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First published online 8 May 2007
doi: 10.1242/jcs.03454

Journal of Cell Science 120, 1852-1858 (2007)
Published by The Company of Biologists 2007
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Research Article

NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death

Maria Grazia Di Certo1,2, Nicoletta Corbi3, Tiziana Bruno4, Simona Iezzi1,4, Francesca De Nicola1,4, Agata Desantis1,3, Maria Teresa Ciotti2, Elisabetta Mattei2, Aristide Floridi1,4, Maurizio Fanciulli4,5 and Claudio Passananti3,5,*

1 Department of Experimental Medicine, Via Vetoio, Coppito 2, University of L'Aquila, 67100 L'Aquila, Italy
2 Istituto di Neurobiologia e Medicina Molecolare, CNR, c/o EBRI, Via del Fosso di Fiorano 64, 00143 Rome, Italy
3 Istituto di Biologia e Patologia Molecolari, CNR, c/o Regina Elena Cancer Institute, Via delle Messi d'Oro 156, 00158 Rome, Italy
4 Laboratory "B", Regina Elena Cancer Institute, Via delle Messi d'Oro 156, 00158 Rome, Italy
5 AIRC-Roman Oncogenomic Center (ROC), Via delle Messi d'Oro 156, 00158 Rome, Italy

* Author for correspondence (e-mail: passananti{at}ifo.it)

Accepted 5 April 2007

Neurotrophin receptor-interacting MAGE homolog (NRAGE) has been recently identified as a cell-death inducer, involved in molecular events driving cells through apoptotic networks during neuronal development. Recently, we have focused on the functional role of Che-1, also known as apoptosis-antagonizing transcription factor (AATF), a protein involved in cell cycle control and gene transcription. Increasing evidence suggests that Che-1 is involved in apoptotic signalling in neural tissues. In cortical neurons Che-1 exhibits an anti-apoptotic activity, protecting cells from neuronal damage induced by amyloid beta-peptide.

Here, we report that Che-1 interacts with NRAGE and that an EGFP-NRAGE fusion protein inhibits nuclear localization of Che-1, by sequestering it within the cytoplasmic compartment. Furthermore, NRAGE overexpression downregulates endogenous Che-1 by targeting it for proteasome-dependent degradation. Finally, we propose that Che-1 is a functional antagonist of NRAGE, because its overexpression completely reverts NRAGE-induced cell-death.

Key words: MAGE, NRAGE, Che-1, AATF, Apoptosis, Neural cell-death, Ubiquitin


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