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Titolo:
Retinoic acid induces proteasome-dependent degradation of retinoic acid receptor alpha (RAR alpha) and oncogenic RAR alpha fusion proteins
Autore:
Zhu, J; Gianni, M; Kopf, E; Honore, N; Chelbi-Alix, M; Koken, M; Quignon, F; Rochette-Egly, C; de The, H;
Indirizzi:
Univ Paris 07, Comite Paris Ligue Natl Contre Canc Convent, Hop St Louis,Lab 11, CNRS,Unite Propre Rech 9051, F-75475 Paris 10, France Univ Paris 07Paris France 10 Propre Rech 9051, F-75475 Paris 10, France Univ Strasbourg 1, CNRS, INSERM, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch, France Univ Strasbourg 1 Illkirch France F-67404 aire, F-67404 Illkirch, France
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 26, volume: 96, anno: 1999,
pagine: 14807 - 14812
SICI:
0027-8424(199912)96:26<14807:RAIPDO>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE PROMYELOCYTIC LEUKEMIA; NUCLEAR-BODIES; HISTONE DEACETYLASE; GROWTH-SUPPRESSOR; NB4 CELLS; PML; ONCOPROTEIN; EXPRESSION; PLZF; DIFFERENTIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: de The, H Univ Paris 07, Hop St Louis, Lab 11, CNRS,Unite Propre Rech 9051, F-75475 Paris 10, France Univ Paris 07 Paris France 10 h 9051, F-75475 Paris 10, France
Citazione:
J. Zhu et al., "Retinoic acid induces proteasome-dependent degradation of retinoic acid receptor alpha (RAR alpha) and oncogenic RAR alpha fusion proteins", P NAS US, 96(26), 1999, pp. 14807-14812

Abstract

Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RAR alpha) catabolism in acute promyelocytic leukemia (APL); we found that, in addition to caspase-mediated PML/RAR alpha cleavage, RA triggers degradation of both PML/RAR alpha and RAR alpha, Similarly, in non-APL cells, RA directly targeted RAR alpha and RAR alpha fusions to the proteasome degradation pathway. Activation of either RAR alpha or RXR alpha by specific agonists induced degradation of both proteins. Conversely, a mutation in RAR alpha that abolishes heterodimer formation and DNA binding, blocked both RAR alpha and RXR alpha degradation. Mutations in the RAR alpha DNA-binding domain or AF-2 transcriptional activation region also impaired RAR alpha catabolism. Hence, our results link transcriptional activation to receptor catabolism and suggest that transcriptional up-regulation of nuclear receptors by their ligands may be a feedback mechanism allowing sustained target-gene activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 00:36:57