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ABSTRACT: The α-ketoglutarate dehydrogenase complex (KGDHC) is an important mitochondrial constituent, and deficiency of KGDHC is associated with a number of neurological
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Inactivation and Reactivation of the Mitochondrial α-Ketoglutarate
Purification of KGDHC from N2a All procedures were carried out at 4 °C unless otherwise indicated. Mitochondria were isolated from N2a cells by modification of a previous method (34).
The α-Ketoglutarate Dehydrogenase Complex as a Hub of
The consequences of KGHDC inhibition on flux were determined. Flux measures with [1- 13 C]-glucose and [U- 13 C] glutamate indicate that inhibition of KGDHC with specific KGDHC
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Alpha-ketoglutarate dehydrogenase complex-dependent succinylation
Clearly, KGHDC can readily donate succinyl groups to albumin. SC increased succinylation in the presence of KGDHC, but not near as much KG and the effects were not additive.
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The α-Ketoglutarate Dehydrogenase Complex as a Hub of Plasticity in
The consequences of KGHDC inhibition on flux were determined. Flux measures with [1- 13 C]-glucose and [U- 13 C] glutamate indicate that inhibition of KGDHC with specific KGDHC
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Reductions in the mitochondrial enzyme α-ketoglutarate
The results suggest that internal antioxidants linked to KGDHC such as thioredoxin/peroxiredoxin are depleted by the reduction in KGHDC. The beneficial effects of the over-expression of OGDH are
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Mitochondrially Mediated Post-Translational Modification of
Reducing the enzyme KGHDC has widespread consequences on cell and brain function. We postulate this is because it is responsible for post-translation modification of thousands of proteins by