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1 to aspects of the catalytic mechanism of l-3-hydroxyacyl-CoA dehydrogenase.
2 may have a Glu474Gln mutation in long-chain hydroxyacyl-CoA dehydrogenase.
3 ied as an essential catalytic residue of L-3-hydroxyacyl-CoA dehydrogenase.
4 fer substantially from the classic, type I 3-hydroxyacyl-CoA dehydrogenases.
5 hase, a marker of oxidative metabolism; beta-hydroxyacyl-CoA dehydrogenase, a marker of lipolytic met
6 mumol.min-1.mg protein-1; P < .05) and beta-hydroxyacyl-CoA dehydrogenase activity (normal, 0.27 +/-
7 etabolize fat, as indicated by measures beta-hydroxyacyl-CoA dehydrogenase activity or its ratio to c
13 a 6.1-fold decrease in the kcat/k(m) of L-3-hydroxyacyl-CoA dehydrogenase and a 10-fold increase in
14 ildren had a deficiency only of long-chain 3-hydroxyacyl-CoA dehydrogenase and presented with hypoket
15 long-chain enoyl-CoA hydratase, long-chain 3-hydroxyacyl-CoA dehydrogenase, and long-chain 3-ketoacyl
16 he only histidine conserved in all known L-3-hydroxyacyl-CoA dehydrogenases, and since its counterpar
17 f which (2-trans enoyl-CoA hydratase and L-3-hydroxyacyl-CoA dehydrogenase) are core activities requi
18 endent pathway is the higher activity of L-3-hydroxyacyl-CoA dehydrogenase as compared with Delta3,De
19 n from a peroxisomal enoyl-CoA hydratase/l-3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme gene p
20 tic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protectiv
21 hway and D-3-hydroxyacyl-CoA dehydratase/D-3-hydroxyacyl-CoA dehydrogenase (D-PBE) of the noninducibl
24 Toxoplasma consisting of one N-terminal d-3-hydroxyacyl-CoA dehydrogenase domain fused to two tandem
25 renal function include enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (EHHADH) and apolipoprotei
31 and glucose; (3) an increase in muscle beta-hydroxyacyl-CoA dehydrogenase (HADH) and adipose lipopro
32 teroid dehydrogenase type 10/short chain L-3-hydroxyacyl-CoA dehydrogenase have been investigated.
33 yl-CoA oxidase (ACOX), enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (HD), and thiolase, has be
34 se (THIO), peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase (HD), peroxisomal membrane
37 ain (C18:0) substrates, whereas the MFP2 L-3-hydroxyacyl-CoA dehydrogenase is active on C6:0, C12:0 a
38 f the second enzyme, enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase (L-PBE) of the inducible p
39 udy, the function of enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase (L-PBE), the second enzyme
40 purification of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase made it possible to charac
41 that His450 is the catalytic residue of L-3-hydroxyacyl-CoA dehydrogenase of the E. coli multifuncti
42 roperties of 3-ketoacyl-CoA thiolase and l-3-hydroxyacyl-CoA dehydrogenase of the mutant complexes we
43 2-terminal hydratase and the COOH-terminal 3-hydroxyacyl-CoA dehydrogenase, result in a unique neurom
47 with inactivating mutations of short-chain 3-hydroxyacyl-CoA dehydrogenase (SCHAD) was examined in mi
49 mutations in the gene encoding short-chain 3-hydroxyacyl-CoA dehydrogenase (SCHAD), a ubiquitously ex
50 Exercise training increased mtDNA and beta-hydroxyacyl-CoA dehydrogenase similarly in WT and CD36-K
51 nsferase, carnitine palmitoyltransferase 1A, hydroxyacyl-CoA-dehydrogenase, Sirtuin 6 (SIRT6), and AM
52 a-peptide (Abeta)-binding protein (ERAB)/L-3-hydroxyacyl-CoA dehydrogenase type II (HADH II) is expre
54 -/-) hearts, we measured the activity of l-3-hydroxyacyl-CoA dehydrogenase, which was acetylated in t
55 37 +/- 8% versus O(TR) 97 +/- 33%) and beta-hydroxyacyl-CoA-dehydrogenase (Y(TR) 31 +/- 7%, versus O
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