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Article: The C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity

TitleThe C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity
Authors
Issue Date2016
PublisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/
Citation
Oxidative Medicine and Cellular Longevity, 2016, v. 2016, p. 4693703:1-16 How to Cite?
AbstractExcessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson’s disease) and contributes to progressive neuronal loss. In this study, we show that cell apoptosis is induced by oxidative stress and that lysosomes play an important role in cell survival under oxidative stress. As a compensatory response to this stress, lysosomal genes were upregulated via induction of transcription factor EB (TFEB). In addition, localization of TFEB to the nucleus was increased by oxidative stress. We also confirmed that TFEB protects cells from oxidative stress both in vitro and in vivo. Finally, we found that C-ETS2 senses oxidative stress, activates TFEB transcription, and mediates the upregulation of lysosomal genes. Our results demonstrate a mechanistic pathway for inducing lysosomal activity during ageing and neurodegeneration.
Persistent Identifierhttp://hdl.handle.net/10722/243567
ISSN
2015 Impact Factor: 4.492
2015 SCImago Journal Rankings: 1.503

 

DC FieldValueLanguage
dc.contributor.authorMa, S-
dc.contributor.authorFang, Z-
dc.contributor.authorLuo, W-
dc.contributor.authorYang, Y-
dc.contributor.authorWang, C-
dc.contributor.authorZhang, Q-
dc.contributor.authorWang, H-
dc.contributor.authorChen, H-
dc.contributor.authorChan, CB-
dc.contributor.authorLiu, Z-
dc.date.accessioned2017-08-25T02:56:34Z-
dc.date.available2017-08-25T02:56:34Z-
dc.date.issued2016-
dc.identifier.citationOxidative Medicine and Cellular Longevity, 2016, v. 2016, p. 4693703:1-16-
dc.identifier.issn1942-0900-
dc.identifier.urihttp://hdl.handle.net/10722/243567-
dc.description.abstractExcessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson’s disease) and contributes to progressive neuronal loss. In this study, we show that cell apoptosis is induced by oxidative stress and that lysosomes play an important role in cell survival under oxidative stress. As a compensatory response to this stress, lysosomal genes were upregulated via induction of transcription factor EB (TFEB). In addition, localization of TFEB to the nucleus was increased by oxidative stress. We also confirmed that TFEB protects cells from oxidative stress both in vitro and in vivo. Finally, we found that C-ETS2 senses oxidative stress, activates TFEB transcription, and mediates the upregulation of lysosomal genes. Our results demonstrate a mechanistic pathway for inducing lysosomal activity during ageing and neurodegeneration.-
dc.languageeng-
dc.publisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/-
dc.relation.ispartofOxidative Medicine and Cellular Longevity-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleThe C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity-
dc.typeArticle-
dc.identifier.emailChan, CB: chancb@hku.hk-
dc.identifier.authorityChan, CB=rp02140-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2016/4693703-
dc.identifier.hkuros274299-
dc.identifier.volume2016-
dc.identifier.spage4693703:1-
dc.identifier.epage16-
dc.publisher.placeUnited States-

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