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1 the thermodynamically stable normal product, crotonyl-CoA.
2 h both crotonyl-ACP and the model substrate, crotonyl-CoA.
3 ylation of glutaryl-CoA to produce CO(2) and crotonyl-CoA.
4 i) of 4.0 and 12.9 microM, respectively, for crotonyl-CoA.
5 loyl-CoA, 3-oxopimeloyl-CoA, glutaconyl-CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as obs
6  positive (+38 mV) than did optimal product (crotonyl-CoA) (+31 mV), a finding opposite of that obser
7            Catalysis of the syn hydration of crotonyl-CoA, absent in the wild-type 4-chlorobenzoyl-Co
8 e catalyzes the oxidation of glutaryl-CoA to crotonyl-CoA and CO(2) in the mitochondrial degradation
9 ation and decarboxylation of glutaryl-CoA to crotonyl-CoA and CO(2).
10 acid of Glu370 also protonates the transient crotonyl-CoA anion following decarboxylation.
11                           Protonation of the crotonyl-CoA anion occurs by a 1,3-prototropic shift cat
12  725 nm-absorbing species is the delocalized crotonyl-CoA anion that follows decarboxylation and that
13 xylation, and Arg94 stabilizes the transient crotonyl-CoA anion.
14  also driven by the concomitant reduction of crotonyl-CoA by NADH, a process called electron bifurcat
15 on of the DeltaacuI::kan mutant phenotype by crotonyl-CoA carboxylase/reductase from R. sphaeroides w
16 sion is based on the following findings: (i) crotonyl-CoA carboxylase/reductase, a key enzyme of the
17 inhibited by a mutation in the gene encoding crotonyl-CoA carboxylase/reductase, demonstrating that a
18 d the midpoint potential for the butyryl-CoA/crotonyl-CoA couple (E(BCoA/CCoA)) to shift 14 mV negati
19 CoA with bulk solvent and (b) protonation of crotonyl-CoA dienolate by solvent-derived protons under
20                           The protonation of crotonyl-CoA dienolate following decarboxylation of glut
21 lar 1,3-prototropic shift for protonation of crotonyl-CoA dienolate.
22 erization of enzyme activity with respect to crotonyl-CoA, hexenoyl-CoA, and dodecenoyl-CoA substrate
23 (2015) discover that levels of intracellular crotonyl-CoA impact the histone acylation landscape, pro
24 ance (lambda(max) approximately 725 nm), and crotonyl-CoA is found as the sole product.
25 e availability of the appropriate substrate (crotonyl-CoA) is limiting.
26  or decreasing the cellular concentration of crotonyl-CoA leads to enhanced or diminished gene expres
27 in the presence and absence of a butyryl-CoA/crotonyl-CoA mixture.
28  recycled, resulting in the simple equation: crotonyl-CoA + NADH + H(+) = butyryl-CoA + NAD(+) with K
29 polymerase (Lpp0650), but not enzymes of the crotonyl-CoA pathway (Lpp0931-0933) are involved in PHB
30 to increase plasmid-based expression of both crotonyl CoA reductase gene (ccr) and the erythromycin r
31    A ccr-blocked mutant showed no detectable crotonyl-CoA reductase activity and, compared to the wil
32                             In addition to a crotonyl-CoA reductase gene (fkbS), at least two other g
33 r the heterologous AT seemed to be limiting, crotonyl-CoA reductase, a primary metabolic enzyme invol
34                The product of orf4* (cer) is crotonyl-CoA reductase, which converts acetoacetyl-CoA t
35 ha, beta-unsaturated thioesters catalysed by crotonyl-CoA reductase/carboxylase (CCRC) homologues.
36 o and in vitro experiments revealed that the crotonyl-CoA reductase/carboxylase SalG has broad substr
37 crR, was shown to regulate the expression of crotonyl-CoA reductase/carboxylase, an enzyme of the eth
38 ds, correlating with the reduced activity of crotonyl-CoA reductase/carboxylase.
39 hydratase catalyzes the hydration of trans-2-crotonyl-CoA to 3(S)-HB-CoA, 3(S)-hydroxybutyryl-CoA wit
40 ase (CCR), which catalyzes the conversion of crotonyl-CoA to butyryl-CoA in the presence of NADPH, wa
41 ans, which couple the exergonic reduction of crotonyl-CoA to butyryl-CoA to the endergonic reduction
42 uced ferredoxin and Dh-FADH(-) that converts crotonyl-CoA to butyryl-CoA.
43 E144-catalyzed stepwise addition of water to crotonyl-CoA which is bound in an s-trans conformation i
44 e regulated by the cellular concentration of crotonyl-CoA, which can be altered through genetic and e
45 a) a rapid exchange of C-4 methyl protons of crotonyl-CoA with bulk solvent and (b) protonation of cr
46 hydrogenase decarboxylates glutaconyl-CoA to crotonyl-CoA without oxidation-reduction reactions of th

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