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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
8          Consistent with the hypothesis, l-3-hydroxyacyl-CoA dehydrogenase activity was inhibited by
9  protein level, and a tendency for reduced 3-hydroxyacyl-CoA dehydrogenase activity.
10 lactate dehydrogenase, pyruvate kinase and 3-hydroxyacyl-CoA dehydrogenase activity.
11 atty acid transporters CD36 and CPT1 or beta-hydroxyacyl-CoA dehydrogenase activity.
12                                Human type II hydroxyacyl-CoA dehydrogenase/amyloid-beta binding alcoh
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
22 metabolic disease states correlated with L-3-hydroxyacyl-CoA dehydrogenase deficiencies.
23                        In 24 children with 3-hydroxyacyl-CoA dehydrogenase deficiency, we used DNA am
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
26                                  A novel L-3-hydroxyacyl-CoA dehydrogenase from human brain has been
27                    The human short chain L-3-hydroxyacyl-CoA dehydrogenase gene is organized into six
28 RAP150, to the mouse enoyl-CoA hydratase/l-3-hydroxyacyl-CoA dehydrogenase gene promoter.
29 tion is encoded by the human short chain L-3-hydroxyacyl-CoA dehydrogenase gene.
30                                          l-3-Hydroxyacyl-CoA dehydrogenase (HAD), the penultimate enz
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
35           Measurement of the activity of L-3-hydroxyacyl-CoA dehydrogenase in cultured skin fibroblas
36                         The activity of beta-hydroxyacyl-CoA dehydrogenase increased with GW610742 (P
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
44                                          l-3-Hydroxyacyl-CoA dehydrogenase reversibly catalyzes the c
45                  Human heart short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) catalyzes the oxid
46            Sequencing of the short-chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) genomic DNA from t
47 with inactivating mutations of short-chain 3-hydroxyacyl-CoA dehydrogenase (SCHAD) was examined in mi
48                  Human brain short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) was found to catal
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
53                     Here, we report that L-3-hydroxyacyl-CoA dehydrogenase type II/amyloid binding al
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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