ライフサイエンスコーパス: acyl-CoA

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

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

3 he formation of a double bond on a saturated acyl-CoA.

4 ed within the reaction centre, orthogonal to acyl-CoA.

5 positioned to encounter the cleavage site in acyl-CoA.

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

7 eous analysis of nucleotides and short-chain acyl-CoAs.

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

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

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

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

12 e a constitutive siphon for long-chain fatty acyl-CoAs.

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

14 LCFA trafficking to ceramides, and restoring acyl CoA, ACSL1 delayed progressive cardiac remodeling a

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

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

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

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

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

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

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

22 x proteins identified included components of acyl-CoA and carbohydrate metabolism and pyrimidine and

23 rances for each of the two substrates, fatty acyl-CoA and diacylglycerol.

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

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

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

27 tracellular transporter and buffer for fatty-acyl-CoA and is active in membrane assembly.

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

29 te gene transcription using a combination of acyl-CoAs and [4Fe4S] cluster.

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

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

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

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

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

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

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

37 Intracellular nucleotides and acyl-CoAs are metabolites that are central to the regula

38 Acyl-CoAs are reactive metabolites that can non-enzymati

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

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

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

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

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

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

45 Acyl-CoA binding of FadR derepresses the transcription o

46 Acyl-CoA binding protein (ACBP)-derived endozepines are

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

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

49 rts have indicated that Arabidopsis thaliana acyl-CoA-binding proteins (ACBPs) are important in seed

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

51 ogical processes related to long chain fatty acyl-CoA biosynthesis and elongation of mono-, poly-unsa

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

53 ts indicate that peroxisomes not only accept acyl-CoAs but can also oxidize acylcarnitines in a simil

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

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

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

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

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

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

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

61 plicated structure-function relationships of acyl-CoA carboxylases, trans-carboxytransferases, malony

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

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

64 Acyl-CoA:cholesterol acyltransferase (ACAT) mediates cel

65 The 25HC-mediated activation of acyl-CoA:cholesterol acyltransferase (ACAT) triggered ra

66 mbrane fusion by activating the ER-localized acyl-CoA:cholesterol acyltransferase (ACAT) which leads

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

68 Short-term pharmacological inhibition of acyl-CoA:cholesterol acyltransferase-mediated cholestero

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

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

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

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

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

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

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

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

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

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

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

82 tative mitochondria-targeted, bacterial-type acyl-CoA dehydrogenase (PtMACAD1) that is present in Str

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

84 Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is the most co

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

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

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

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

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

94 Changes in medium-chain acyl-CoA dehydrogenase expression and acylcarnintine flu

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

96 Moreover, the FAO enzyme very-long-chain acyl-CoA dehydrogenase physically interacted with TFP, t

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

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

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

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

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

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

103 lglycerol (TAG) is mediated primarily by the acyl-CoA-dependent enzyme diacylglycerol acyltransferase

104 oxidized 2-arachidonoyl-lysophospholipids by acyl-CoA-dependent sn-1 acyltransferase(s).

105 erases, which catalyze the final reaction in acyl-CoA-dependent TAG biosynthesis, interact with the a

106 Strikingly, the FadR theme of acyl-CoA-dependent transcriptional regulation is found i

107 xidation of n-alkanes to their corresponding acyl-CoA derivatives including AlkB and AlmA, two CYP153

108 ure and directly binds to CoA or short-chain acyl-CoA derivatives to form a homotetramer that covers

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

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

111 Triacylglycerol synthesis is catalysed by acyl-CoA diacylglycerol acyltransferase (DGAT) enzymes(2

112 most oilseeds, two evolutionarily unrelated acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes,

113 arily triglycerides (TGs) synthesized by two acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes.

114 glycerol-3-phosphate acyltransferase (GPAT), acyl-CoA:diacylglycerol acyltransferase (DGAT), and phos

115 Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a k

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

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

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

119 catalyzes beta-oxidation of long chain fatty acyl-CoAs, employing 2-enoyl-CoA hydratase (ECH), 3-hydr

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

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

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

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

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

125 yl-CoA thioesterases (Acots) hydrolyze fatty acyl-CoA esters.

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

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

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

129 is the recognition of free acyl coenzyme A (acyl-CoA) from the lipid bilayer.

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

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

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

133 This is the first demonstration of reduced acyl CoA in failing hearts of humans and mice, and sugge

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

135 AD site to the KT site is unique in that the acyl-CoA intermediate can be transferred between the two

136 or syntrophic reverse electron transfer from acyl-CoA intermediates to formate was detected.

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

138 tly converts long chain fatty acyl-ACP/fatty acyl-CoA into hydrocarbon.

139 erase that catalyzes the hydrolysis of fatty acyl-CoAs into free fatty acids plus CoASH.

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

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

142 t of cytoplasmic long chain acyl-coenzyme A (acyl-CoA) into the mitochondrial matrix, which requires

143 Thus, lysine N-acylation by acyl-CoAs is enhanced by nucleotide-binding sites and ma

144 d highlight the maintenance of optimal fatty acyl-CoA levels as key to ER homeostasis.

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

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

147 ited to ER microdomains containing the fatty acyl-CoA ligase ACSL3, where nascent LDs bud.

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

149 CSL1 accelerated LCFA uptake, preventing C16 acyl CoA loss post-TAC.

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

151 mes regulating long-chain acetyl-coenzyme A (Acyl-CoA) metabolism.

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

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

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

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

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

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

158 Acyl-CoA mutases are a growing class of adenosylcobalami

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

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

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

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

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

164 oss-of-function mutations in the peroxisomal acyl-CoA oxidase 1 (ACOX1) gene cause neurodegeneration

165 Acyl-CoA oxidase 1 (Acox1), the enzyme that catalyzes th

166 ein 70 (PMP70) (modest down-regulation), and acyl-CoA oxidase 1 (ACOX1).

167 out of the peroxisomal beta-oxidation enzyme acyl-CoA oxidase 1 (Acox1-AKO) was not sufficient to aff

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

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

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

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

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

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

174 02 (CrACX2), a gene encoding a member of the acyl-CoA oxidase/dehydrogenase superfamily.

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

176 bidopsis mutant defective in two peroxisomal acyl-CoA oxidases does not metabolize ascr#18 and does n

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

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

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

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

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

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

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

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

185 mitochondrial CoA and shifts in the cardiac acyl-CoA profile paralleled changes in fatty acid oxidat

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

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

188 morphology that is specifically adapted for acyl-CoA recognition and autoacylation.

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

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

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

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

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

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

195 sterase activity with kinetic parameters and acyl-CoA selectivity comparable with acyl-CoA thioestera

196 e the enantiomeric specificity and saturated acyl-CoA selectivity of microsomal sn-1 acyltransferase(

197 Recently discovered acylation by reactive acyl-CoA species is considered a novel regulatory mechan

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

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

200 sn-1 acyltransferase activity for saturated acyl-CoA species.

201 Thus, DGAT isoforms with different acyl-CoA specificities are differentially active in the

202 We characterized the acyl-CoA specificities of all DGAT isoforms in oilseed r

203 four DGAT1 isoforms showed similar and broad acyl-CoA specificities.

204 However, DGAT2 isoforms had much narrower acyl-CoA specificities: two DGAT2 isoforms were highly a

205 portance, which a DGAT isoform with suitable acyl-CoA specificity may have, when aiming for high cont

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

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

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

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

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

211 f DGATs were similar with most of the tested acyl-CoA substrates in both cultivars, MAPLUS had 6- to

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

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

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

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

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

217 Differences in FAE1 enzyme affinity for the acyl-CoA substrates, as well as the balance between the

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

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

220 denosylcobalamin cofactor and four different acyl-CoA substrates.

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

222 ty of human PORCN across a spectrum of fatty acyl-CoAs suggested that the kink in the unsaturated acy

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

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

225 luding Acsl5 and Acsf2 (encode regulators of acyl-CoA synthesis), Slc27a2 (encodes a fatty acid trans

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

227 ember 4, fatty acid synthase, and long-chain acyl-CoA synthetase (3), and glucose transport genes (gl

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

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

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

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

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

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

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

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

236 enzymes and provide direct evidence that the acyl-CoA synthetase ACS-7, which was previously implicat

237 acs-13 encodes a homolog of the human acyl-CoA synthetase ACSL1, and localizes to the mitochon

238 tal muscle (Acsl1(M) (-/-)) severely reduces acyl-CoA synthetase activity and fatty acid oxidation.

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

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

241 lsugar accumulation due to trichome specific acyl-CoA synthetase and enoyl-CoA hydratase genes.

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

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

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

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

246 Loss of long-chain acyl-CoA synthetase isoform-1 (ACSL1) in mouse skeletal

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

248 l glutathione peroxidase 4 overexpression or acyl-CoA synthetase long chain family member 4 depletion

249 A28:g.23380074_23483377del, containing genes Acyl-CoA Synthetase Long Chain Family Member 5 (ACSL5) a

250 Acyl-CoA synthetase long-chain family member 4 (ACSL4) i

251 increased expression of 15-lipoxygenase and acyl-CoA synthetase long-chain family member 4 (enzyme t

252 Fatty acid transport protein 4 (FATP4) is an acyl-CoA synthetase that is required for normal permeabi

253 tion, activation of the carboxylate anion by acyl-CoA synthetase(s), and re-esterification to the sn-

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

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

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

257 ynthesis, as an inhibitor of host long-chain acyl CoA synthetases, key enzymes for glycerolipid biosy

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

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

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

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

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

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

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

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

266 It hydrolyzes long-chain fatty acyl-CoAs that are derived from lipid droplets, preventi

267 FadR is a transcription factor regulated by acyl-CoA thioester binding that optimizes fatty acid (FA

268 ithin a hydrophobic channel, positioning the acyl-CoA thioester bond near an invariant catalytic hist

269 h transporter from Arabidopsis has intrinsic acyl-CoA thioesterase (ACOT) activity, important for phy

270 The expression of the Acyl-CoA thioesterase (ACOT) family was induced upon CR,

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

272 ers and acyl-CoA selectivity comparable with acyl-CoA thioesterase 1 (ACOT1).

273 ty acid metabolism-associated genes [ Acot1 (Acyl-CoA thioesterase 1), Fabp1 (fatty acid-binding prot

274 MBLAC2 has acyl-CoA thioesterase activity with kinetic parameters a

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

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

277 Acyl-CoA thioesterases (Acots) hydrolyze fatty acyl-CoA

278 changes in fatty acid oxidation enzymes and acyl-CoA thioesterases, suggesting limitations of CoA av

279 Acyl-CoA thioesters were the preferred acyl donors, whil

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

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

282 ve energy metabolism by restoring long-chain acyl CoA through ASCL1 activation and mechanical unloadi

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

284 (TAG) synthesis, the esterification of fatty acyl-CoA to diacylglycerol.

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

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

287 A (CoA) diphosphatase that hydrolyzes fatty acyl-CoA to yield acyl 4'-phosphopantetheine.

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

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

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

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

292 In parallel, acyl CoA was measured in tissue obtained from heart fail

293 Long-chain acyl CoA was similarly reduced in human failing myocardi

294 Here, we report that the genetic deletion of Acyl-CoA:wax alcohol acyltransferase 2 (AWAT2) causes th

295 nd allosterically enhance Them1 catalysis of acyl-CoA, whereas 18:1 LPC destabilizes and inhibits act

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

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

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

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

300 the activity of PORCN with a range of fatty acyl-CoAs with varying length and unsaturation.