http://www.cnr.it/ontology/cnr/individuo/prodotto/ID167780
NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death (Articolo in rivista)
- Type
- Label
- NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Di Certo MG; Corbi N; Bruno T; Iezzi S; De Nicola F; Desantis A; Ciotti MT; Mattei E; Floridi A; Fanciulli M; Passananti C. (literal)
- Pagina inizio
- Pagina fine
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- Impact Factor = 6.427 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- a = CNR, Institute of Neurobiology and Molecular Medicine, Rome, Italy;
b = CNR, Institute of Biology and Molecular Pathology, Rome, Italy;
c = Istituto Regina Elena, Rome, Italy;
d = Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy. (literal)
- Titolo
- NRAGE associates with the anti-apoptotic factor Che-1 and regulates its degradation to induce cell death (literal)
- 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. (literal)
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- Autore CNR
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