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TLDc proteins: new players in the oxidative stress response and neurological disease

Finelli, Matt�a J.; Oliver, Peter L.

TLDc proteins: new players in the oxidative stress response and neurological disease Thumbnail


Authors

Matt�a J. Finelli

Peter L. Oliver



Contributors

Matt�a J. Finelli
Researcher

Peter L. Oliver
Project Leader

Abstract

Oxidative stress (OS) arises from an imbalance in the cellular redox state, which can lead to intracellular damage and ultimately cell death. OS occurs as a result of normal ageing, but it is also implicated as a common etiological factor in neurological disease; thus identifying novel proteins that modulate the OS response may facilitate the design of new therapeutic approaches applicable to many disorders. In this review, we describe the recent progress that has been made using a range of genetic approaches to understand a family of proteins that share the highly conserved TLDc domain. We highlight their shared ability to prevent OS-related cell death and their unique functional characteristics, as well as discussing their potential application as new neuroprotective factors. Furthermore, with an increasing number of pathogenic mutations leading to epilepsy and hearing loss being discovered in the TLDc protein TBC1D24, understanding the function of this family has important implications for a range of inherited neurological diseases.

Citation

Finelli, M. J., & Oliver, P. L. (2017). TLDc proteins: new players in the oxidative stress response and neurological disease. Mammalian Genome, 28(9-10), 395-406. https://doi.org/10.1007/s00335-017-9706-7

Journal Article Type Article
Acceptance Date Jul 3, 2017
Online Publication Date Jul 13, 2017
Publication Date 2017-10
Deposit Date Jul 25, 2021
Publicly Available Date Jul 27, 2021
Journal Mammalian Genome
Print ISSN 0938-8990
Electronic ISSN 1432-1777
Publisher Springer Verlag
Peer Reviewed Peer Reviewed
Volume 28
Issue 9-10
Pages 395-406
DOI https://doi.org/10.1007/s00335-017-9706-7
Keywords Genetics
Public URL https://nottingham-repository.worktribe.com/output/5832605
Publisher URL https://link.springer.com/article/10.1007%2Fs00335-017-9706-7

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