ライフサイエンスコーパス: CoA

1 expression displayed DGAT activity with 10:0-CoA and the diacylglycerol didecanoyl, that was approxim

2 ith the previously described CvLPAT2, a 10:0-CoA-specific Cuphea LPAT, increased 10:0 amounts to 25 m

3 ity studies showed that LPEAT1 utilized 16:0-CoA at the highest rate of 11 tested acyl-CoAs, whereas

4 rease in acylation activity of LPE with 16:0-CoA compared with wild-type membranes, whereas the acyla

5 sted acyl-CoAs, whereas LPEAT2 utilized 20:0-CoA as the best acyl donor.

6 e membranes, whereas the acylation with 18:1-CoA was much less affected, demonstrating that other lys

7 Furthermore, C22:1-CoA was 2.3-fold higher in insulin-resistant mice and co

8 on insulin sensitivity, we identified C22:1-CoA, C2-carnitine, and C16-ceramide as the best classifi

9 sent several cocrystal structures of BjaI, a CoA-dependent LuxI homolog that represent views of enzym

10 ux through the key fluoromalonyl coenzyme A (CoA) building block, thereby offering the potential to g

11 all molecule inhibitor of acetyl coenzyme A (CoA) carboxylase (ACC), the enzyme that controls the fir

12 he reduction of hydroxycinnamoyl-coenzyme A (CoA) esters using NADPH to produce hydroxycinnamyl aldeh

13 lastidial lipids, while the 16:4-coenzyme A (CoA) species was not detected.

14 n bond forming step between acyl coenzyme A (CoA) substrates offer a versatile route for biological s

15 idylethanolamine (LPE) with acyl-coenzyme A (CoA), designated LYSOPHOSPHATIDYLETHANOLAMINE ACYLTRANSF

16 l and committed step in the acyl-coenzyme A (CoA)-dependent biosynthesis of triacylglycerol (TAG).

17 lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (ACLY) from mitoc

18 ate is being used to synthesize cytosolic Ac-CoA by ACSS2.

19 imary enzyme involved in making cytosolic Ac-CoA in cells with abundant nutrients.

20 osphate, acetoacetyl coenzyme A (acetoacetyl-CoA), butyryl CoA, acetoacetate, and beta-hydroxybutyrat

21 ne and nicotinamide nucleotides, acetoacetyl-CoA, H2O2, reduced glutathione, and 2-monoacylglycerol w

22 sor for lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (ACLY) fr

23 ic infection, a specific inhibitor of acetyl CoA carboxylase 1, 5-(tetradecyloxy)-2-furoic acid, was

24 nd early pharmaceutical inhibition of acetyl CoA carboxylase 1, the rate limiting step of FAS, inhibi

25 Acetyl-CoA has diverse fates in metabolism and can be derived f

26 Acetyl-CoA stimulates cell growth under nutrient-limiting condi

27 Acetyl coenzyme A (acetyl-CoA) generated from glucose and acetate uptake is import

28 olic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acetylation and gene regulatio

29 ce utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

30 he availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for metabolic regulation of

31 -485 competes with acetyl coenzyme A (acetyl-CoA).

32 evealed the greatest activity against acetyl-CoA, and structure-guided mutagenesis of putative active

33 ior to agmatine to generate an AgmNAT*acetyl-CoA*agmatine ternary complex prior to catalysis.

34 ty acid oxidation, activated the AMPK-acetyl-CoA carboxylase pathway, and promoted inefficient metabo

35 leave out how and why ATP, NADH, and acetyl-CoA (Figure 1 ) at the molecular level play such central

36 ns, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing TPT were crucial to T

37 rotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable intermediates.

38 vels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Acc1).

39 as a protease subunit (clpP)-like and acetyl-CoA carboxylase subunit D (accD)-like open reading frame

40 enine dinucleotide, reduced form) and acetyl-CoA levels.

41 out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation represent

42 nformations in succinyl-CoA-bound and acetyl-CoA-bound forms.

43 rbon flow via OAA-malate-pyruvate and acetyl-CoA-fatty acid pathways in TRCs.

44 asticity and establish a link between acetyl-CoA generation 'on-site' at chromatin for histone acetyl

45 shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2 We conclude that CR m

46 om mitochondria-derived citrate or by acetyl-CoA synthetase short-chain family member 2 (ACSS2) from

47 ate-malate shuttle supplies cytosolic acetyl-CoA and plastidic glycolysis and malic enzyme support th

48 etate levels resulting from decreased acetyl-CoA synthetase activity.

49 exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels resultin

50 acid cycle influx of pyruvate-derived acetyl-CoA relative to beta-oxidation-derived acetyl-CoA, are s

51 oA relative to beta-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulated gluco

52 uding Acc1p, the rate-limiting enzyme acetyl-CoA carboxylase.

53 ere we show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) directly regulates histone acet

54 he first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient cells

55 he formation of N-acetylagmatine from acetyl-CoA and agmatine.

56 the transfer of an acetyl moiety from acetyl-CoA to the C-4 amino group of UDP-d-viosamine.

57 the transfer of an acetyl group from acetyl-CoA to the sn-3 position of diacylglycerol to form 3-ace

58 es that commonly produce ethanol from acetyl-CoA with acetaldehyde as intermediate and play a key rol

59 ng conditions, but how cells generate acetyl-CoA under starvation stress is less understood.

60 However, how acetyl-CoA is produced under nutritional stress is unclear.

61 ed in fatty acid synthesis, including acetyl-CoA carboxylase, and three out of five putative type II

62 Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with expressi

63 evating glucose uptake, and increased acetyl-CoA levels, leading to more ROS generation in hypoxic YC

64 ere observed with a HFD despite lower acetyl-CoA levels.

65 sing an ordered sequential mechanism; acetyl-CoA binds prior to agmatine to generate an AgmNAT*acetyl

66 ivated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphorylation at S659, which

67 rate ( 0.03 h(-1)) of key metabolite acetyl-CoA reached to P7 strain's metabolism limitation regime.

68 l fatty acid synthesis genes, namely, acetyl-CoA carboxylase, fatty acid synthase, SREBP1c, chREBP, g

69 A decrease in ACSS2 lowers nuclear acetyl-CoA levels, histone acetylation, and responsive expressi

70 g the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the transc

71 ytic genes and a significant delay of acetyl-CoA accumulation and reentry into growth from quiescence

72 onsuming a HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

73 in mice by liver-specific knockout of acetyl-CoA carboxylase (ACC) genes and treat the mice with the

74 The synthesis of acetyl-CoA depends primarily on the PDH-catalyzed conversion of

75 atalyzing the reversible synthesis of acetyl-CoA from CO and a methyl group through a series of nicke

76 , the spatial and temporal control of acetyl-CoA production by ACLY participates in the mechanism of

77 increased ACC levels and the ratio of acetyl-CoA to free CoA in these animals, indicating increased f

78 ble NADH-mediated interconversions of acetyl-CoA, acetaldehyde, and ethanol but seemed to be poised t

79 gulated, leading to the production of acetyl-CoA, which can feed TAG accumulation upon exposure to NO

80 r nuclear ACLY-mediated production of acetyl-CoA, which promotes histone acetylation, BRCA1 recruitme

81 and liver, but the impact of diet on acetyl-CoA and histone acetylation in these tissues remains unk

82 ipid biosynthetic precursors NADPH or acetyl-CoA.

83 e reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

84 elective binding of succinyl-CoA over acetyl-CoA.

85 cells oxidize fatty acids to produce acetyl-CoA for epigenetic modifications critical to lymphangiog

86 etylation turnover to locally produce acetyl-CoA for histone H3 acetylation in these regions and prom

87 ATP citrate-lyase produces acetyl-CoA in the nucleus and cytosol and regulates histone ace

88 hich results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen species se

89 -responsive factor Oaf1 in regulating acetyl-CoA production in glucose grown cells.

90 n cultured adipocytes also suppressed acetyl-CoA and histone acetylation levels.

91 ass in the cytosol, which synthesizes acetyl-CoA from acetate.

92 d histone acetylation levels and that acetyl-CoA abundance correlates with acetylation of specific hi

93 Our results also demonstrated that acetyl-CoA or acetyl-phosphate could acetylate MDH chemically i

94 p300 HAT complexes and shows that the acetyl-CoA binding site is stably formed in the absence of cofa

95 dditional suppressor mutations in the acetyl-CoA binding site of pyruvate carboxylase (PycA) rescued

96 l histone lysines correlated with the acetyl-CoA: (iso)butyryl-CoA ratio in liver.

97 ytic activity and is not sensitive to acetyl-CoA activation, in contrast to other PC enzymes.

98 talyzes the conversion of pyruvate to acetyl-CoA.

99 matrix where it converts pyruvate to acetyl-CoA.

100 oryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl transf

101 f an alpha-methyl branched dicarboxylic acid CoA thioester.

102 Since acrylate/acryloyl-CoA is probably produced by other metabolism, and AcuI a

103 se propionate-CoA ligase (PrpE) and acryloyl-CoA reductase (AcuI) as the key enzymes involved and thr

104 Acrylate and its metabolite acryloyl-CoA are toxic if allowed to accumulate within cells.

105 P1's interaction with and inhibition of acyl CoA-synthetase ligase (ACSL) activity.

106 ifference in their ability to use C18:0 acyl-CoA as a substrate.

107 rmed that conversion is performed by an acyl-CoA dehydrogenase and a subsequent hydratase yielding an

108 t genetic analysis identified ACS-4, an acyl-CoA synthetase and its FA-CoA product, as key germline f

109 CT775 accepts both acyl-ACP and acyl-CoA as acyl donors and, 1- or 2-acyl isomers of lysophos

110 s within many activated fatty acids and acyl-CoA substrates.

111 y acid synthase (FASN) and medium chain acyl-CoA dehydrogenase (MCAD) protein within the same cells i

112 it directly interacts with medium-chain acyl-CoA dehydrogenase (MCAD).

113 erentiation by attenuating medium-chain acyl-CoA dehydrogenase activity and that inhibition of this a

114 acetylation of mitochondrial long-chain acyl-CoA dehydrogenase, a known SIRT3 deacetylation target; i

115 on histones in vitro using short-chain acyl-CoA donors, proving that they are less efficient towards

116 ACBP binds very-long-chain acyl-CoA esters, which is required for its ability to stimula

117 xicity overexpressing ACSL1 (long-chain acyl-CoA synthetase 1) in cardiomyocytes, we show that modest

118 KEY POINTS: Long-chain acyl-CoA synthetase 6 (ACSL6) mRNA is present in human and ra

119 ABSTRACT: Long-chain acyl-CoA synthetases (ACSL 1 to 6) are key enzymes regulating

120 indicate that inhibition of long-chain acyl-CoA synthetases with triacsin C, a fatty acid analogue,

121 belongs to the family of FAD-dependent acyl-CoA dehydrogenase (ACD) and is a key enzyme of the ethyl

122 In conclusion, ACSL6 drives acyl-CoA toward lipid synthesis and its downregulation improv

123 er enzyme will accept the other's fatty acyl-CoA or peptide substrates.

124 -based peptide derived from human fatty acyl-CoA reductase 1 in complex with heme exhibited a signifi

125 morphology through the long-chain fatty acyl-CoA synthetase Faa1, independently of the RNA methylatio

126 itochondria-associated long-chain fatty acyl-CoA thioesterase that is activated upon binding phosphat

127 2/PC-TP complex directs saturated fatty acyl-CoA toward beta-oxidation.

128 as found to have an allosteric site for acyl-CoA/CoA.

129 eins, we observed the formation of four acyl-CoA intermediates, including a unique 4-phosphovaleryl-C

130 the expression of 28 transcripts [e.g., acyl-CoA oxidase 1 (ACOX1) and FAT atypical cadherin 1 (FAT1)

131 t demonstrated that CrACX2 is a genuine acyl-CoA oxidase, which is responsible for the first step of

132 Hepatic acyl-CoA thioesterase 1 (ACOT1) catalyzes the conversion of a

133 ynthase AasC but inhibitors of the host acyl-CoA synthetase enymes ACSL also impaired growth of C.t.

134 Under increasing acyl-CoA levels, the binding of acyl-CoA with this noncatalyt

135 other hand, is prevented under limiting acyl-CoA conditions (low acyl-CoA-to-CoA ratio), whereby CoA

136 under limiting acyl-CoA conditions (low acyl-CoA-to-CoA ratio), whereby CoA acts as a noncompetitive

137 enzymes regulating the partitioning of acyl-CoA species toward different metabolic fates such as lip

138 hioesterase activity against a range of acyl-CoA substrates revealed the greatest activity against ac

139 reasing acyl-CoA levels, the binding of acyl-CoA with this noncatalytic site facilitates homotropic a

140 po-CBP HAT domain is similar to that of acyl-CoA-bound p300 HAT complexes and shows that the acetyl-C

141 DGAT11-113) regulates activity based on acyl-CoA/CoA levels.

142 ta-oxidation involving H2 O2 -producing acyl-CoA oxidation activity has already evolved in the microb

143 t with the peroxisomal membrane protein acyl-CoA binding domain containing 5 (ACBD5) and that this in

144 ic lipid droplets (LDs) through reduced acyl-CoA production and increased lipid utilization in the mi

145 rACX2), a gene encoding a member of the acyl-CoA oxidase/dehydrogenase superfamily.

146 sis, DAG requires a fatty acid from the acyl-CoA pool or phosphatidylcholine.

147 We show that the acyl-CoA synthetase ACS-7, which localizes to lysosome-relate

148 fatty acid export in cells lacking the acyl-CoA synthetases Faa1 and Faa4.

149 rmation of triacylglycerol (TAG) by the acyl-CoA-dependent acylation of sn-1,2-diacylglycerol catalyz

150 es evidence that diet can impact tissue acyl-CoA and histone acetylation levels and that acetyl-CoA a

151 tone acyl-PTM abundances in response to acyl-CoA supplementation in in nucleo reactions.

152 ctural and storage lipids together with acyl-CoA analysis further help to determine mechanisms possib

153 in plastidial lipids, TAGs, as well as acyl-CoAs.

154 ant in limiting the use of longer chain acyl-CoAs by this enzyme.

155 gnificant flux of nascent and elongated acyl-CoAs into the sn-3 position of TAG.

156 a coli catalyzed the oxidation of fatty acyl-CoAs into trans-2-enoyl-CoA and produced H2 O2 .

157 ssette (ABC) half-transporters of fatty acyl-CoAs with both distinct and overlapping substrate specif

158 ells, showing their transformation into acyl-CoAs and subsequent click chemistry-based detection, to

159 they are less efficient towards larger acyl-CoAs.

160 marks, revealing that concentrations of acyl-CoAs affect histone acyl-PTM abundances by both enzymati

161 xamined the effects of HFD on levels of acyl-CoAs and histone acetylation in mouse white adipose tiss

162 (R (2) > 0.99) between the abundance of acyl-CoAs and their corresponding acyl-PTMs.

163 e 1 (ACOT1) catalyzes the conversion of acyl-CoAs to fatty acids (FAs) and CoA.

164 :0-CoA at the highest rate of 11 tested acyl-CoAs, whereas LPEAT2 utilized 20:0-CoA as the best acyl

165 We also observe that acyl-CoAs can acylate histones through non-enzymatic mechanis

166 dehydrogenases are substituted by 'ancient' CoA-dependent pyruvate and alpha-ketoglutarate ferredoxi

167 ersion of acyl-CoAs to fatty acids (FAs) and CoA.

168 is, glutathione metabolism, pantothenate and CoA biosynthesis, and butanoate metabolism.

169 natal diagnosis of coarctation of the aorta (CoA) is still challenging and affected by high rates of

170 er metallireducens uses the class II benzoyl-CoA reductase complex for this reaction.

171 atic and QM/MM calculations to model benzoyl-CoA reduction by BamB.

172 of our calculations, we propose that benzoyl-CoA reduction is initiated by a hydrogen atom transfer f

173 were pinpointed as being involved in binding CoA-conjugated phenylpropanoids.

174 acetyl coenzyme A (acetoacetyl-CoA), butyryl CoA, acetoacetate, and beta-hydroxybutyrate.

175 Butyryl-CoA and isobutyryl-CoA interacted with the acetyltransfe

176 correlated with the acetyl-CoA: (iso)butyryl-CoA ratio in liver.

177 n rearrangement of isobutyryl-CoA to butyryl-CoA.

178 bCCR1 displayed higher affinity for caffeoyl-CoA or p-coumaroyl-CoA than for feruloyl-CoA, the enzyme

179 anism and substrate specificity of cinnamoyl-CoA reductases from sorghum (Sorghum bicolor), a strateg

180 ficity for feruloyl-CoA over other cinnamoyl-CoA thioesters, and the T154Y mutation in SbCCR1 led to

181 e report that CLYBL operates as a citramalyl-CoA lyase in mammalian cells.

182 Cells lacking CLYBL accumulate citramalyl-CoA, an intermediate in the C5-dicarboxylate metabolic p

183 We tested the corresponding CoA esters of isomers and analogues of this compound for

184 isplayed greater activity toward p-coumaroyl-CoA than did SbCCR1, which could imply a role in the syn

185 her affinity for caffeoyl-CoA or p-coumaroyl-CoA than for feruloyl-CoA, the enzyme showed significant

186 3-oxopimeloyl-CoA, glutaconyl-CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable i

187 esults in increased affinity for NADH and DD-CoA turnover but with a reduction in Vmax for DD-CoA, im

188 turnover but with a reduction in Vmax for DD-CoA, impairing overall activity.

189 t to facilitate substrate turnover in the DD-CoA binding region of the protein.

190 free extracts, yielding 2,3-dehydropimeloyl-CoA, 3-hydroxypimeloyl-CoA, 3-oxopimeloyl-CoA, glutacony

191 zymatically reduced to cyclohexa-1,5-dienoyl-CoA.

192 dation of fatty acyl-CoAs into trans-2-enoyl-CoA and produced H2 O2 .

193 S1 impedes ECHS1 activity by impairing enoyl-CoA binding, promoting ECHS1 degradation and blocking it

194 show that exceeding nutrients suppress Enoyl-CoA hydratase-1 (ECHS1) activity by inducing its acetyla

195 Herein, we report that enoyl-CoA hydratase-1 (ECHS1), the enzyme involved in the oxid

196 ACD) and is a key enzyme of the ethylmalonyl-CoA pathway for acetate assimilation.

197 unprecedented variation of the ethylmalonyl-CoA pathway.

198 ied ACS-4, an acyl-CoA synthetase and its FA-CoA product, as key germline factors that mediate the ro

199 Feruloyl CoA 6'-hydroxylase is a controlling enzyme in the biosyn

200 contains a seven membered family of feruloyl CoA 6'-hydroxylase genes, four of which are expressed in

201 ava, where it significantly reduced feruloyl CoA 6'-hydroxylase gene expression, scopoletin accumulat

202 rs strong substrate specificity for feruloyl-CoA over other cinnamoyl-CoA thioesters, and the T154Y m

203 oyl-CoA or p-coumaroyl-CoA than for feruloyl-CoA, the enzyme showed significantly higher activity for

204 s to enzyme acylation with the fluoromalonyl-CoA extender unit.

205 l ACP-linked intermediate with fluoromalonyl-CoA allows insertion of fluorinated extender units at 43

206 identified, and 12 (922 fetuses at risk for CoA) articles were included.

207 C levels and the ratio of acetyl-CoA to free CoA in these animals, indicating increased fatty acid ox

208 yme that can oxidize succinyl-CoA to fumaryl-CoA is sought after.

209 ypimeloyl-CoA, 3-oxopimeloyl-CoA, glutaconyl-CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA a

210 oA dehydrogenase and a subsequent glutaconyl-CoA decarboxylase.

211 stream metabolites pimeloyl-CoA and glutaryl-CoA was proved in cell free extracts, yielding 2,3-dehyd

212 ta-oxidation, a non-decarboxylating glutaryl-CoA dehydrogenase and a subsequent glutaconyl-CoA decarb

213 ions, acute phase response pathway, glutaryl-CoA/tryptophan degradations and EIF2/AMPK/mTOR signaling

214 Statins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase in

215 )-localized 3-hydroxy-3-methylglutaryl (HMG) CoA reductase.

216 hibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic acid m

217 HMG-CoA reductase inhibitors such as statins are cholesterol

218 , 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the main t

219 ycerol, diacylglycerol, malonyl-CoA, and HMG-CoA.

220 CSA13 inhibited colonic HMG-CoA reductase activity in an FPRL1-dependent manner.

221 atment and variants in the gene encoding HMG-CoA reductase are associated with reductions in both the

222 Statins lower cholesterol by inhibiting HMG-CoA reductase, the rate-limiting enzyme of the metabolic

223 brosis via FPRL1-dependent modulation of HMG-CoA reductase pathway.

224 the rate-limiting enzyme in the pathway, HMG-CoA reductase (HMGCR).

225 omes ([S]-LIP), that are loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evaluated

226 partially rescued by treatment with the HMG-CoA reductase inhibitor simvastatin.

227 utaconyl-CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable intermediates.

228 Two hydroxycinnamoyl-CoA transferases (HCT/HQT) have been involved in CGA pro

229 A null mutant of 3-hydroxyisobutyryl-CoA hydrolase (CHY4, At4g31810) resulted in an embryo le

230 g 2,3-dehydropimeloyl-CoA, 3-hydroxypimeloyl-CoA, 3-oxopimeloyl-CoA, glutaconyl-CoA, crotonyl-CoA, 3-

231 and the previously observed 3-hydroxyvaleryl-CoA product.

232 Butyryl-CoA and isobutyryl-CoA interacted with the acetyltransferase P300/CBP-assoc

233 carbon skeleton rearrangement of isobutyryl-CoA to butyryl-CoA.

234 tochondrial B12 metabolism and that itaconyl-CoA is a cofactor-inactivating, substrate-analog inhibit

235 Among other genes, a beta-ketoacyl CoA synthase gene (PotriKCS1) was downregulated in leave

236 ondrial metabolism, anaplerosis, and malonyl-CoA/lipid signaling in beta-cell metabolic signaling and

237 onoacylglycerol, diacylglycerol, and malonyl-CoA; the predominance of KATP/Ca(2+) signaling control b

238 1-monoacylglycerol, diacylglycerol, malonyl-CoA, and HMG-CoA.

239 the formation of palmitic acid from malonyl-CoA, drove NF2-deficient cells into apoptosis.

240 ular some Krebs cycle intermediates, malonyl-CoA, and lower ADP levels.

241 gents that inhibit the production of malonyl-CoA reduced their sensitivity to FASN inhibitors.

242 them sensitive to elevated levels of malonyl-CoA, as occurs following blockade of FASN, suggesting ne

243 inyl-CoA to alpha,beta-unsaturated mesaconyl-CoA and shows only about 0.5% activity with succinyl-CoA

244 ein (SRP) or anti-3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) antibodies (Abs), and the titer of

245 h variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.

246 ese 10 genes, the 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2 (HMGCS2) was the highest upregulated gene

247 nzymes methionine synthase and methylmalonyl-CoA mutase, respectively.

248 he mitochondrial B12-dependent methylmalonyl-CoA mutase (MUT).

249 r characterized and homologous methylmalonyl-CoA mutase/G-protein chaperone system.

250 ecarboxylative condensation of methylmalonyl-CoA with S-propionyl-N-acetylcysteamine catalyzed by the

251 denosylcobalamin cofactor onto methylmalonyl-CoA mutase (MCM) and precludes loading of inactive cofac

252 se structural homolog of (2S)-methylsuccinyl-CoA and an essential intermediate in central carbon meta

253 (2S)-methylsuccinyl-CoA dehydrogenase (MCD) belongs to the family of FAD-dep

254 talyzes the oxidation of (2S)-methylsuccinyl-CoA to alpha,beta-unsaturated mesaconyl-CoA and shows on

255 ributed to increased intracellular myristoyl CoA levels.

256 acid increased the biosynthesis of myristoyl CoA and myristoylated Src and promoted Src kinase-mediat

257 We identified the myristoyl-CoA analogue B13 as a small-molecule inhibitor of NMT1 e

258 ferent ultrasound signs for the detection of CoA were associated with an increased detection rate.

259 The detection rate of CoA may improve when a multiple-criteria prediction mode

260 carrier protein (ACP)-coupled fatty acids or CoA-aryl/acyl moieties as progenitors.

261 yl-CoA, 3-hydroxypimeloyl-CoA, 3-oxopimeloyl-CoA, glutaconyl-CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA

262 ratively analyze beta-oxidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from Sham and

263 is: the condensation of serine and palmitoyl-CoA.

264 ediates, including a unique 4-phosphovaleryl-CoA and the previously observed 3-hydroxyvaleryl-CoA pro

265 BioW is a pimeloyl-CoA synthetase that converts pimelic acid to pimeloyl-Co

266 he potential downstream metabolites pimeloyl-CoA and glutaryl-CoA was proved in cell free extracts, y

267 etase that converts pimelic acid to pimeloyl-CoA.

268 er catabolic pathway proceeding via pimeloyl-CoA.

269 of different ultrasound signs in predicting CoA prenatally.

270 We propose propionate-CoA ligase (PrpE) and acryloyl-CoA reductase (AcuI) as t

271 ith an alpha-methyl branch using a propionyl-CoA extender unit.

272 enase, converts 1,2-propanediol to propionyl-CoA.

273 Recent evidences suggest that stearoyl-CoA-desaturase 1 (SCD1), the enzyme involved in monounsa

274 native TCA cycle, in which acetate:succinate CoA-transferase (ASCT) replaces the enzymatic step typic

275 We show that succinyl-coenzyme A (succinyl-CoA) binds to KAT2A.

276 zymatic step typically performed by succinyl-CoA synthetase (SCS), has arisen in diverse bacterial gr

277 fferent structural conformations in succinyl-CoA-bound and acetyl-CoA-bound forms.

278 emonstrate that local generation of succinyl-CoA by the nuclear alpha-KGDH complex coupled with the s

279 nt role in the selective binding of succinyl-CoA over acetyl-CoA.

280 enting the nonspecific oxidation of succinyl-CoA, which is a close structural homolog of (2S)-methyls

281 however, an enzyme that can oxidize succinyl-CoA to fumaryl-CoA is sought after.

282 -CoA at 2.3 A resolution shows that succinyl-CoA binds to a deep cleft of KAT2A with the succinyl moi

283 SIRT5 largely reversed the succinyl-CoA-driven lysine succinylation.

284 substrate specificity of MCD toward succinyl-CoA through active-site mutagenesis.

285 In vitro, succinyl-CoA was used to succinylate liver mitochondrial membrane

286 tic domain of KAT2A in complex with succinyl-CoA at 2.3 A resolution shows that succinyl-CoA binds to

287 shows only about 0.5% activity with succinyl-CoA.

288 Among treated patients the CoA segment (the maxillary length) and the ANB angle (th

289 imiting acyl-CoA conditions (low acyl-CoA-to-CoA ratio), whereby CoA acts as a noncompetitive feedbac

290 ditions (low acyl-CoA-to-CoA ratio), whereby CoA acts as a noncompetitive feedback inhibitor through

291 the structure of malonate decarboxylase with CoA in the active site of MdcD-MdcE.

292 2, and P=0.02, respectively) in fetuses with CoA in comparison with controls, although aortic isthmus

293 hypoplasia were more common in fetuses with CoA than in controls (odds ratio, 26.0; 95% confidence i

294 e diameter z score was lower in fetuses with CoA than in healthy fetuses (P</=0.001), but the ascendi

295 uct diameter ratio was lower in fetuses with CoA than in those without CoA (P<0.001).

296 diameter z score was higher in fetuses with CoA than in those without CoA (P=0.01).

297 ea view (P<0.001) were lower in fetuses with CoA.

298 o acid residues in the loop interacting with CoA were identified, revealing details of this important

299 er in fetuses with CoA than in those without CoA (P<0.001).

300 er in fetuses with CoA than in those without CoA (P=0.01).