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NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death.
- Source :
-
Journal of cell science [J Cell Sci] 2007 Jun 01; Vol. 120 (Pt 11), pp. 1852-8. Date of Electronic Publication: 2007 May 08. - Publication Year :
- 2007
-
Abstract
- 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.
- Subjects :
- Animals
Antigens, Neoplasm chemistry
Apoptosis Regulatory Proteins chemistry
Cell Death
Cell Nucleus metabolism
HeLa Cells
Humans
Mice
NIH 3T3 Cells
Neoplasm Proteins chemistry
Protein Binding
Protein Transport
Repressor Proteins chemistry
Transcription Factors chemistry
Antigens, Neoplasm metabolism
Apoptosis Regulatory Proteins metabolism
Neoplasm Proteins metabolism
Protein Processing, Post-Translational
Repressor Proteins metabolism
Transcription Factors metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0021-9533
- Volume :
- 120
- Issue :
- Pt 11
- Database :
- MEDLINE
- Journal :
- Journal of cell science
- Publication Type :
- Academic Journal
- Accession number :
- 17488777
- Full Text :
- https://doi.org/10.1242/jcs.03454