ライフサイエンスコーパス: fatty acyl-CoA

1 for vesicle budding from the Golgi, PI, and fatty acyl CoA.

2 physiological ligands such as bilirubin and fatty acyl CoA.

3 nd metabolism by converting fatty acids into fatty acyl-CoA.

4 and a final reduction to form the elongated fatty acyl-CoA.

5 tional activation is prevented by long chain fatty acyl-CoA.

6 or, triacsin C, evidence of its mediation by fatty acyl-CoA.

7 of MPYS interact with activated fatty acid, fatty acyl-CoA.

8 lability of glycerol-3-phosphate (Gro3P) and fatty acyl-CoA.

9 inhibited by ACPSH but not by fatty acid or fatty-acyl CoA.

10 s that catalyze the hydrolysis of long chain fatty acyl CoAs.

11 atalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs.

12 t activity toward the long chain unsaturated fatty acyl-CoAs.

13 no change in the concentration of any other fatty acyl-CoAs.

14 of processes sensitive to unbound long chain fatty acyl-CoAs.

15 a key enzyme in the synthesis of desaturated fatty acyl-CoAs.

16 h use two substrates, namely sphinganine and fatty acyl-CoAs.

17 ar head groups with acylating agents such as fatty acyl-CoAs.

18 nthesized fatty acids to their corresponding fatty acyl-CoAs.

19 roduces the first double bond into saturated fatty acyl-CoAs.

20 odimerize and form peroxisomal importers for fatty acyl-CoAs.

21 provide a constitutive siphon for long-chain fatty acyl-CoAs.

22 st both saturated and unsaturated long-chain fatty acyl-CoAs.

23 erase activity which catalyzes hydrolysis of fatty acyl-CoAs.

24 Long-chain (C16 to C20) fatty acyl-CoAs accumulate in kat2 seedlings, indicating

25 re, it is not known whether interaction with fatty acyl-CoA alters the structure of HNF-4alpha.

26 Less is known about the source of the fatty acyl-CoAs, although a number of cytosolic proteins

27 Fatty acyl CoA and cholesterol are the substrates for ch

28 The effect of fatty acyl CoA and fatty acid on the solution structure

29 Fatty acyl-CoA and cholesterol are two substrates for ch

30 tion results in an increase in intracellular fatty acyl-CoA and DAG concentrations, which results in

31 T2 activity was dependent on the presence of fatty acyl-CoA and diacylglycerol, indicating that this

32 te entrances for each of the two substrates, fatty acyl-CoA and diacylglycerol.

33 transporters, led accumulation of long-chain fatty acyl-coA and triacylglycerol in insulin-resistant

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

35 rsors for phosphatidic acid (PA) (long-chain fatty acyl-CoAs and lysophosphatidic acid [LPA]) were no

36 ted clear preference to long chain saturated fatty acyl-CoAs and oleoyl-CoA as acyl donors, which is

37 ve with both medium-and long-chain saturated fatty acyl-CoAs and showed maximal activity with C14-CoA

38 low micromolar concentrations of long chain fatty acyl-CoAs and the non-hydrolyzable thioether analo

39 gands are in the nanomolar range, long chain fatty acyl-CoAs and unsaturated fatty acids may both rep

40 to the similar affinities of PPAR alpha for fatty acyl-CoAs and unsaturated fatty acids, CoA thioest

41 an intracellular transporter and buffer for fatty-acyl-CoA and is active in membrane assembly.

42 s to FATP4 on mitochondria for conversion to fatty-acyl-CoAs and subsequent oxidation.

43 Further, ligands such as fatty acids, fatty acyl CoAs, and/or CoASH differentially modulate th

44 nizes a broad range of medium and long chain fatty acyl-CoA, and its activity was not affected by Ca(

45 CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid int

46 iated with the levels of a broad spectrum of fatty acyl-CoAs, and were elevated in human prostate tum

47 low micromolar concentrations of long chain fatty acyl-CoAs (apparent Ki approximately 1 muM).

48 ol acyltransferase, an enzyme that also uses fatty acyl CoA as a substrate.

49 cerol synthesis, by using diacylglycerol and fatty acyl CoA as substrates.

50 erol (TG) synthesis using diacylglycerol and fatty acyl CoA as substrates.

51 r fatty acid-acyl carrier protein (ACP) over fatty acyl-CoA as the acyl substrate for signal synthesi

52 DHHC enzymes use fatty acyl-CoA as the ubiquitous fatty acyl donor and be

53 4 nM K(d) values) for unsaturated long chain fatty acyl-CoAs as well as unsaturated long chain fatty

54 SCP-2 bound fluorescent fatty acyl-CoAs at a single site with high affinity.

55 rict control of the metabolism of long-chain fatty acyl-CoAs because of the multiplicity of their cel

56 Isoforms I and II both had two fatty acid or fatty acyl CoA binding sites.

57 significantly and differentially altered by fatty acyl-CoA binding.

58 data show for the first time that SCP-2 is a fatty acyl-CoA-binding protein.

59 f biological processes related to long chain fatty acyl-CoA biosynthesis and elongation of mono-, pol

60 2-6His hydrolyzes both medium and long chain fatty acyl-CoAs but has highest activity toward the long

61 oA thioesterase (Acot) gene family hydrolyze fatty acyl-CoAs, but their biological functions remain i

62 Acot) gene family catalyze the hydrolysis of fatty acyl-CoAs, but their biological functions remain u

63 ming; EC 6.2.1.3) catalyzes the formation of fatty acyl-CoA by a two-step process that proceeds throu

64 (ACBP) stimulates utilization of long-chain fatty acyl-CoA by a variety of membrane-bound enzymes, i

65 atalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs by branched-chain acyl-CoA oxidase (pris

66 The long-chain fatty acyl-CoA can be effectively extracted from frozen

67 d-derived metabolites (i.e., diacylglycerol, fatty acyl CoA, ceramides).

68 played distinct specificities for fatty acid/fatty acyl CoA chain length and unsaturation.

69 the time trends in activities depend on the fatty-acyl CoA chain lengths of the different ceramide s

70 ctivity was accompanied by a 28% increase in fatty acyl-CoA concentration.

71 method for the quantification of long-chain fatty acyl-CoA concentrations and enrichment.

72 the catalytic alpha,beta-dehydrogenation of fatty acyl-CoAs consists of two C-H bond dissociation pr

73 old increase in liver triglyceride and total fatty acyl-CoA content without any significant increase

74 iated with 30% increases in triglyceride and fatty acyl-CoA contents in the liver of rosiglitazone-tr

75 iated with 50% decreases in triglyceride and fatty acyl-CoA contents in the skeletal muscle of rosigl

76 ed to a significant reduction in heart total fatty acyl-CoA (control, 99.5 +/- 3.8; hLpL0, 36.2 +/- 3

77 -1) (P < 0.05) after acipimox; intramuscular fatty acyl CoA decreased from 10.3 +/- 1.9 to 4.54 +/- 0

78 KijD3 places it into the well-characterized fatty acyl-CoA dehydrogenase superfamily.

79 te dehydrogenase kinase, medium-chain length fatty acyl-CoA dehydrogenase, ubiquinone-cytochrome c re

80 Two fatty acyl-CoA dehydrogenases (designated FadE1 and FadE

81 broad range of substrate specificity toward fatty acyl-CoA derivatives and monoacylglycerols, among

82 in (ACBP) has high affinity for medium chain fatty acyl-CoAs, direct interaction of ACBP with >14-car

83 ed 10-18-carbon and unsaturated 14-20-carbon fatty acyl-CoAs displaced SCP-2-bound fluorescent ligand

84 The medium-to-long-chain fatty acyl-CoAs displayed the smallest K(m) values.

85 gher specific activity with unsaturated long fatty acyl-CoA donors.

86 HNF-4alphaLBD intrinsic Trp fluorescence by fatty acyl-CoAs (e.g. pamitoyl-, stearoyl-, linoleoyl-,

87 action is the initial step of the microsomal fatty acyl-CoA elongation pathway responsible for format

88 (TFP) catalyzes beta-oxidation of long chain fatty acyl-CoAs, employing 2-enoyl-CoA hydratase (ECH),

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

90 ated fatty acids (e.g. arachidonic acid) and fatty acyl-CoA esters (e.g. arachidonoyl-CoA) has been r

91 ness of the biological impacts of long-chain fatty acyl-CoA esters (LCACoAs), our knowledge about the

92 Long-chain fatty acyl-CoA esters activated PP5 at physiological con

93 dely expressed protein that binds long-chain fatty acyl-CoA esters and plays a role in fatty acyl-CoA

94 concentrations of five individual long-chain fatty acyl-CoA esters extracted from muscle tissue sampl

95 tive tissues, where it hydrolyzes long-chain fatty acyl-CoA esters to free fatty acids and CoA.

96 ity of saturated fatty acids, the effects of fatty acyl-CoA esters were examined.

97 Fatty acyl-CoA esters were the substrate of FAR1, and th

98 Acyl-CoA thioesterases (Acots) hydrolyze fatty acyl-CoA esters.

99 (ACSs, EC 6.2.1.3) catalyze the formation of fatty acyl-CoAs from free fatty acid, ATP, and CoA.

100 s autophagy proteins as well as medium-chain fatty acyl CoA generated by peroxisomes.

101 of the peroxisome to hijack the medium chain fatty acyl-CoA generated from the beta-oxidation pathway

102 e activity of iPLA 2beta can lead to reduced fatty acyl-CoA generation and impair fatty acid oxidatio

103 es the idea that manipulating the pathway of fatty acyl-CoA generation will impact a wide variety of

104 Cellular unbound long chain fatty acyl-CoAs (>14 carbon) are potent regulators of ge

105 , direct interaction of ACBP with >14-carbon fatty acyl-CoAs has not been established.

106 l analysis of ACSLs levels and the amount of fatty acyl-CoAs illustrated that ACSL1 were significantl

107 of short-chain acylcarnitines and long-chain fatty acyl CoAs in HK2 cells but not in Acsl1KO cells, c

108 the levels of long-chain acylcarnitines and fatty acyl CoAs in HK2 cells, and these increases were a

109 ACSL1 increased the biosynthesis of fatty acyl-CoAs including C16:0-, C18:0-, C18:1-, and C1

110 Both glycerol 3-phosphate and fatty acyl-CoA increased the GPAT activity, and the acti

111 effect on cholesterol transfer, and 5 mol % fatty acyl-CoAs increased transfer rates, demonstrating

112 yme catalyzes the synthesis of omega-hydroxy fatty acyl-CoA intermediates in the pathway to cutin syn

113 ficiently converts long chain fatty acyl-ACP/fatty acyl-CoA into hydrocarbon.

114 esaturase, an enzyme that converts saturated fatty acyl-CoAs into cis-Delta-9 unsaturated fatty acids

115 hioesterase that catalyzes the hydrolysis of fatty acyl-CoAs into free fatty acids plus CoASH.

116 Escherichia coli catalyzed the oxidation of fatty acyl-CoAs into trans-2-enoyl-CoA and produced H2 O

117 The fatty acyl-CoA is largely buried in the N-terminal lobe,

118 hospholipids; and reduced hepatic long-chain fatty acyl-CoAs (LCA-CoA).

119 Increases in intramyocellular long-chain fatty acyl-CoAs (LCACoA) have been implicated in the pat

120 chain fatty acid (LCFA) but also long chain fatty acyl CoA (LCFA-CoA), the physiological significanc

121 Although it is hypothesized that long-chain fatty acyl CoAs (LCFA-CoAs) and long-chain fatty acids (

122 long chain fatty acid (LCFA) and long chain fatty acyl-CoA (LCFA-CoA) binding site(s) remains to be

123 binding protein ACBP may modulate long-chain fatty acyl-CoA (LCFA-CoA) distribution, its physiologica

124 high affinity (Kd=0.06-12 nm) for long chain fatty acyl-CoAs (LCFA-CoA) and low affinity (Kd=58-296 n

125 estore the hypothalamic levels of long-chain fatty acyl-CoAs (LCFA-CoAs) and to normalize food intake

126 IT2 and highlight the maintenance of optimal fatty acyl-CoA levels as key to ER homeostasis.

127 ciated PI 3-kinase activity and increases in fatty acyl-CoA levels in skeletal muscle.

128 e associated with decreases in intramuscular fatty acyl-CoA levels.

129 om K(d) values) obtained with a radiolabeled fatty acyl-CoA ligand binding assay raised questions reg

130 han those previously derived by radiolabeled fatty acyl-CoA ligand binding assay.

131 RpfB is predicted to be a long-chain fatty acyl CoA ligase, and RpfF shows some relatedness t

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

133 Combining DNA encoding the fatty acyl-CoA ligase with suitable lipid precursors ena

134 -CoA thioesters generated enzymatically by a fatty acyl-CoA ligase.

135 -related lipopeptide, was mis-annotated as a fatty acyl-CoA ligase; however, it is in fact a FAAL tha

136 as either fatty acyl-AMP ligases (FAALs) or fatty acyl-CoA ligases based on sequence analysis.

137 ycle proteins and co-transfected with either fatty acyl:CoA ligases (ACSLs) 1, 3, or 6 or the SLC27A

138 FadR, in conjunction with long-chain fatty acyl-CoA, long-chain acyl-ACP, ppGpp and cAMP, are

139 One key enzyme in the Lands' cycle is fatty acyl-CoA:lysophosphatidylcholine acyltransferase (

140 ed the levels of triacylglycerol, long-chain fatty acyl-coA, malonyl-CoA, fatty acid oxidation, AMP-a

141 m iPLA(2)gamma(-/-) mice were insensitive to fatty acyl-CoA-mediated augmentation of calcium-induced

142 ranscription was found to be closely tied to fatty acyl-CoA metabolism.

143 Collectively, these results demonstrate that fatty acyl-CoA modulates phosphofructokinase activity th

144 A binding protein (ACBP) maintains a pool of fatty acyl-CoA molecules in the cell and plays a role in

145 in the endoplasmic reticulum, where each use fatty acyl-CoAs of defined chain length for ceramide syn

146 e cytochrome P450 enzyme CYP86A22 is the key fatty acyl-CoA omega-hydroxylase essential for the produ

147 tochrome P450 gene CYP86A22, which encodes a fatty acyl-CoA omega-hydroxylase involved in estolide bi

148 effects of saturated versus polyunsaturated fatty acyl-CoAs on HNF-4alpha LBD secondary structure co

149 ded on the concentration of MGAT substrates (fatty acyl CoA or monoacylglycerol).

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

151 ion system, which consists of three enzymes: fatty acyl-CoA oxidase (ACOX), enoyl-CoA hydratase/3-hyd

152 rat enoyl-CoA hydratase (HD) and peroxisomal fatty acyl-CoA oxidase (ACOX).

153 efective in ACX3, two of the six Arabidopsis fatty acyl-CoA oxidase (ACX) genes.

154 t in PPARalpha (PPARalpha(-/-)), peroxisomal fatty acyl-CoA oxidase (AOX(-/-)), and in both PPARalpha

155 ta-oxidation pathway in mice at the level of fatty acyl-CoA oxidase (AOX), the first and rate-limitin

156 We previously generated mice lacking fatty acyl-CoA oxidase (AOX), the first enzyme of the L-

157 oxisome proliferators, whereas those lacking fatty acyl-CoA oxidase (AOX-/-), the first enzyme of the

158 Fatty acyl-CoA oxidase (FACO) activity and mRNA were inc

159 n phytanoyl-CoA alpha hydroxylase (PAHX) and fatty acyl-CoA oxidase (FACO) mRNA levels during differe

160 efective in ACX1, ACX3, or ACX4 have reduced fatty acyl-CoA oxidase activity on specific substrates.

161 t of the PPARalpha-responsive genes encoding fatty acyl-CoA oxidase and cytochrome P450 4A1.

162 transfected with H2O2-generating peroxisomal fatty acyl-CoA oxidase cDNA, which encodes the first and

163 l of constitutively active human peroxisomal fatty acyl-CoA oxidase gene promoter.

164 element (PPRE) found in the promoter of the fatty acyl-CoA oxidase gene.

165 PPAR alpha and of the classical peroxisomal fatty acyl-CoA oxidase in energy metabolism, and in the

166 Cardiac fatty acyl-CoA oxidase mRNA levels increased at doses in

167 om mice deficient in PPAR alpha, peroxisomal fatty acyl-CoA oxidase, and some of the other enzymes of

168 ased expression of mRNAs for the peroxisomal fatty acyl-CoA oxidase, bifunctional enzyme, or thiolase

169 le of catalyzing straight-chain acyl-CoAs by fatty acyl-CoA oxidase, L-bifunctional protein, and thio

170 st and rate-limiting enzyme of this cycle is fatty acyl-CoA oxidase.

171 catalyzed hydrolysis of saturated long-chain fatty acyl-CoAs (palmitoyl-CoA approximately myristoyl-C

172 arboxylase 2 [ACC2], a critical regulator of fatty acyl-CoA partitioning between cytosol and mitochon

173 responsible for the biosynthesis of the 16:3 fatty acyl-CoA precursor, we identified and cloned three

174 y acids (9Z-16:1 and 9Z-18:1) from saturated fatty acyl-CoA precursors.

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

176 ited broad starter-unit specificities toward fatty acyl-CoAs ranging in sizes between C6 and C16 and

177 Furthermore, the finding that saturated fatty acyl-CoAs, rather than saturated fatty acids, are

178 We demonstrate that FATTY ACYL-COA REDUCTASE (AsFAR) plays an essential role

179 ion in jojoba requires, in addition to WS, a fatty acyl-CoA reductase (FAR) and an efficient fatty ac

180 oduced in yeast via targeted expression of a fatty acyl-CoA reductase (TaFAR) in the peroxisome of Sa

181 Peroxisomal fatty acyl-CoA reductase 1 (FAR1) is a rate-limiting enz

182 Peroxisomal fatty acyl-CoA reductase 1 (Far1) is essential for suppl

183 in another gene in plasmalogen biosynthesis, fatty acyl-CoA reductase 1 (FAR1), in two families affec

184 Coexpression of cDNAs specifying fatty acyl-CoA reductase 1 and wax synthase led to the s

185 A 23mer His-based peptide derived from human fatty acyl-CoA reductase 1 in complex with heme exhibite

186 a two step biosynthetic pathway catalyzed by fatty acyl-CoA reductase and wax synthase enzymes.

187 Mutant lines in a Fatty acyl-CoA Reductase gene expressed exclusively in t

188 like the root endodermis, we focused on two Fatty acyl-CoA Reductase genes that were specifically ac

189 synthesis in mammals is accomplished by two fatty acyl-CoA reductase isozymes that are expressed at

190 of CER4-6, which encodes an alcohol-forming fatty acyl-CoA reductase, was elevated 120-fold in iw1Iw

191 de, indicating that the gene encodes a novel fatty acyl-CoA reductase.

192 We further demonstrate that FATTY ACYL-CoA REDUCTASEs (FARs) FAR5 (At3g44550), FAR4

193 bited high affinity for saturated long chain fatty acyl-CoAs, regardless of chain length (1-13 nM K(d

194 er axis involving accumulation of long-chain fatty acyl-CoA, release of cholecystokinin, and subseque

195 In addition, there was no change in fatty acyl-CoA selectivity.

196 The corresponding fatty acyl-CoA serves as a starter unit for polyketide s

197 chain acyl-CoA synthetase-1 and its product fatty acyl-CoA, shown previously to be required for budd

198 hase activity that utilizes an atypical 16:3 fatty acyl-CoA starter unit, resulting in the formation

199 ) derived from an unusual 16:3Delta(9,12,15) fatty acyl-CoA starter unit.

200 RS enzymes capable of accepting a variety of fatty acyl-CoA starter units in recombinant enzyme studi

201 -alkylresorcinols using medium to long-chain fatty acyl-CoA starter units via iterative condensations

202 Each inhibitor binds DGAT1's fatty acyl-CoA substrate binding tunnel that opens to th

203 ch increased the SPT affinity toward the C18 fatty acyl-CoA substrate by twofold and significantly el

204 i 2,4-dienoyl-CoA reductase with NADP+ and a fatty acyl-CoA substrate reveals a possible mechanism fo

205 esterol ester formation from cholesterol and fatty acyl CoA substrates.

206 interacts with proteins that synthesize its fatty acyl CoA substrates.

207 a higher specific activity toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapenta

208 so determined that Hhat can utilize multiple fatty acyl-CoA substrates for fatty acid transfer to Shh

209 ER membrane is impermeable to the long-chain fatty acyl-CoA substrates of these enzymes.

210 With fatty acyl-CoA substrates of varying chain lengths, it w

211 purified protein was shown to be active with fatty acyl-CoA substrates that ranged from C(8) to C(16)

212 iolase superfamily enzyme that condenses two fatty acyl-CoA substrates to produce a beta-ketoacid pro

213 Substantial hydrolysis of fatty acyl-CoA substrates to the corresponding fatty aci

214 instead produced triketide alkylpyrones from fatty acyl-CoA substrates with shorter chain lengths.

215 dest preference for palmitoyl-CoA over other fatty acyl-CoA substrates.

216 cy and provide substrate specificity for the fatty acyl-CoA substrates.

217 dria, and relatively specific for long chain fatty acyl-CoA substrates.

218 y for both phenylacetyl-CoA and medium-chain fatty-acyl CoA substrates.

219 ectivity of human PORCN across a spectrum of fatty acyl-CoAs suggested that the kink in the unsaturat

220 iacylglycerol acyltransferase by determining fatty acyl-CoA supply.

221 ne fatty acid binding protein (FABP-pm), and fatty acyl CoA synthase (FACS) were detectable.

222 y acid transport related proteins as well as fatty acyl CoA synthase are expressed in keratinocytes a

223 ome proliferator response element-containing fatty acyl CoA synthase gene, although it cannot be rule

224 ve fatty acid transport related proteins and fatty acyl CoA synthase, an enzyme that facilitates the

225 ases (ACSLs) 1, 3, or 6 or the SLC27A family fatty acyl-CoA synthase FATP2/SLCA27A2 to test their eff

226 GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related pr

227 apidly converted to 5HD-CoA by mitochondrial fatty acyl CoA synthetase and acted as a weak substrate

228 mportant lysine residue in a number of FadD (fatty acyl CoA synthetase) enzymes is acetylated by KATm

229 ochondrial HMG-CoA synthase and increases in fatty acyl-CoA synthetase (3-8-fold) and carnitine palmi

230 These data support the hypothesis that fatty acyl-CoA synthetase (Faa1p or Faa4p) functions as

231 In Saccharomyces cerevisiae Fat1p and fatty acyl-CoA synthetase (FACS) are hypothesized to cou

232 Fatty acyl-CoA synthetase (FACS, fatty acid:CoA ligase,

233 Fatty acyl-CoA synthetase (fatty acid:CoA ligase, AMP-fo

234 uced function of peroxisomal very long chain fatty acyl-CoA synthetase (VLCS) that leads to severe an

235 Expression of the fatty acyl-CoA synthetase ACSVL3 was found to be markedl

236 the fatty acid transport and very long-chain fatty acyl-CoA synthetase activities were distinguishabl

237 of fatty acid accumulation, very long-chain fatty acyl-CoA synthetase activities, and the fatty acid

238 lted in either wild-type or nearly wild-type fatty acyl-CoA synthetase activity profiles; 2) those th

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

240 d vacuolar morphology through the long-chain fatty acyl-CoA synthetase Faa1, independently of the RNA

241 This region of fatty acyl-CoA synthetase from E. coli, 431NGWLHTGDIAVMD

242 The E. coli fatty acyl-CoA synthetase has remarkable amino acid simi

243 s, suppression was completely blocked by the fatty acyl-CoA synthetase inhibitor, triacsin C, evidenc

244 We propose that this sequence represents the fatty acyl-CoA synthetase signature motif (FACS signatur

245 ing the ATP/AMP binding domain and the 25-aa fatty acyl-CoA synthetase signature motif, but displays

246 Eighteen site-directed mutations within the fatty acyl-CoA synthetase structural gene (fadD) corresp

247 Fatty acid transport protein 4 (FATP4) is a fatty acyl-CoA synthetase that preferentially activates

248 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, and troglitazone, an enhancer

249 Triacsin C, an inhibitor of fatty acyl-CoA synthetase, prevented the increase in PFK

250 were reversed by triacsin C, an inhibitor of fatty acyl-CoA synthetase, the enzyme that generates LC-

251 acellular trafficking were also found in the fatty acyl-CoA synthetase-deficient strains.

252 Long-chain fatty acyl-CoA synthetases (ACSLs), a group of rate-limi

253 ghly conserved amino acid residues in the 12 fatty acyl-CoA synthetases compared.

254 o metabolic utilization proceeds through the fatty acyl-CoA synthetases Faa1p and Faa4p.

255 ce, DGWLHTGDIGXWXPXGXLKIIDRKK, common to all fatty acyl-CoA synthetases for which sequence informatio

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

257 he family of both prokaryotic and eukaryotic fatty acyl-CoA synthetases, indicating a common ancestry

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

259 ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in ins

260 It hydrolyzes long-chain fatty acyl-CoAs that are derived from lipid droplets, pr

261 that requires peroxisomal beta-oxidation and fatty acyl CoA thioesterase activity.

262 d that membranes from infected cells possess fatty acyl-CoA thioesterase activity, which is stimulate

263 em2) is a mitochondria-associated long-chain fatty acyl-CoA thioesterase that is activated upon bindi

264 e superfamily member 1 (Them1), a long-chain fatty acyl-CoA thioesterase that is enriched in BAT, sup

265 e superfamily member 2 (Them2), a long-chain fatty acyl-CoA thioesterase that is highly expressed in

266 fat inducible thioesterase) is a long-chain fatty acyl-CoA thioesterase that is highly expressed in

267 e superfamily member 1 (Them1), a long chain fatty acyl-CoA thioesterase.

268 odel and experimental analysis indicate that fatty acyl CoA thioesters, the proposed HNF4alpha ligand

269 lysolipids undergo spontaneous coupling with fatty acyl-CoA thioesters generated enzymatically by a f

270 Fatty acyl-CoA thioesters have recently been proposed to

271 esterase activity directed toward long chain fatty acyl-CoA thioesters, thus distinguishing the catal

272 ing was reversed upon addition of long-chain fatty acyl-CoA thioesters.

273 an indirect route of provision of ER luminal fatty acyl-CoA through a luminal carnitine acyltransfera

274 ally activated by small molecules as well as fatty acyl-CoAs through a mechanism involving Ser108 wit

275 atalyzed by acyl-CoA oxidase (AOX), converts fatty acyl-CoA to 2-trans-enoyl-CoA.

276 me acyl-CoA oxidase (ACOX), which oxidizes a fatty acyl-CoA to a 2-trans-enoyl-CoA.

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

278 tilizes lysophosphatidylcholine (LysoPC) and fatty acyl-CoA to produce various phosphatidylcholine (P

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

280 ected ion monitoring was used to analyze the fatty acyl-CoAs to achieve reliable quantification of th

281 PT) I catalyzes the conversion of long-chain fatty acyl-CoAs to acyl carnitines in the presence of l-

282 CPT-I converts long-chain fatty acyl-CoAs to acylcarnitines for translocation acro

283 CPTI) catalyzes the conversion of long-chain fatty acyl-CoAs to acylcarnitines in the presence of l-c

284 nd CPT1b catalyze acyl transfer from various fatty acyl-CoAs to carnitine, whereas CPT1c does not.

285 esterases (Acots) catalyze the hydrolysis of fatty acyl-CoAs to form free fatty acids plus CoA, but t

286 catalyzes the flavin-dependent oxidation of fatty acyl-CoAs to the corresponding trans-2-enoyl-CoAs.

287 s, the Them2/PC-TP complex directs saturated fatty acyl-CoA toward beta-oxidation.

288 in fatty acyl-CoA esters and plays a role in fatty acyl-CoA transport and pool formation.

289 rated that high affinity ligands (long chain fatty acyl-CoAs, unsaturated fatty acids), but not weak

290 rotein-2 (SCP-2) to interact with long chain fatty acyl-CoAs was examined.

291 Third, binding of fatty acyl-CoAs was specific as the binding affinities o

292 h catalyzes the conversion of fatty acids to fatty acyl-CoA, was inhibited with triacsin C, the incre

293 Fatty acyl CoAs were more effective than fatty acids in

294 Both fluorescent fatty acyl-CoAs were located within a very ordered (limi

295 ence of elevated tissue levels of long-chain fatty acyl CoA, which can impair beta-cell cell function

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

297 -binding cassette (ABC) half-transporters of fatty acyl-CoAs with both distinct and overlapping subst

298 Thus, native liver ACBP binds >14-carbon fatty acyl-CoAs with nanomolar affinity at a single bind

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

300 resistance and intramuscular accumulation of fatty acyl-CoA without alteration in whole-body adiposit