ライフサイエンスコーパス: acyl-CoA

1 ty of glycerol-3-phosphate (Gro3P) and fatty acyl-CoA.

2 ants could acylate GPC with acyl groups from acyl-CoA.

3 ting in retention of TAG and accumulation of acyl CoAs.

4 ATP and its key negative regulators, acetyl(acyl)-CoA.

5 catalytic yet essential and binds long-chain acyl-CoAs.

6 s the first double bond into saturated fatty acyl-CoAs.

7 ichment data were obtained in the respective acyl-CoAs.

8 ize and form peroxisomal importers for fatty acyl-CoAs.

9 that they are less efficient towards larger acyl-CoAs.

10 ratio in plastidial lipids, TAGs, as well as acyl-CoAs.

11 Acyl CoA:1,2-diacylglycerol acyltransferase (DGAT)-2 is

12 n in transacylation activity at the level of acyl-CoA:1-acylglycerol-sn-3-phosphate acyltransferase.

13 Furthermore, the RSV induction of acyl-CoA activity in mouse liver resulted in increases i

14 Specifically, acyl-CoA/acyl-ACP processing enzymes were targeted to th

15 ol acyltransferase (PDAT) and diacylglycerol:acyl CoA acyltransferase play overlapping roles in triac

16 tone marks, revealing that concentrations of acyl-CoAs affect histone acyl-PTM abundances by both enz

17 structural and storage lipids together with acyl-CoA analysis further help to determine mechanisms p

18 rDGTT3 possess distinct specificities toward acyl CoAs and diacylglycerols, and may work in concert s

19 Harnessing lipogenic pathways and rewiring acyl-CoA and acyl-ACP (acyl carrier protein) metabolism

20 Acyl-CoA and acyl-acyl carrier protein (ACP) synthetases

21 relatively promiscuous, accepting a range of acyl-CoA and amine substrates.

22 Fatty acyl-CoA and cholesterol are two substrates for choleste

23 the C143S co-crystal structure contains both acyl-CoA and fatty acid, defining how a second substrate

24 rovides evidence that diet can impact tissue acyl-CoA and histone acetylation levels and that acetyl-

25 eta(117)) is positioned to deprotonate bound acyl-CoA and initiate carbon-carbon bond formation.

26 ceramide synthases use very-long-chain fatty acyl-CoA and trihydroxy LCB substrates, and LOH2 (At3g19

27 , whereas muscle total carnitine, long-chain acyl-CoA and whole-body energy expenditure did not chang

28 we examined the effects of HFD on levels of acyl-CoAs and histone acetylation in mouse white adipose

29 for phosphatidic acid (PA) (long-chain fatty acyl-CoAs and lysophosphatidic acid [LPA]) were not decr

30 ian cells, showing their transformation into acyl-CoAs and subsequent click chemistry-based detection

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

32 acyl CoAs, CrDGTT2 preferred monounsaturated acyl CoAs, and CrDGTT3 preferred C16 CoAs.

33 ve lower ECHA activity, increased long-chain acyl-CoAs, and decreased ATP in the heart under fasting

34 active towards short-chain and medium-chain acyl-CoAs, and we have named it long-chain acyl-CoA carb

35 loops protruding into the binding pocket of acyl-CoA are determined by the individual arrangement of

36 Acyl-CoAs are substrates for energy production; stored w

37 TG) synthesis using diacylglycerol and fatty acyl CoA as substrates.

38 ked difference in their ability to use C18:0 acyl-CoA as a substrate.

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

40 Surprisingly, the content of muscle acyl-CoA at exhaustion was markedly elevated, indicating

41 ontrol of the metabolism of long-chain fatty acyl-CoAs because of the multiplicity of their cellular

42 teract with the peroxisomal membrane protein acyl-CoA binding domain containing 5 (ACBD5) and that th

43 Acyl-CoA binding domain-containing 7 (Acbd7) is a paralo

44 ralog gene of the diazepam-binding inhibitor/Acyl-CoA binding protein in which single nucleotide poly

45 The human orthologue of Atg37, acyl-CoA-binding domain containing protein 5 (ACBD5), is

46 nd the Golgin-160-associated protein, ACBD3 (acyl-CoA-binding domain-containing 3), and acetylation r

47 Here we describe a new, conserved acyl-CoA-binding protein, Atg37, that is an integral per

48 erichia coli FadR (EcFadR) contains only one acyl-CoA-binding site in each monomer, crystallographic

49 the apo-CBP HAT domain is similar to that of acyl-CoA-bound p300 HAT complexes and shows that the ace

50 oesterase (Acot) gene family hydrolyze fatty acyl-CoAs, but their biological functions remain incompl

51 ism of intracellular FA is the conversion to acyl-CoA by long chain acyl-CoA synthetases (Acsls).

52 erminant in limiting the use of longer chain acyl-CoAs by this enzyme.

53 The acyl moiety of acyl-CoA can be bulky or lengthy, allowing a large exten

54 We also observe that acyl-CoAs can acylate histones through non-enzymatic mec

55 Cellular metabolites, such as acyl-CoA, can modify proteins, leading to protein posttr

56 tructures of the unusual beta-subunit of the acyl-CoA carboxylase (YCC) responsible for this reaction

57 he 3.0 A crystal structure of the long-chain acyl-CoA carboxylase holoenzyme from Mycobacterium avium

58 n acyl-CoAs, and we have named it long-chain acyl-CoA carboxylase.

59 of two distinct lineages of biotin-dependent acyl-CoA carboxylases, one carboxylating the alpha carbo

60 ime trends in activities depend on the fatty-acyl CoA chain lengths of the different ceramide species

61 proteins that are believed to contribute to acyl-CoA channeling, the metabolic consequences of loss

62 cancer specimens and cell lines, mediated by acyl-CoA cholesterol acyltransferase-1 (ACAT-1) enzyme.

63 Acyl-CoA:cholesterol acyltransferase 1 (Acat1) converts

64 Acyl-CoA:cholesterol acyltransferase 1 (ACAT1) is a resi

65 at the expression of Niemann Pick C1 Like 1, Acyl-CoA:Cholesterol acyltransferase 1, and microsomal t

66 g excess LDL-cholesterol to be esterified by acyl-CoA:cholesterol acyltransferase and stored in lipid

67 targeting long-chain acyl-CoA synthetase and acyl-CoA:cholesterol acyltransferase, respectively.

68 (BnaDGAT11-113) regulates activity based on acyl-CoA/CoA levels.

69 ion was found to have an allosteric site for acyl-CoA/CoA.

70 his review, we will discuss the evidence for acyl-CoA compartmentalization, highlight the key modes o

71 mes play an important role in regulating the acyl-CoA composition in plant cells by transferring poly

72 third group generates minimal activity with acyl-CoA compounds that bind non-selectively to the prot

73 , we demonstrate that the physiologic pH and acyl-CoA concentrations of the mitochondrial matrix are

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

75 id dehydrogenase activity) as well as 3-keto-acyl-CoA conjugates and exhibits strong cofactor selecti

76 ree DGTTs: CrDGTT1 preferred polyunsaturated acyl CoAs, CrDGTT2 preferred monounsaturated acyl CoAs,

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

78 Long-chain acyl-CoA dehydrogenase (LCAD) is a key mitochondrial fat

79 Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial fatty a

80 g the fatty acid oxidation enzyme long-chain acyl-CoA dehydrogenase (LCAD).

81 fatty acid synthase (FASN) and medium chain acyl-CoA dehydrogenase (MCAD) protein within the same ce

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

83 Very long acyl-CoA dehydrogenase (VLCAD) deficiency is a genetic p

84 Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is an inherite

85 Acyl-CoA dehydrogenase 9 (ACAD9) is an assembly factor f

86 Medium-chain acyl-CoA dehydrogenase and acyl-CoA dehydrogenase 9, two related enzymes with lysin

87 nserved Caenorhabditis elegans gene acdh-11 (acyl-CoA dehydrogenase [ACDH]) facilitates heat adaptati

88 cid oxidation enzyme integrity, medium-chain acyl-CoA dehydrogenase activity and fat oxidation are el

89 differentiation by attenuating medium-chain acyl-CoA dehydrogenase activity and that inhibition of t

90 confirmed that conversion is performed by an acyl-CoA dehydrogenase and a subsequent hydratase yieldi

91 Medium-chain acyl-CoA dehydrogenase and acyl-CoA dehydrogenase 9, two

92 he powerful epoxyketone residue involving an acyl-CoA dehydrogenase and an unconventional free-standi

93 y to receive electrons from the medium chain acyl-CoA dehydrogenase and the glutaryl-CoA dehydrogenas

94 Multiple acyl-CoA dehydrogenase deficiencies (MADDs) are a hetero

95 elements: the nuclear pore complex (NPC) and acyl-CoA dehydrogenase family member-10 (ACAD10).

96 regulatory circuit involving a heat-induced acyl-CoA dehydrogenase that controls the lipid saturatio

97 ased acetylation of mitochondrial long-chain acyl-CoA dehydrogenase, a known SIRT3 deacetylation targ

98 xidation, such as cytochrome c, medium-chain acyl-CoA dehydrogenase, and adipocyte protein 2.

99 the fatty acid oxidation enzyme medium-chain acyl-CoA dehydrogenase, we tested whether acetylation-de

100 rally distinct subfamily of acyl coenzyme A (acyl-CoA) dehydrogenase (ACAD) enzymes that are alpha2be

101 7 and Phe-320, which are conserved among all acyl-CoA dehydrogenases and coordinate the enzyme-bound

102 The same mechanism may regulate other acyl-CoA dehydrogenases.

103 he formation of triacylglycerol (TAG) by the acyl-CoA-dependent acylation of sn-1,2-diacylglycerol ca

104 Sl-ASAT3 was shown to encode an acyl-CoA-dependent acyltransferase that catalyzes the tr

105 sed fatty acid flux into multiple long-chain acyl-CoA-dependent pathways.

106 Enhancement of acyl-CoA-dependent triacylglycerol (TAG) synthesis in ve

107 Here, we demonstrate that long chain acyl-CoA derivatives (oleoyl-CoA and, to lesser extent,

108 Our data suggest that long chain acyl-CoA derivatives serve as biological indicators of t

109 or production of other chemicals, especially acyl-CoA-derived molecules.

110 he discovery and optimization of a series of acyl CoA:diacylglycerol acyltransferase 1 (DGAT1) inhibi

111 ympathetic activity, increased expression of acyl CoA:diacylglycerol acyltransferase-2 in the liver,

112 We identified several genes encoding acyl-CoA:diacylglycerol acyltransferases (DGATs) and pho

113 Indirect evidence suggests that acyl-CoAs do not wander freely within cells, but instead

114 tions on histones in vitro using short-chain acyl-CoA donors, proving that they are less efficient to

115 ylCoA synthase, a subunit of the cytoplasmic acyl-CoA elongase complex that controls the production o

116 acids and the subsequent reduction of fatty acyl-CoAs enabled the efficient synthesis of fatty alcoh

117 in contrast to yeast cells, very long-chain acyl-CoA esters are transported into peroxisomes by ABCD

118 the orientation of the hydroxyl group of the acyl-CoA esters by H-bond formation, thus determining st

119 he capacity of ACOT7 to hydrolyze long-chain acyl-CoA esters suggests potential roles in beta-oxidati

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

121 Besides interconversion of hydroxylated acyl-CoA esters, wild-type HCM as well as HcmA I90V and

122 l enzymes that convert fatty acids (FA) into acyl-CoA for use in metabolic pathways.

123 peroxisome to hijack the medium chain fatty acyl-CoA generated from the beta-oxidation pathway and c

124 ylglycerol acyltransferase and mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase and an

125 In addition to acyl-CoA, GPCAT efficiently utilizes LPC and lysophospha

126 We previously showed that the Delta(9) acyl-CoA integral membrane desaturase Ole1p from Sacchar

127 ced through the use of key enzymes acting on acyl-CoA intermediates, a carboxylic acid reductase from

128 proteins, we observed the formation of four acyl-CoA intermediates, including a unique 4-phosphovale

129 , resulting in increased reesterification of acyl-CoAs into diacylglycerol and triacylglycerol, with

130 a significant flux of nascent and elongated acyl-CoAs into the sn-3 position of TAG.

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

132 When acyl CoA is abundant, transient H2O2 oxidative stress or

133 that accumulation of amphipathic, long-chain acyl-CoA (LC-CoA) metabolites stimulates lipoapoptosis b

134 Acyl-CoA levels, ATP/ADP increases, membrane depolarizat

135 Under increasing acyl-CoA levels, the binding of acyl-CoA with this nonca

136 own did not alter FA oxidation or long chain acyl-CoA levels.

137 functionally replace the paradigm bacterial acyl-CoA ligase, Escherichia coli FadD, in the E. coli s

138 SF processing and was predicted to encode an acyl-CoA ligase.

139 ed lipopeptide, was mis-annotated as a fatty acyl-CoA ligase; however, it is in fact a FAAL that tran

140 ther fatty acyl-AMP ligases (FAALs) or fatty acyl-CoA ligases based on sequence analysis.

141 -CoA ligase (SPO2934) and other unidentified acyl-CoA ligases.

142 roteins and co-transfected with either fatty acyl:CoA ligases (ACSLs) 1, 3, or 6 or the SLC27A family

143 reaction catalyzed by the reverse action of acyl-CoA:lysophosphatidylcholine acyltransferase (LPCAT)

144 Acyl-CoA:lysophosphatidylcholine acyltransferase (LPCAT)

145 togenesis is a critical regulator of hepatic acyl-CoA metabolism, glucose metabolism, and TCA cycle f

146 s and that succinyl-CoA is the most abundant acyl-CoA molecule in the heart.

147 Here, by profiling acyl-CoA molecules in various mouse tissues, we have dis

148 abolic pathways that activate fatty acids to acyl-CoA molecules.

149 l in the enterocytes, a process catalyzed by acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2.

150 Acyl-CoA:monoacylglycerol acyltransferases (MGATs) and d

151 l findings identify critical determinants of acyl-CoA mutase substrate specificity and predict new ac

152 mutase substrate specificity and predict new acyl-CoA mutase-catalyzed reactions.

153 a novel 5'-deoxyadenosylcobalamin-dependent acyl-CoA mutase.

154 trate specificity and the catalytic scope of acyl-CoA mutases and could benefit engineering efforts f

155 Acyl-CoA mutases are a growing class of adenosylcobalami

156 ng of substrate specificity and catalysis in acyl-CoA mutases, however, is incomplete.

157 rane class of desaturases such as the Delta9-acyl-CoA, Ole1p, from yeast, which requires two catalyti

158 ND blockade, MEND is restored by cytoplasmic acyl CoA or CoA.

159 neither enzyme will accept the other's fatty acyl-CoA or peptide substrates.

160 Acyl CoA Oxidase 2 (ACOX2) encodes branched-chain acyl-C

161 e, we determine the crystal structure of the acyl-CoA oxidase 1 (ACOX-1) homodimer and the ACOX-2 hom

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

163 biogenesis and metabolism (e.g., PEX13p and acyl-CoA oxidase 1).

164 Thus, ATP may serve as a regulator of acyl-CoA oxidase activity, thereby directly linking asca

165 Mutations in the acyl-CoA oxidase genes acox-1, -2, and -3 led to specifi

166 lone or in pairs and purified, the resulting acyl-CoA oxidase homo- and heterodimers displayed differ

167 CoA Oxidase 2 (ACOX2) encodes branched-chain acyl-CoA oxidase, a peroxisomal enzyme believed to be in

168 result demonstrated that CrACX2 is a genuine acyl-CoA oxidase, which is responsible for the first ste

169 02 (CrACX2), a gene encoding a member of the acyl-CoA oxidase/dehydrogenase superfamily.

170 basis for the substrate specificities of the acyl-CoA oxidases and reveal why some of these enzymes h

171 to be made for the roles of uncharacterized acyl-CoA oxidases in C. elegans and in other nematode sp

172 arkably, we show that most of the C. elegans acyl-CoA oxidases that participate in ascaroside biosynt

173 When the acyl-CoA oxidases were expressed alone or in pairs and p

174 Here we show that three acyl-CoA oxidases, which catalyze the first step in thes

175 Acyl-CoA oxidases, which catalyze the first step in thes

176 FA beta-oxidation involving H2 O2 -producing acyl-CoA oxidation activity has already evolved in the m

177 This review evaluates the evidence for acyl-CoA partitioning by reviewing experimental data on

178 teins, and the potential role of maladaptive acyl-CoA partitioning in the pathogenesis of metabolic d

179 diagram potential mechanisms for controlling acyl-CoA partitioning.

180 nic acid (18:3(cisDelta9,12,15)) in both the acyl-CoA pool and seed oil of the former (48.4%-48.9% an

181 Our results indicated that both the acyl-CoA pool and seed oil of transgenic Arabidopsis lin

182 er, alterations in the FA composition of the acyl-CoA pool did not always correlate with those seen i

183 y fatty acids produced on PC directly to the acyl-CoA pool for further metabolism or catabolism.

184 ynthesis, DAG requires a fatty acid from the acyl-CoA pool or phosphatidylcholine.

185 ) can transfer PUFAs on PC directly into the acyl-CoA pool, making these PUFAs available for the diac

186 ong-chain monounsaturated fatty acids in the acyl-CoA pool.

187 by type III polyketide synthases using fatty acyl-CoA precursors.

188 aline pH and high concentrations of reactive acyl-CoAs present in the mitochondrial matrix.

189 plasmic lipid droplets (LDs) through reduced acyl-CoA production and increased lipid utilization in t

190 Their acyl-CoA products regulate metabolic enzymes and signali

191 overed that different tissues have different acyl-CoA profiles and that succinyl-CoA is the most abun

192 Acyl-CoA profiling of these plants revealed a major redu

193 We demonstrate that FATTY ACYL-COA REDUCTASE (AsFAR) plays an essential role in th

194 in yeast via targeted expression of a fatty acyl-CoA reductase (TaFAR) in the peroxisome of Saccharo

195 Peroxisomal fatty acyl-CoA reductase 1 (Far1) is essential for supplying f

196 ther gene in plasmalogen biosynthesis, fatty acyl-CoA reductase 1 (FAR1), in two families affected by

197 r His-based peptide derived from human fatty acyl-CoA reductase 1 in complex with heme exhibited a si

198 artmentalization, highlight the key modes of acyl-CoA regulation, and diagram potential mechanisms fo

199 s involving accumulation of long-chain fatty acyl-CoA, release of cholecystokinin, and subsequent neu

200 o-crystal structure possesses a single bound acyl-CoA representing the Michaelis complex with the fir

201 This compartmentalization of acyl-CoAs resulted in both an excessive glucose requirem

202 red for activation of the heterodimer or for acyl-CoA selectivity suggests that the ssSPTs have addit

203 e key enzymes regulating the partitioning of acyl-CoA species toward different metabolic fates such a

204 e key enzymes regulating the partitioning of acyl-CoA species toward different metabolic fates such a

205 ereas the levels of many of the medium-chain acyl-CoA species were significantly reduced.

206 cid, consisting of enzymes that condense two acyl-CoAs, stereospecifically reduce the resulting beta-

207 sn-2 position on lysophosphatidic acid by an acyl CoA substrate to produce the phosphatidic acid prec

208 reased the SPT affinity toward the C18 fatty acyl-CoA substrate by twofold and significantly elevated

209 e show that human TE1 efficiently hydrolyzes acyl-CoA substrate mimetics.

210 to our knowledge, into the determinants for acyl-CoA substrate specificity.

211 both phenylacetyl-CoA and medium-chain fatty-acyl CoA substrates.

212 acts with proteins that synthesize its fatty acyl CoA substrates.

213 er specific activity toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapentaenoyl-

214 of thioesterase activity against a range of acyl-CoA substrates revealed the greatest activity again

215 ssment of SpPaaI activity against a range of acyl-CoA substrates showed activity for both phenylacety

216 binding and isomerization of highly branched acyl-CoA substrates such as 2-hydroxyisobutyryl- and piv

217 superfamily enzyme that condenses two fatty acyl-CoA substrates to produce a beta-ketoacid product a

218 d produced triketide alkylpyrones from fatty acyl-CoA substrates with shorter chain lengths.

219 This enzyme can accept a broad range of acyl-CoA substrates, allowing us to interrogate differen

220 It has preference for long-chain acyl-CoA substrates, although it is also active towards

221 denosylcobalamin cofactor and four different acyl-CoA substrates.

222 oyl-CoA) than toward short-chain or aromatic acyl-CoA substrates.

223 bonds within many activated fatty acids and acyl-CoA substrates.

224 synthetic pathway in vitro using sucrose and acyl-CoA substrates.

225 isplayed a dual specificity for medium-chain acyl-CoAs substrates and phenylacetyl-CoA substrates, an

226 n histone acyl-PTM abundances in response to acyl-CoA supplementation in in nucleo reactions.

227 ACSLs) 1, 3, or 6 or the SLC27A family fatty acyl-CoA synthase FATP2/SLCA27A2 to test their effect on

228 nings, followed by coenzyme A (CoA) release, acyl CoA synthesis, and membrane protein palmitoylation.

229 TP openings, depleting fatty acids, blocking acyl CoA synthesis, metabolizing CoA, or inhibiting palm

230 stion was markedly elevated, indicating that acyl-CoAs synthesized by other ACSL isoforms were not av

231 CoA toxicity in mycobacteria by inactivating acyl CoA synthetase (ACS).

232 nt lysine residue in a number of FadD (fatty acyl CoA synthetase) enzymes is acetylated by KATmt in a

233 tal muscle-specific deficiency of long-chain acyl-CoA synthetase (ACSL)1.

234 , which each have very long-chain fatty acid acyl-CoA synthetase (VLCFA-ACS) activity, as negative re

235 hearts with a temporally induced knockout of acyl-CoA synthetase 1 (Acsl1(T-/-)) are virtually unable

236 The enzyme acyl-CoA synthetase 1 (ACSL1) is induced by peroxisome p

237 Long-chain acyl-CoA synthetase 1 (ACSL1) plays a key role in fatty

238 ipotoxicity overexpressing ACSL1 (long-chain acyl-CoA synthetase 1) in cardiomyocytes, we show that m

239 A comparative analysis demonstrates that the acyl-CoA synthetase 3 is recruited early to the assembly

240 Here we show that long-chain acyl-CoA synthetase 4a (Acsl4a), an LC-PUFA activating e

241 Long-chain acyl-CoA synthetase 6 (ACSL6) mRNA is present in human a

242 KEY POINTS: Long-chain acyl-CoA synthetase 6 (ACSL6) mRNA is present in human a

243 We show that the acyl-CoA synthetase ACS-7, which localizes to lysosome-r

244 tic Acsl1 mRNA and protein levels as well as acyl-CoA synthetase activity.

245 esis of TAGs and CEs by targeting long-chain acyl-CoA synthetase and acyl-CoA:cholesterol acyltransfe

246 In contrast, adipocyte acyl-CoA synthetase and diacylglycerol acyltransferase a

247 equent genetic analysis identified ACS-4, an acyl-CoA synthetase and its FA-CoA product, as key germl

248 t did not acetylate the wild-type long-chain acyl-CoA synthetase B (RpLcsB; formerly Rpa2714) enzyme

249 Here we show that the Drosophila fatty acyl-CoA synthetase CG6178, which cannot use d-luciferin

250 CP) synthase AasC but inhibitors of the host acyl-CoA synthetase enymes ACSL also impaired growth of

251 olar morphology through the long-chain fatty acyl-CoA synthetase Faa1, independently of the RNA methy

252 oA hydrolase (HIBCH, p = 8.42 x 10(-89)) and acyl-CoA synthetase family member 3 (ACSF3, p = 3.48 x 1

253 2 cell lysates with (2E)-hexadecenal and the acyl-CoA synthetase inhibitor triacsin C.

254 Thus, long-chain acyl-CoA synthetase isoform 1 (ACSL1) deficiency in the

255 ation of fatty acids by one of 13 long-chain acyl-CoA synthetase isoforms.

256 dy revealed a central role of the long-chain acyl-CoA synthetase LCS2 in the production of triacylgly

257 ion into TAG, with long lasting increases in acyl-CoA synthetase long 1 (ACSL1) and diacylglycerol ac

258 that requires activation by very long-chain acyl-CoA synthetase-1 (ACSVL1) to modulate both targets,

259 y CDCP1's interaction with and inhibition of acyl CoA-synthetase ligase (ACSL) activity.

260 he CYP77A and CYP86A subfamilies, LONG-CHAIN ACYL-COA SYNTHETASE2, GLYCEROL-3-PHOSPHATE SN-2-ACYLTRAN

261 The NDP-forming acyl-CoA synthetases (ACDs) catalyze the conversion of v

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

263 Long-chain acyl-CoA synthetases (ACSL 1 to 6) are key enzymes regul

264 Long-chain acyl-CoA synthetases (ACSLs) are key host-cell enzymes t

265 is the conversion to acyl-CoA by long chain acyl-CoA synthetases (Acsls).

266 C transporter and the peroxisomal long chain acyl-CoA synthetases (LACS)6 and -7.

267 as palustris (RpPat) inactivates AMP-forming acyl-CoA synthetases by acetylating the epsilon-amino gr

268 l for fatty acid export in cells lacking the acyl-CoA synthetases Faa1 and Faa4.

269 rases are thought to have evolved from fatty acyl-CoA synthetases present in all insects.

270 dings indicate that inhibition of long-chain acyl-CoA synthetases with triacsin C, a fatty acid analo

271 Firefly luciferase is homologous to fatty acyl-CoA synthetases.

272 for RpPat, all of which are also AMP-forming acyl-CoA synthetases.

273 The AMP-forming acyl coenzyme A (acyl-CoA) synthetases are a large class of enzymes found

274 aldehyde dehydrogenase enzymes to produce an acyl-CoA that is ultimately used in substrate-level phos

275 d activation of the free fatty acids to give acyl-CoAs that can be utilized to restore membrane lipid

276 a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with glucose-deri

277 Members of the acyl-CoA thioesterase (Acot) gene family hydrolyze fatty

278 Hepatic acyl-CoA thioesterase 1 (ACOT1) catalyzes the conversion

279 membranes from infected cells possess fatty acyl-CoA thioesterase activity, which is stimulated by A

280 s a mitochondria-associated long-chain fatty acyl-CoA thioesterase that is activated upon binding pho

281 Encoding acyl-CoA thioesterase-7 (Acot7) is one of approximately

282 the long-chain cytoplasmic acyl coenzyme A (acyl-CoA) thioesterase 7 (ACOT7) to regulate lipid reten

283 f enzymes related to beta-oxidation, such as acyl-CoA thioesterase2, acyl-activating enzyme isoform1,

284 ur-step reaction mechanism of ACDs, coupling acyl-CoA thioesters with ATP synthesis.

285 bled by direct carboxylation of medium chain acyl-CoA thioesters.

286 istage conformational change upon binding of acyl-CoA, thus allowing the uploading of Tei pseudoaglyc

287 inolenoyl groups from PC were transferred to acyl-CoA to a similar extent.

288 All enzymes utilize acyl-CoA to acylate GPC, forming lyso-PC, and they show

289 T) superfamily of enzymes that typically use acyl-CoA to modify diverse bacterial, archaeal, and euka

290 essed by the binding of either ATP.Mg(2+) or acyl-CoA to PANK3, is highly cooperative indicating that

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

292 nted under limiting acyl-CoA conditions (low acyl-CoA-to-CoA ratio), whereby CoA acts as a noncompeti

293 Them2/PC-TP complex directs saturated fatty acyl-CoA toward beta-oxidation.

294 In conclusion, ACSL6 drives acyl-CoA toward lipid synthesis and its downregulation i

295 ed by a network of proteins that channel the acyl-CoAs toward or away from specific metabolic pathway

296 ABCD2 (D2) is a peroxisomal long-chain acyl-CoA transporter that is highly induced by fenofibra

297 ic patterns of myocardial acylcarnitines and acyl-CoAs were analyzed using ultra-HPLC-MS/MS.

298 ed 16:0-CoA at the highest rate of 11 tested acyl-CoAs, whereas LPEAT2 utilized 20:0-CoA as the best

299 PpORS condenses a very long chain fatty acyl-CoA with four molecules of malonyl-CoA and catalyze

300 r increasing acyl-CoA levels, the binding of acyl-CoA with this noncatalytic site facilitates homotro

301 ng cassette (ABC) half-transporters of fatty acyl-CoAs with both distinct and overlapping substrate s