Activation of c-Jun N-terminal kinase antagonizes an anti-apoptotic action of Bcl-2

Jihyun Park, Injung Kim, Young Jun Oh, Ko Woon Lee, Pyung Lim Han, Eui Ju Choi

Research output: Contribution to journalArticlepeer-review

121 Citations (Scopus)


Bcl-2 is an intracellular membrane-associated protein that prevents cell death induced by a variety of apoptotic stimuli. A mechanism by which Bcl-2 exerts an anti-cell death effect is, however, not fully understood. In the present study, Bcl-2 suppressed cell death of N18TG neuroglioma cells caused by various apoptotic stresses, including etoposide, staurosporine, anisomycin, and ultraviolet irradiation. Concomitantly, Bcl-2 disrupted a signaling cascade to the c-Jun N-terminal kinase activation induced by the apoptotic stresses. Bcl-2 also prevented the etoposide-induced stimulation of MEKK1. Furthermore, overexpression of c-Jun N-terminal kinase antagonized the death-protective function of Bcl-2. These data suggest that suppression of the c-Jun N-terminal kinase signaling pathway may be critical for Bcl-2 action.

Original languageEnglish
Pages (from-to)16725-16728
Number of pages4
JournalJournal of Biological Chemistry
Issue number27
Publication statusPublished - 1997 Jul 4

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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