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1 deficiency of mitochondrial medium- or very long-chain acyl-CoA dehydrogenase.
2 -CoA dehydrogenase family except for IVD and long-chain acyl-CoA dehydrogenase.
3 mice decreased acetylation of mitochondrial long-chain acyl-CoA dehydrogenase, a known SIRT3 deacety
4 iltration analysis indicated that, like very-long-chain acyl-CoA dehydrogenase, ACAD-9 is a dimer, in
5 of 3-mercaptopropionic acid, an inhibitor of long chain acyl-CoA dehydrogenase, and partially inhibit
6 olic enzymes, such as acetyl-CoA synthetase, long-chain acyl-CoA dehydrogenase, and 3-hydroxy-3-methy
7 specificity, it appears that ACAD9 and very-long-chain acyl-CoA dehydrogenase are unable to compensa
9 ce carrying the targeted inactivation of the long chain acyl CoA dehydrogenase gene (Acadl) are also
10 bution and gene regulation of ACAD9 and very-long-chain acyl-CoA dehydrogenase identify the presence
11 e, very long chain acyl-CoA synthetase, very long chain acyl-CoA dehydrogenase) in livers of the etha
12 CoA dehydrogenase (IVD), and Glu261 in human long chain acyl-CoA dehydrogenase (LCAD), has been sugge
15 ) deficiency, none have been documented with long-chain acyl-CoA dehydrogenase (LCAD) deficiency.
18 stance, we studied mice with a deficiency of long-chain acyl-CoA dehydrogenase (LCAD), a key enzyme i
20 base-arrangement has been altered to that of long chain acyl-CoA dehydrogenase (LCADH), Glu376Gly/Thr
22 chain acyl-CoA dehydrogenase (LCAD) and very long-chain acyl-CoA dehydrogenase revealed that 5-trans-
23 er between the two human genes encoding very long chain acyl-CoA dehydrogenase (VLCAD) and postsynapt
26 h many patients have been found to have very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency, no
29 tion that is highly homologous to human very-long-chain acyl-CoA dehydrogenase was identified by larg
30 urated acyl-CoAs are poor substrates of very long-chain acyl-CoA dehydrogenase when compared with myr
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