ライフサイエンスコーパス: CoA

1 nearly equal substrate preferences to C16:0-CoA and 18:1-CoA whereas OsDGAT1-2 displayed substrate s

2 -2 displayed substrate selectivity for C16:0-CoA over 18:1-CoA, indicating that these enzymes have co

3 idney mitochondria, as was activity for C4:0-CoA, a unique Acot9 substrate.

4 substrate preferences to C16:0-CoA and 18:1-CoA whereas OsDGAT1-2 displayed substrate selectivity fo

5 ubstrate selectivity for C16:0-CoA over 18:1-CoA, indicating that these enzymes have contrasting subs

6 had 6- to 14-fold higher activity with 22:1-CoA than did MONOLIT.

7 atically affects the specificity toward 22:1-CoA.

8 AAE13 as the best candidate for generating a CoA ester of tiglic acid (Taxol B side chain), TmAAE3 an

9 rt the cryo-EM structure of hNatB bound to a CoA-alphaSyn conjugate, together with structure-guided a

10 Acetate, a precursor of acetyl coenzyme A (CoA) (a product of fatty acid beta-oxidation [FAO]), or

11 the low molecular weight thiols coenzyme A (CoA) and glutathione in S47 cells.

12 ER protein FIT2 as a fatty acyl-coenzyme A (CoA) diphosphatase that hydrolyzes fatty acyl-CoA to yie

13 abolic fluxes to generate acetyl-Coenzyme A (CoA) from glucose resulting in augmented histone acetyla

14 rearranged AML by linking acetyl-coenzyme A (CoA) homeostasis to Bromodomain and Extra-Terminal domai

15 LCFA) uptake and activation with coenzyme A (CoA), mediating the fate of LCFA.

16 on the energy landscape of acyl-coenzyme A (CoA)-binding protein (ACBP).

17 including glutathione (GSH) and coenzyme A (CoA).

18 nce of the gene encoding butyryl-coenzyme A (CoA):acetate-CoA-transferase, a major enzyme in butyrate

19 KAN) and result in low levels of coenzyme-A (CoA) in the CNS due to impaired production of phosphopan

20 ne encoding butyryl-coenzyme A (CoA):acetate-CoA-transferase, a major enzyme in butyrate metabolism (

21 Acetyl-CoA carboxylase (ACCase) catalyzes the first committed s

22 Acetyl-CoA carboxylase 1 (Acc1) connects central energy metabol

23 Acetyl-CoA is the substrate for de novo lipogenesis as well as

24 ated metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic functions, including ener

25 the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an arylamine substrate using fola

26 The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element for a wide range of

27 is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes two oxidative decar

28 thesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular building block.

29 increasing FAO via deletion of ACC2 (acetyl-CoA-carboxylase 2) in phenylephrine-stimulated cardiomyo

30 in levels in chicken liver, activated acetyl-CoA carboxylase (ACCalpha), and increased FASN, ATP citr

31 Sphingosine kinase1 (SphK1) is an acetyl-CoA dependent acetyltransferase which acts on cyclooxyge

32 g appreciation that molecules such as acetyl-CoA act as a shared currency between metabolic flux and

33 ingosine (N-AS) is first generated by acetyl-CoA and sphingosine through SphK1.

34 thesis (FAS) is partially mediated by acetyl-CoA carboxylase (ACCase), the first committed step for t

35 ed flux of [U-(13)C]glucose to [(13)C]acetyl-CoA and M2 and M4 isotopomers of tricarboxylic acid (TCA

36 They convert acetyl-CoA to ethanol via an acetaldehyde intermediate during e

37 pathway in the peroxisome to convert acetyl-CoA to several commercially important monoterpenes and a

38 on is controlling nuclear-cytoplasmic acetyl-CoA synthesis.

39 ency markedly lowered total cytosolic acetyl-CoA levels, which led to decreased Raptor acetylation an

40 e results identify peroxisome-derived acetyl-CoA as a key metabolic regulator of autophagy that contr

41 ichloroacetic acid treatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited autoph

42 CSH) module, flanked by four flexible acetyl-CoA synthetase homology (ASH) domains; CoA is bound at t

43 which transfers the acetyl group from acetyl-CoA to EctB-formed l-2,4-diaminobutyrate (DAB), yielding

44 cleaves cytosolic citrate to generate acetyl-CoA, and is upregulated after consumption of carbohydrat

45 D(+) and by SpxB and PDHc to generate acetyl-CoA.

46 ing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses the conversion of

47 dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis.

48 ersion of bolus fructose into hepatic acetyl-CoA and fatty acids.

49 oute from dietary fructose to hepatic acetyl-CoA and lipids remains unknown.

50 pase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux, while also in

51 presses a multicomponent, heteromeric acetyl-CoA carboxylase (htACCase), which catalyzes the generati

52 ch a cell responds to fluctuations in acetyl-CoA levels remain elusive.

53 The metabolic intermediate acetyl-CoA links anabolic and catabolic processes and coordinat

54 Intracellular acetyl-CoA concentrations are associated with nutrient availabi

55 nucleolus as an important hub linking acetyl-CoA fluctuations to cellular stress responses.

56 biota(9), and this supplies lipogenic acetyl-CoA independently of ACLY(10).

57 ation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention.

58 onment," the hepatocyte diverted more acetyl-CoA away from lipogenesis toward ketogenesis and TCA cyc

59 is a major source of nucleocytosolic acetyl-CoA, a fundamental building block of carbon metabolism i

60 r(4-6), in which carbon precursors of acetyl-CoA are converted into fatty acids.

61 s to AMPK-mediated phosphorylation of acetyl-CoA carboxylase and polyunsaturated fatty acid biosynthe

62 e homology domain in the mechanism of acetyl-CoA formation.

63 ux was secondary to greater levels of acetyl-CoA from metabolic reprogramming to beta oxidation.

64 The majority of acetyl-CoA generated by PFL was used to regenerate NAD(+) with

65 se in a manner that is independent of acetyl-CoA metabolism.

66 late the nucleo-cytoplasmic levels of acetyl-CoA using clustered regularly interspaced short palindro

67 acetate and decreased accumulation of acetyl-CoA-derived intermediates of central metabolism.

68 bial acetate feeds lipogenic pools of acetyl-CoA.

69 activity as a competitive analogue of acetyl-CoA.

70 TCA cycle by reducing the amounts of Acetyl-CoA.

71 from glucose and palmitate to produce Acetyl-CoA, and secretion of heparan sulfate proteoglycan (comp

72 ionally implicate mTORC2 in promoting acetyl-CoA synthesis from acetate through acetyl-CoA synthetase

73 e decarboxylation steps to regenerate acetyl-CoA.

74 tory element-binding protein [SREBP], acetyl-CoA carboxylase [ACC], peroxisome proliferator-activator

75 of AMPK and of its downstream target acetyl-CoA carboxylase.

76 mobile systemic insecticide targeting acetyl-CoA carboxylase (ACC) of pest insects and mites upon fol

77 inical and clinical data suggest that acetyl-CoA carboxylase (ACC) inhibitors have the potential to r

78 e omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleolus, imp

79 n (p.Arg53His) and two at or near the acetyl-CoA binding site (p.Cys369Ser and p.Ser413Ala).

80 used in capsule production, while the acetyl-CoA generated by SpxB and PDHc was utilized primarily fo

81 ted that GCBCs generate most of their acetyl-CoA and acetylcarnitine from FAs.

82 yl-CoA synthesis from acetate through acetyl-CoA synthetase 2 (ACSS2).

83 decreased carbon flux from glucose to acetyl-CoA in the TAZ-KO cells to a ~50% decrease in pyruvate d

84 s) and eat it (degrade acyl chains to acetyl-CoA).

85 ACL), an enzyme converting citrate to acetyl-CoA, is highly induced in the kidney of overweight or ob

86 ne reductase to acetyl-P, and then to acetyl-CoA, which is condensed with another CO(2) to form pyruv

87 yruvate metabolism was shunted toward acetyl-CoA production.

88 ACLY with acetyl-CoA and oxaloacetate products shows the products bound i

89 tive-site A cluster of wild-type (WT) Acetyl-CoA Synthase (ACS) and two variants, F229W and F229A.

90 s, two aldehyde dehydrogenases, a fatty-acid-CoA ligase, a fatty acid desaturase and associated oxido

91 Many bacteria use AMP-forming acid:CoA ligases to convert organic acids into their correspo

92 oup has shown that the activity of many acid:CoA ligases is posttranslationally controlled by acylati

93 We identified eight new acid:CoA ligases in S. lividans TK24.

94 sis, as an inhibitor of host long-chain acyl CoA synthetases, key enzymes for glycerolipid biosynthes

95 Acyl-CoA binding of FadR derepresses the transcription of the

96 Acyl-CoA oxidase 1 (Acox1), the enzyme that catalyzes the fir

97 Acyl-CoA synthetase long-chain family member 4 (ACSL4) is one

98 Acyl-CoA thioesters were the preferred acyl donors, while acy

99 Acyl-CoA:cholesterol acyltransferase (ACAT) mediates cellular

100 Acyl-CoA:cholesterol acyltransferases 1 and 2 (ACAT1/2) conve

101 Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a key en

102 he recognition of free acyl coenzyme A (acyl-CoA) from the lipid bilayer.

103 cytoplasmic long chain acyl-coenzyme A (acyl-CoA) into the mitochondrial matrix, which requires the a

104 id metabolism-associated genes [ Acot1 (Acyl-CoA thioesterase 1), Fabp1 (fatty acid-binding protein 1

105 ACOX1 (acyl-CoA oxidase 1) encodes the first and rate-limiting enzym

106 acid transport protein 4 (FATP4) is an acyl-CoA synthetase that is required for normal permeability

107 se activity with kinetic parameters and acyl-CoA selectivity comparable with acyl-CoA thioesterase 1

108 ges in fatty acid oxidation enzymes and acyl-CoA thioesterases, suggesting limitations of CoA availab

109 We reasoned that protein-bound acyl-CoA could also facilitate S -> N-transfer of acyl groups

110 iacylglycerol synthesis is catalysed by acyl-CoA diacylglycerol acyltransferase (DGAT) enzymes(2-4),

111 is a transcription factor regulated by acyl-CoA thioester binding that optimizes fatty acid (FA) met

112 zed 2-arachidonoyl-lysophospholipids by acyl-CoA-dependent sn-1 acyltransferase(s).

113 chondrial CoA and shifts in the cardiac acyl-CoA profile paralleled changes in fatty acid oxidation e

114 rial C(12) oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macr

115 down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accu

116 with early induction of the long-chain acyl-CoA synthetase 1 (ACSL1).

117 organic acids into their corresponding acyl-CoA derivatives, which can then enter metabolism.

118 ated for human DHHC20 and for different acyl-CoA forms, also in a POPC membrane.

119 s for each of the two substrates, fatty acyl-CoA and diacylglycerol.

120 l processes related to long chain fatty acyl-CoA biosynthesis and elongation of mono-, poly-unsaturat

121 onverts long chain fatty acyl-ACP/fatty acyl-CoA into hydrocarbon.

122 hlight the maintenance of optimal fatty acyl-CoA levels as key to ER homeostasis.

123 synthesis, the esterification of fatty acyl-CoA to diacylglycerol.

124 oA) diphosphatase that hydrolyzes fatty acyl-CoA to yield acyl 4'-phosphopantetheine.

125 llular transporter and buffer for fatty-acyl-CoA and is active in membrane assembly.

126 hology that is specifically adapted for acyl-CoA recognition and autoacylation.

127 .23380074_23483377del, containing genes Acyl-CoA Synthetase Long Chain Family Member 5 (ACSL5) and Zi

128 MBLAC2 has acyl-CoA thioesterase activity with kinetic parameters and ac

129 ioned to encounter the cleavage site in acyl-CoA.

130 e fusion by activating the ER-localized acyl-CoA:cholesterol acyltransferase (ACAT) which leads to th

131 LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C(12).

132 teins identified included components of acyl-CoA and carbohydrate metabolism and pyrimidine and CoA b

133 acids and stimulated gene expression of acyl-CoA dehydrogenases in the liver.

134 g Acsl5 and Acsf2 (encode regulators of acyl-CoA synthesis), Slc27a2 (encodes a fatty acid transporte

135 losterically enhance Them1 catalysis of acyl-CoA, whereas 18:1 LPC destabilizes and inhibits activity

136 Strikingly, the FadR theme of acyl-CoA-dependent transcriptional regulation is found in a d

137 The 25HC-mediated activation of acyl-CoA:cholesterol acyltransferase (ACAT) triggered rapid i

138 hort-term pharmacological inhibition of acyl-CoA:cholesterol acyltransferase-mediated cholesterol est

139 we report that the genetic deletion of Acyl-CoA:wax alcohol acyltransferase 2 (AWAT2) causes the obs

140 tathione peroxidase 4 overexpression or acyl-CoA synthetase long chain family member 4 depletion dimi

141 f-function mutations in the peroxisomal acyl-CoA oxidase 1 (ACOX1) gene cause neurodegeneration via d

142 sis mutant defective in two peroxisomal acyl-CoA oxidases does not metabolize ascr#18 and does not re

143 cently discovered acylation by reactive acyl-CoA species is considered a novel regulatory mechanism i

144 enantiomeric specificity and saturated acyl-CoA selectivity of microsomal sn-1 acyltransferase(s) an

145 rmation of a double bond on a saturated acyl-CoA.

146 r accumulation due to trichome specific acyl-CoA synthetase and enoyl-CoA hydratase genes.

147 Ts were similar with most of the tested acyl-CoA substrates in both cultivars, MAPLUS had 6- to 14-fo

148 erences in FAE1 enzyme affinity for the acyl-CoA substrates, as well as the balance between the diffe

149 es and provide direct evidence that the acyl-CoA synthetase ACS-7, which was previously implicated in

150 a hydrophobic channel, positioning the acyl-CoA thioester bond near an invariant catalytic histidine

151 thin the reaction centre, orthogonal to acyl-CoA.

152 e mitochondria-targeted, bacterial-type acyl-CoA dehydrogenase (PtMACAD1) that is present in Strameno

153 nd acyl-CoA selectivity comparable with acyl-CoA thioesterase 1 (ACOT1).

154 Acyl-CoAs are reactive metabolites that can non-enzymatically

155 d the ability to desaturate 24C and 26C acyl-CoAs while maintaining its Delta9-regioselectivity.

156 Thus, lysine N-acylation by acyl-CoAs is enhanced by nucleotide-binding sites and may con

157 ides (NAD(+) and NADH), and short-chain acyl-CoAs (acetyl, malonyl, succinyl, and propionyl).

158 It hydrolyzes long-chain fatty acyl-CoAs that are derived from lipid droplets, preventing th

159 so that we are able to redirect 89% of acyl-CoAs from the synthesis of neutral lipids to alka(e)nes

160 However, SPT can also metabolize other acyl-CoAs, in the range of C(14) to C(18), forming a variety

161 We find that acyl-CoAs, rather than free fatty acids (FFAs), are the prefe

162 a new PANk2(-/-) knockout model that allows CoA regeneration in brain cells to be evaluated and desc

163 tification of the biomolecules AMP, ATP, and CoA, which are fundamental for numerous biochemical proc

164 of ACLY in the presence of ATP, citrate and CoA substrates reveals a phospho-citryl-CoA intermediate

165 FAD and CoA are accommodated in the DXO/Rai1 active site by adop

166 d carbohydrate metabolism and pyrimidine and CoA biosynthesis, whereas no components related to eithe

167 oplasty for native coarctation of the aorta (CoA) is successful in children and adults but in neonate

168 Furthermore, as CoA contains an ADP backbone this may extend beyond CoA-

169 tains an ADP backbone this may extend beyond CoA-binding sites and include abundant Rossmann-fold mot

170 complex with DAB, (iv) in complex with both CoA and DAB, and (v) in the presence of the product N-ga

171 )) transfers one electron further to butyryl-CoA dehydrogenase (Bcd); two such transfers enable Bcd t

172 enable Bcd to reduce crotonyl-CoA to butyryl-CoA.

173 of transcripts encoding functional caffeoyl CoA- and caffeic acid 3-O-methyltransferases (CCoAOMT an

174 shikimate esterase1 Upregulation of caffeoyl-CoA O-methyltransferase1 and downregulation of F5Hs are

175 erase (HCT) or loss of function of cinnamoyl CoA reductase 1 (CCR1) express a suite of pathogenesis-r

176 and CoA substrates reveals a phospho-citryl-CoA intermediate in the ASH domain.

177 enzyme scaffold most related to contemporary CoA ligases toward more specialized functions including

178 Knockout of lignin-associated 4-coumarate:CoA ligases (4CLs) in herbaceous species mainly reduces

179 such transfers enable Bcd to reduce crotonyl-CoA to butyryl-CoA.

180 se enzymes can also remove FAD and dephospho-CoA (dpCoA) non-canonical caps from RNA, and we have nam

181 ance and highlight mitochondrial 2,4-dienoyl-CoA reductase (DECR1), an auxiliary enzyme of beta-oxida

182 cetyl-CoA synthetase homology (ASH) domains; CoA is bound at the CSH-ASH interface in mutually exclus

183 chome specific acyl-CoA synthetase and enoyl-CoA hydratase genes.

184 report a previously unassigned modular enoyl-CoA hydratase (mECH) domain and the assembly of enzyme c

185 upregulation of ech-1.1 (a homolog of enoyl-CoA hydratase involved in fatty acid beta-oxidation) and

186 and a C-terminal module homologous to enoyl-CoA hydratases/isomerases.

187 ere the crystal structure of the mouse Esco2/CoA complex at 1.8 angstrom resolution.

188 ation of Taz(KD) mitochondria with exogenous CoA partially rescued pyruvate and palmitoylcarnitine ox

189 myl-THF to produce formyl-coenzyme A (formyl-CoA) as a central reaction intermediate.

190 In a second step, formyl-CoA is decarbonylated, resulting in free CoA and carbon

191 myl-CoA is decarbonylated, resulting in free CoA and carbon monoxide.

192 hylglyoxal, 4-hydroxynonenal, and glutaconyl-CoA), or metabolites that act as competitive analogs aga

193 s defective in CaiB which catalyzes glutaryl-CoA synthesis from glutarate and succinyl-CoA.

194 an enzyme upstream of the defective glutaryl-CoA dehydrogenase, has been investigated as a potential

195 ate carbon atoms being derived from glutaryl-CoA, an intermediate in lysine degradation.

196 ere, we show that loss of DHTKD1 in glutaryl-CoA dehydrogenase-deficient HEK-293 cells leads to a 2-f

197 and a significantly reduced rate of glutaryl-CoA production by dihydrolipoamide succinyl-transferase

198 an alternative enzymatic source of glutaryl-CoA.

199 ated degradation (ERAD) of ubiquitinated HMG CoA reductase (HMGCR), the rate-limiting enzyme of the m

200 HMG-CoA reductase (HMGR) undergoes feedback-regulated degrad

201 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment for dyslipid

202 r (IGF1R) inhibitor, and fluvastatin, an HMG-CoA reductase inhibitor, as potential chemopreventive ag

203 Statins are HMG-CoA reductase inhibitors that are known to inhibit cellu

204 reduction from medications that inhibit HMG-CoA reductase; further research is needed to understand

205 Interestingly, HMG-CoA reductase, the rate-limiting enzyme in cholesterol s

206 re was genetically proxied inhibition of HMG-CoA reductase and secondary exposures were genetically p

207 Genetically proxied inhibition of HMG-CoA reductase was significantly associated with lower od

208 used to proxy therapeutic inhibition of HMG-CoA reductase, Niemann-Pick C1-Like 1 (NPC1L1) and propr

209 he primary analysis, genetically proxied HMG-CoA reductase inhibition equivalent to a 1-mmol/L (38.7-

210 2 mutation carriers, genetically proxied HMG-CoA reductase inhibition was associated with lower ovari

211 On the basis of a 17-HOPC-CoA -docked model, we propose a catalytic mechanism wher

212 a proton from the D-ring hydroxyl of 17-HOPC-CoA and Tyr-344 as the general acid that protonates the

213 of the mitochondrial enzyme beta-hydroxyacyl-CoA-dehydrogenase (HADH) can indicate previous freezing.

214 ding protein), and Hadh (encodes hydroxyacyl-CoA dehydrogenase).

215 through down-regulation of hydroxycinnamoyl CoA:shikimate/quinate hydroxycinnamoyl transferase (HCT)

216 the 3-HIB-forming enzyme 3-hydroxyisobutyryl-CoA hydrolase decreases release of 3-HIB and lipid accum

217 determined that two of the newly identified CoA ligases were under NAD(+) -dependent sirtuin deacyla

218 ncorporation of the prodrug-derived PPA into CoA.

219 encodes an epidermally-expressed 3-KETOACYL-CoA SYNTHASE (KCS) belonging to a functionally uncharact

220 ex that catalyzes thiolysis of beta-ketoacyl-CoA esters as part of fatty acid beta-oxidation.

221 ane suberin biosynthetic genes beta-ketoacyl-CoA synthase (ShKCS20) and caffeic acid-O-methyltransfer

222 We have studied the beta-ketoacyl-CoA synthase from the high erucic feedstock Thlaspi arve

223 itigate beta-oxidation overload and maintain CoA availability.

224 zygous mutation p.L81R and pR212W in malonyl CoA-acyl carrier protein transacylase (MCAT), a mitochon

225 ed in vitro lysine N-malonylation by malonyl-CoA near nucleotide-binding sites which overlaps with in

226 e for the citrate-derived metabolite malonyl-CoA in the effect of LPS in macrophages.

227 l-thioesters are reactive centers of malonyl-CoA and malonyl- S-acyl carrier protein, essential to fa

228 uggest that metabolic outsourcing of malonyl-CoA may be a strategy by which the soma communicates nut

229 Separation of malonyl-CoA production from its site of utilization facilitates

230 ionally, we demonstrate that loss of malonyl-CoA production in the intestine negatively impacts germl

231 plex to facilitate the generation of malonyl-CoA.

232 hemical (etomoxir) or physiological (malonyl-CoA) inhibitors, did not reduce MDV replication, indicat

233 We provide evidence that malonyl-CoA, the rate-limiting substrate for fatty acid synthesi

234 , ATP, malonate, coenzyme A, and the malonyl-CoA ligase MatB, venemycin production can be monitored b

235 hich catalyzes the generation of the malonyl-CoA precursor of de novo fatty acid biosynthesis.

236 limiting enzymes: 3-hydroxy-3-methylglutaryl CoA reductase and squalene monooxygenase.

237 tein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP-citrate lyase (ACLY) in a

238 Both 3-Hydroxy-3-Methylglutaryl-CoA Reductase and Proprotein Convertase Subtilisin/Kexin

239 a ketosynthase, a 3-hydroxy-3-methylglutaryl-CoA synthase, a dehydratase, a decarboxylase and a dedic

240 ession of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the rate-limiting e

241 ystathionine beta synthase and methylmalonyl-CoA-mutase to be common to 3 out of 4 datasets.

242 ity of the downstream enzymes, methylmalonyl-CoA mutase and methionine synthase.

243 assan protein EcPKS1 uses only methylmalonyl-CoA as a substrate, otherwise unknown in animal lipid me

244 n escort, delivering AdoCbl to methylmalonyl-CoA mutase (MCM).

245 Deficiencies in mitochondrial CoA and shifts in the cardiac acyl-CoA profile parallele

246 DmdC, a MMPA-CoA dehydrogenase, catalyzes the dehydrogenation of MMPA

247 enase, catalyzes the dehydrogenation of MMPA-CoA to generate MTA-CoA with Glu435 as the catalytic bas

248 dehydrogenation of MMPA-CoA to generate MTA-CoA with Glu435 as the catalytic base.

249 e efficacy of balloon angioplasty for native CoA during infancy beyond the neonatal period was examin

250 who underwent balloon angioplasty for native CoA.

251 Balloon angioplasty of native CoA is effective and safe in infants aged 3 to 12 months

252 statistical analysis, to show that octanoyl-CoA binding increases the activation free energy for the

253 s in terms of key interactions that octanoyl-CoA establishes with the four alpha-helices of ACBP and

254 light into the control of the activities of CoA ligases involved in the activation of organic acids

255 ion capacities, implicating dysregulation of CoA-dependent intermediary metabolism rather than respir

256 nzymes (AAEs) that catalyze the formation of CoA esters of different organic acids relevant for the N

257 e flavin of FAD and the pantetheine group of CoA contact the same region at the bottom of the active

258 capable of regenerating excellent levels of CoA in this system.

259 CoA thioesterases, suggesting limitations of CoA availability or "trapping" in Taz(KD) mitochondrial

260 ure of human DGAT1 in complex with an oleoyl-CoA substrate.

261 A structure obtained with oleoyl-CoA substrate resolved at approximately 3.2 angstrom sho

262 structures of mammalian DXO with 3'-FADP or CoA and fission yeast Rai1 with 3'-FADP provide elegant

263 by the conjugation of l-serine and palmitoyl-CoA.

264 uinone Oxidoreductase 1, Carnitine Palmitoyl-CoA Transferase and mitochondrial respiratory complexes

265 y acyl chain, usually derived from palmitoyl-CoA, to specific cysteine residues on target proteins, w

266 shows a conformational change that prohibits CoA binding.

267 tabolism caused by a deficiency of propionyl CoA carboxylase which often manifests with frequent meta

268 iency of the mitochondrial enzyme, propionyl-CoA carboxylase (PCC) composed of six alpha (PCCA) and s

269 d 2-ketobutyrate biosynthesis from propionyl-CoA and formate.

270 e general acid that protonates the propionyl-CoA anion following C-C bond cleavage.

271 2)-enolate recombination, yielding propionyl-CoA.

272 enous PPA is a recent strategy to reactivate CoA biosynthesis in PKAN patients.

273 SNO-CoA reductases require NADPH, whereas enzymatic reductio

274 gested an AKR1A1 substrate preference of SNO-CoA > GSNO.

275 he SNO group that mediate recognition of SNO-CoA by SCoR.

276 Finally, we discovered that the SNO-CoA/SCoR system has a role in mitochondrial metabolism.

277 Stearoyl CoA desaturase 1 (SCD1) is a critical lipogenic enzyme t

278 Stearoyl-CoA desaturase 1 (SCD1) is a membrane-embedded metalloen

279 phenotypic shift was controlled by stearoyl-CoA desaturase-1 (SCD1), an enzyme responsible for the d

280 tivator of the key lipogenic enzyme stearoyl-CoA desaturase (SCD) and that SCD is required for MITF(H

281 the crystal structure of the mouse stearoyl-CoA desaturase (mSCD1) it was proposed that Tyr-104, a s

282 r cells into an active inhibitor of stearoyl-CoA desaturase (SCD).

283 ences in central adiposity and SCD (stearoyl-CoA desaturase)-1 enzyme activity index.

284 itro expression and activity of the Stearoyl-CoA Desaturase 1 (SCD1), the hepatic Delta9-desaturase i

285 y maintaining the expression of the stearoyl-CoA desaturase FAT-7, an oxygen consuming, rate-limiting

286 at ADT induced upregulation of the succinate-CoA ligase GDP-forming beta subunit (SUCLG2), which regu

287 ET depends strongly on whether the succinyl CoA (SCoA) cosubstrate is bound at the MmOGOR active sit

288 Succinyl-CoA ligase (SCL) deficiency causes a mitochondrial encep

289 5'-aminolevulinate from glycine and succinyl-CoA.

290 yl-CoA synthesis from glutarate and succinyl-CoA.

291 tricarboxylic acid cycle (TCA) gene succinyl-CoA ligase subunit-beta (SUCLA2), causing global protein

292 Thus, increased succinyl-CoA levels contribute to the pathology of SCL deficiency

293 and precludes binding of substrate succinyl-CoA.

294 Here, we show that succinyl-CoA accumulates in cells derived from patients with rece

295 ) converts 2-oxoglutarate (2-OG) to succinyl-CoA concomitant with the reduction of NAD(+).

296 Balloon angioplasty increased the CoA diameter from 2.7+/-1 mm to 4.6+/-1.2 mm.

297 a mechanism of electrostatic pivoting of the CoA moiety, mediated by a set of conserved positively ch

298 at approximately 3.2 angstrom shows that the CoA moiety binds DGAT1 on the cytosolic side and the acy

299 date for esterification of benzoic acid with CoA (Taxol side chain).

300 ) (i) for its apo-form, (ii) in complex with CoA, (iii) in complex with DAB, (iv) in complex with bot