NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death
Author(s) -
Maria Grazia Di Certo,
Nicoletta Corbi,
Tiziana Bruno,
Simona Iezzi,
Francesca De Nicola,
Agata Desantis,
Maria Teresa Ciotti,
Elisabetta Mattei,
Aristide Floridi,
Maurizio Fanciulli,
Claudio Passananti
Publication year - 2007
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.03454
Subject(s) - microbiology and biotechnology , biology , programmed cell death , apoptosis , transcription factor , neuroscience , neurotrophin , cancer research , cell , receptor , gene , genetics
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.
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