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Modulation of proteostasis by transcription factor NRF2 and impact in neurodegenerative diseases

AutorPajares, Marta; Cuadrado, Antonio ; Rojo, Ana I.
Palabras claveNeurodegenerative diseases
Oxidative stress
Autophagy
Ubiquitin
Proteasome
Unfolded protein response
Fecha de publicación2017
EditorElsevier
CitaciónRedox Biology 11: 543-553 (2017)
ResumenNeurodegenerative diseases are linked to the accumulation of specific protein aggregates, suggesting an intimate connection between injured brain and loss of proteostasis. Proteostasis refers to all the processes by which cells control the abundance and folding of the proteome thanks to a wide network that integrates the regulation of signaling pathways, gene expression and protein degradation systems. This review attempts to summarize the most relevant findings about the transcriptional modulation of proteostasis exerted by the transcription factor NRF2 (nuclear factor (erythroid-derived 2)-like 2). NRF2 has been classically considered as the master regulator of the antioxidant cell response, although it is currently emerging as a key component of the transduction machinery to maintain proteostasis. As we will discuss, NRF2 could be envisioned as a hub that compiles emergency signals derived from misfolded protein accumulation in order to build a coordinated and perdurable transcriptional response. This is achieved by functions of NRF2 related to the control of genes involved in the maintenance of the endoplasmic reticulum physiology, the proteasome and autophagy.
Versión del editorhttps://doi.org/10.1016/j.redox.2017.01.006
URIhttp://hdl.handle.net/10261/150802
DOI10.1016/j.redox.2017.01.006
Identificadoresdoi: 10.1016/j.redox.2017.01.006
issn: 2213-2317
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