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Title: | RTP801/REDD1: a stress coping regulator that turns into a troublemaker in neurodegenerative disorders |
Author: | Canal de la Iglesia, Mercè Romaní Aumedes, Joan Martín Flores, Núria Pérez Fernández, Víctor Malagelada Grau, Cristina |
Keywords: | Malalties neurodegeneratives Degeneració (Patologia) Malaltia de Parkinson Cicle cel·lular Neurodegenerative Diseases Degeneration (Pathology) Parkinson's disease Cell cycle |
Issue Date: | 2-Oct-2014 |
Publisher: | Frontiers Media |
Abstract: | Mechanistic target of Rapamycin (mTOR) pathway regulates essential processes directed to preserve cellular homeostasis, such as cell growth, proliferation, survival, protein synthesis and autophagy. Importantly, mTOR pathway deregulation has been related to many diseases. Indeed, it has become a hallmark in neurodegenerative disorders, since a fine-tuned regulation of mTOR activities is crucial for neuron function and survival. RTP801/REDD1/Dig2 has become one of the most puzzling regulators of mTOR. Although the mechanism is not completely understood, RTP801 inactivates mTOR and Akt via the tuberous sclerosis complex (TSC1/TSC2) in many cellular contexts. Intriguingly, RTP801 protects dividing cells from hypoxia or H2O2-induced apoptosis, while it sensitizes differentiated cells to stress. Based on experimental models of Parkinson's disease (PD), it has been proposed that at early stages of the disease, stress-induced RTP801 upregulation contributes to mTOR repression, in an attempt to maintain cell function and viability. However, if RTP801 elevation is sustained, it leads to neuron cell death by a sequential inhibition of mTOR and Akt. Here, we will review RTP801 deregulation of mTOR in a context of PD and other neurodegenerative disorders. |
Note: | Reproducció del document publicat a: https://doi.org/10.3389/fncel.2014.00313 |
It is part of: | Frontiers in Cellular Neuroscience, 2014, vol. 8, num. 313 |
URI: | http://hdl.handle.net/2445/120879 |
Related resource: | https://doi.org/10.3389/fncel.2014.00313 |
ISSN: | 1662-5102 |
Appears in Collections: | Articles publicats en revistes (Biomedicina) Publicacions de projectes de recerca finançats per la UE |
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