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Título

Lafora disease fibroblasts exemplify the molecular interdependence between thioredoxin 1 and the proteasome in mammalian cells

AutorGarcía-Giménez, José Luis; Seco-Cervera, Marta; Aguado, Carmen; Dasí, Francisco; Romá-Mateo, Carlos ; Priego, Sonia; Markovic, Jelena; Knecht, Erwin; Sanz, Pascual ; Pallardó, Federico V.
Palabras claveThioredoxin 1
Proteasome
Cell proliferation
Lafora disease
Antioxidant enzymes
Rare diseases
Fecha de publicación9-jul-2013
EditorElsevier
CitaciónFree Radical Biology and Medicine; 65:347-59. (2013)
ResumenThioredoxin 1 (Trx1) is a key regulator of cellular redox balance and participates in cellular signaling events. Recent evidence from yeast indicates that members of the Trx family interact with the 20S proteasome, indicating redox regulation of proteasome activity. However, there is little information about the interrelationship of Trx proteins with the proteasome system in mammalian cells, especially in the nucleus. Here, we have investigated this relationship under various cellular conditions in mammalian cells. We show that Trx1 levels and its subcellular localization (cytosol, endoplasmic reticulum, and nucleus) depend on proteasome activity during the cell cycle in NIH3T3 fibroblasts and under stress conditions, when proteasomes are inhibited. In addition, we also studied in these cells how the main cellular antioxidant systems are stimulated when proteasome activity is inhibited. Finally, we describe a reduction in Trx1 levels in Lafora disease fibroblasts and demonstrate that the nuclear colocalization of Trx1 with 20S proteasomes in laforin-deficient cells is altered compared with control cells. Our results indicate a close relationship between Trx1 and the 20S nuclear proteasome and give a new perspective to the study of diseases or physiopathological conditions in which defects in the proteasome system are associated with oxidative stress.
Descripción13 páginas, 8 figuras (que no aparecen en este documento, se pueden consultar en: http://www.sciencedirect.com/science/article/pii/S0891584913003274#ec0005)
Versión del editorhttp://dx.doi.org/10.1016/j.freeradbiomed.2013.07.001
URIhttp://hdl.handle.net/10261/116950
DOI10.1016/j.freeradbiomed.2013.07.001
ISSN0891-5849
E-ISSN1873-4596
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