c‐Jun, a signal‐transducing transcription factor of the AP‐1 family, normally implicated in cell cycle progression, differentiation and cell transformation, recently has also been linked to apoptosis. To explore further the functional roles of c‐Jun, a conditional allele was generated by fusion of c‐Jun with the hormone‐binding domain of the human estrogen receptor (ER). Here we demonstrate that increased c‐Jun activity is sufficient to trigger apoptotic cell death in NIH 3T3 fibroblasts. c‐Jun‐induced apoptosis is evident at high serum levels, but is enhanced further in factor‐deprived fibroblasts. Furthermore, apoptosis by c‐Jun is not accompanied by an increase in DNA synthesis. Constitutive overexpression of the apoptosis inhibitor protein Bcl‐2 delays the c‐Jun‐mediated cell death. The regions of c‐Jun necessary for apoptosis induction include the amino‐terminal transactivation and the carboxy‐terminal leucine zipper domain, suggesting that c‐Jun may activate cell death by acting as a transcriptional regulator. We further show that α‐fodrin, a substrate of the interleukin 1β‐converting enzyme (ICE) and CED‐3 family of cysteine proteases, becomes proteolytically cleaved in cells undergoing cell death by increased c‐Jun activity. Moreover, cell‐permeable irreversible peptide inhibitors of the ICE/CED‐3 family of cysteine proteases prevented the cell death.
The EMBO Journal – Wiley
Published: Apr 1, 1997
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