of cytochrome C, BIP suppresses Bax-dependent apoptosis. In this study, we observed that BIP inhibited staurosporine-induced neuronal death in cultured cerebral cortex and cerebellar granule cells, but BIP failed to rescue granule cells from trophic signal deprivation-induced neuronal death, although both staurosporine-induced and trophic signal deprivation-induced neuronal death are dependent on Bax. These findings suggest that the mechanisms of the Bax activation may differ depending on the type of cell death induction, and thus BIP exhibits selective suppression of a subtype of Bax-dependent neuronal death.

Original languageEnglish
Pages (from-to)211-217
Number of pages7
JournalAnimal Cells and Systems
Issue number4
Publication statusPublished - 2008 Dec 1



  • Bax
  • Bax-inhibiting peptide (BIP)
  • Cerebellar granule neuron
  • Neuronal apoptosis
  • Potassiumserum deprivation
  • Staurosporine

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Animal Science and Zoology

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