Induction of apoptosis by the transcription factor c‐Jun

Induction of apoptosis by the transcription factor c‐Jun 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The EMBO Journal Wiley

Induction of apoptosis by the transcription factor c‐Jun

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Publisher
Wiley
Copyright
Copyright © 2013 Wiley Periodicals, Inc
ISSN
0261-4189
eISSN
1460-2075
D.O.I.
10.1093/emboj/16.7.1695
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

The EMBO JournalWiley

Published: Apr 1, 1997

References

  • Apoptosis and programmed cell death in immunity
    Cohen, Cohen; Duke, Duke; Fadok, Fadok; Sellins, Sellins
  • Expression of the papillomavirus E2 protein in HeLa cells leads to apoptosis
    Desaintes, Desaintes; Demeret, Demeret; Goyat, Goyat; Yaniv, Yaniv; Thierry, Thierry
  • Mechanism and function of cell death
    Ellis, Ellis; Yuan, Yuan; Horvitz, Horvitz
  • Altered gene expression in neurons during programmed cell death: identification of c‐ jun as necessary for neuronal apoptosis
    Estus, Estus; Zaks, Zaks; Freeman, Freeman; Gruda, Gruda; Bravo, Bravo; Johnson, Johnson
  • Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation
    Gavrieli, Gavrieli; Sherman, Sherman; Ben‐Sasson, Ben‐Sasson
  • Inhibitors of protein synthesis and RNA synthesis prevent neuronal death caused by nerve growth factor deprivation
    Martin, Martin; Schmidt, Schmidt; DiStefano, DiStefano; Lowry, Lowry; Carter, Carter; Johnson, Johnson
  • Tissue transglutaminase is specifically expressed in neonatal rat liver undergoing apoptosis upon epidermal growth factor stimulation
    Piacentini, Piacentini; Autuori, Autuori; Dini, Dini; Farrace, Farrace; Ghibelli, Ghibelli; Piredda, Piredda; Fesus, Fesus
  • Bcl‐2 and the regulation of programmed cell death
    Reed, Reed
  • Cell death: the significance of apoptosis
    Wyllie, Wyllie; Kerr, Kerr; Currie, Currie

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