Matt�a J. Finelli
TLDc proteins: new players in the oxidative stress response and neurological disease
Finelli, Matt�a J.; Oliver, Peter L.
Authors
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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