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1 This was attributed to inhibition of the alpha-ketoglutarate dehydrogenase complex.
2 notransferase, alanine aminotransferase, and alpha-ketoglutarate dehydrogenase complex.
3 respiration by reversible inhibition of the alpha-ketoglutarate dehydrogenase complex.
4 ced CoA to the reduction of NAD(+) using the alpha-ketoglutarate dehydrogenase complex.
5 ymes of central metabolism, the pyruvate and alpha-ketoglutarate dehydrogenase complexes.
6 d restored full activity to the pyruvate and alpha-ketoglutarate dehydrogenase complexes.
7 component of the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes.
9 d its target DLST-the E2 subcomponent of the alpha-ketoglutarate dehydrogenase complex, a rate-contro
10 hydrolipoamide dehydrogenase subunits of the alpha-ketoglutarate dehydrogenase complex (alphaKGDH), a
12 Lipoamide dehydrogenase, a component of the alpha-ketoglutarate dehydrogenase complex and two other
13 sferase to supply alpha-ketoglutarate to the alpha-ketoglutarate dehydrogenase complex and would, in
14 oteins, we demonstrate that the pyruvate and alpha-ketoglutarate dehydrogenase complexes directly cat
15 oxymethyl transferase, and components of the alpha-ketoglutarate dehydrogenase complex in conjunction
16 drogenase complex (OGHDC) (also known as the alpha-ketoglutarate dehydrogenase complex) is a rate-lim
18 m for 24 h, resulted in a pronounced loss of alpha-ketoglutarate dehydrogenase complex (KGDHC) activi
21 Brain metabolism and the activity of the alpha-ketoglutarate dehydrogenase complex (KGDHC), a mit
24 activity of a key mitochondrial enzyme, the alpha-ketoglutarate dehydrogenase complex (KGDHC), decli
27 osttranslational lipoylation of pyruvate and alpha-ketoglutarate dehydrogenase complexes, resulting i
29 ion of ThPP levels causes dysfunction of the alpha-ketoglutarate dehydrogenase complex, which explain
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