Altered mitochondrial acetylation profiles in a kainic acid model of temporal lobe epilepsy.
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ABSTRACT:
SUBMITTER: Gano LB
PROVIDER: S-EPMC6082368 | biostudies-literature | 2018 Aug
REPOSITORIES: biostudies-literature
Publications
Altered mitochondrial acetylation profiles in a kainic acid model of temporal lobe epilepsy.
Gano Lindsey B LB Liang Li-Ping LP Ryan Kristen K Michel Cole R CR Gomez Joe J Vassilopoulos Athanassios A Reisdorph Nichole N Fritz Kristofer S KS Patel Manisha M
Free radical biology & medicine 20180517
Impaired bioenergetics and oxidative damage in the mitochondria are implicated in the etiology of temporal lobe epilepsy, and hyperacetylation of mitochondrial proteins has recently emerged as a critical negative regulator of mitochondrial functions. However, the roles of mitochondrial acetylation and activity of the primary mitochondrial deacetylase, SIRT3, have not been explored in acquired epilepsy. We investigated changes in mitochondrial acetylation and SIRT3 activity in the development of ...[more]
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