ライフサイエンスコーパス: long-chain acyl-CoA

1 nM (short-chain acyl-CoAs) and 4.2 nM (very-long-chain acyl-CoAs).

2 y with the above substrates but carboxylated long chain acyl-CoA.

3 riacylglycerol, diacylglycerol, ceramide, or long-chain acyl-CoA.

4 talyzes the condensation of malonyl-CoA with long-chain acyl-CoA.

5 rom the active site to assist the binding of long chain acyl-CoAs.

6 e could affect the ability of PhlD to accept long chain acyl-CoAs.

7 tabolize seed storage lipid, and accumulated long-chain acyl-CoAs.

8 with 3-day-old acx2-1 seedlings accumulating long-chain acyl-CoAs.

9 talyzes the condensation of malonyl-CoA with long-chain acyl-CoAs.

10 ft BGC and that MFT production is induced by long-chain acyl-CoAs.

11 hA6 is non-catalytic yet essential and binds long-chain acyl-CoAs.

12 n by controlling the mitochondrial uptake of long-chain acyl-CoAs.

13 ation of glycerol 3-phosphate with saturated long-chain acyl-CoAs.

14 monstrates maximum activity with unsaturated long-chain acyl-CoAs.

15 f developing seeds of E. alatus contain both long-chain acyl-CoA and acetyl-CoA sn-1,2-diacylglycerol

16 proteins generated phosphatidylcholine from long-chain acyl-CoA and lysoPC when expressed in Escheri

17 However, whereas muscle total carnitine, long-chain acyl-CoA and whole-body energy expenditure di

18 AtACX2 was active with long-chain acyl-CoAs and showed maximal activity with C1

19 ids (diacylglycerol and triglyceride but not long chain acyl CoAs) and improved hepatic insulin sensi

20 cerol, diacylglycerol, and ceramide (but not long-chain acyl-CoA) and decreased insulin-stimulated [(

21 FadR DNA binding is antagonized by long chain acyl-CoAs, and thus FadR acts as a sensor of

22 of lipid intermediates, including ceramide, long-chain acyl CoA, and diacylglycerol, were also decre

23 confers feedback inhibition by free CoA and long-chain acyl-CoA, and increases the regulation of Pan

24 KO) mice have lower ECHA activity, increased long-chain acyl-CoAs, and decreased ATP in the heart und

25 ude of its regulatory response, and it bound long chain acyl-CoAs appreciably more strongly than the

26 Here we report that long chain acyl-CoAs are more potent inhibitors of bSULT

27 In plants and other eukaryotes, long-chain acyl-CoAs are assumed to be imported into per

28 part of metabolomics, and medium- to (very) long-chain acyl-CoAs are focus of lipidomics studies.

29 diates iPLA2beta autoacylation, and identify long-chain acyl-CoAs as potential candidates mediating c

30 to the previous proposal that AccD4-5 accept long-chain acyl-CoAs as their substrates, both crystal s

31 is for the unusual ability of PhlD to accept long chain acyl-CoAs, both site-directed mutagenesis and

32 o be present for the transfer of medium- and long-chain acyl-CoAs by hChAT.

33 The 3.0 A crystal structure of the long-chain acyl-CoA carboxylase holoenzyme from Mycobact

34 medium-chain acyl-CoAs, and we have named it long-chain acyl-CoA carboxylase.

35 patic ACSL activity and a 25-35% decrease in long chain acyl-CoA content.

36 ce carrying the targeted inactivation of the long chain acyl CoA dehydrogenase gene (Acadl) are also

37 CoA dehydrogenase (IVD), and Glu261 in human long chain acyl-CoA dehydrogenase (LCAD), has been sugge

38 base-arrangement has been altered to that of long chain acyl-CoA dehydrogenase (LCADH), Glu376Gly/Thr

39 er between the two human genes encoding very long chain acyl-CoA dehydrogenase (VLCAD) and postsynapt

40 Very long chain acyl-CoA dehydrogenase (VLCAD; ACADVL) was fo

41 e, very long chain acyl-CoA synthetase, very long chain acyl-CoA dehydrogenase) in livers of the etha

42 of 3-mercaptopropionic acid, an inhibitor of long chain acyl-CoA dehydrogenase, and partially inhibit

43 Crystal structures of human long-chain acyl-CoA dehydrogenase (LCAD) and the catalyt

44 A kinetic study of long-chain acyl-CoA dehydrogenase (LCAD) and very long-c

45 Long-chain acyl-CoA dehydrogenase (LCAD) catalyzes the i

46 ) deficiency, none have been documented with long-chain acyl-CoA dehydrogenase (LCAD) deficiency.

47 Long-chain acyl-CoA dehydrogenase (LCAD) is a key mitoch

48 Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondr

49 stance, we studied mice with a deficiency of long-chain acyl-CoA dehydrogenase (LCAD), a key enzyme i

50 nother mitochondrial C(12) oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed

51 mice lacking the fatty acid oxidation enzyme long-chain acyl-CoA dehydrogenase (LCAD).

52 Very-long-chain acyl-CoA dehydrogenase (VLCAD) catalyzes the

53 Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is

54 Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is

55 h many patients have been found to have very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency, no

56 ifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which

57 Very-long-chain acyl-CoA dehydrogenase (VLCAD) is a major enz

58 Very-long-chain acyl-CoA dehydrogenase (VLCAD) is a member of

59 Very long-chain acyl-CoA dehydrogenase (VLCAD) is an inner mi

60 specificity, it appears that ACAD9 and very-long-chain acyl-CoA dehydrogenase are unable to compensa

61 In three patients with very-long-chain acyl-CoA dehydrogenase deficiency, this treat

62 bution and gene regulation of ACAD9 and very-long-chain acyl-CoA dehydrogenase identify the presence

63 Moreover, the FAO enzyme very-long-chain acyl-CoA dehydrogenase physically interacted

64 With the exception of long-chain acyl-CoA dehydrogenase protein level, which w

65 chain acyl-CoA dehydrogenase (LCAD) and very long-chain acyl-CoA dehydrogenase revealed that 5-trans-

66 tion that is highly homologous to human very-long-chain acyl-CoA dehydrogenase was identified by larg

67 urated acyl-CoAs are poor substrates of very long-chain acyl-CoA dehydrogenase when compared with myr

68 mice decreased acetylation of mitochondrial long-chain acyl-CoA dehydrogenase, a known SIRT3 deacety

69 iltration analysis indicated that, like very-long-chain acyl-CoA dehydrogenase, ACAD-9 is a dimer, in

70 olic enzymes, such as acetyl-CoA synthetase, long-chain acyl-CoA dehydrogenase, and 3-hydroxy-3-methy

71 deficiency of mitochondrial medium- or very long-chain acyl-CoA dehydrogenase.

72 -CoA dehydrogenase family except for IVD and long-chain acyl-CoA dehydrogenase.

73 aled increased fatty acid flux into multiple long-chain acyl-CoA-dependent pathways.

74 Here, we demonstrate that long chain acyl-CoA derivatives (oleoyl-CoA and, to less

75 Our data suggest that long chain acyl-CoA derivatives serve as biological indi

76 nd S. pneumoniae can utilize both short- and long-chain acyl CoA derivatives but prefer long-chain Co

77 , but instead, to an impaired ability to use long-chain acyl-CoAs derived from the diet, even when th

78 ycerol acetyltransferase activity but lacked long-chain acyl-CoA diacylglycerol acyltransferase activ

79 yl-CoA levels in vivo, lower hepatic lipids (long-chain acyl-CoAs, diacylglycerol, and triglycerides)

80 provide evidence that in this organism very long chain acyl-CoA esters are hydrolyzed by the Pxa1p-P

81 es, other metabolic intermediates, including long chain acyl-CoA esters, may also be involved.

82 he form of reactive oxygen species (ROS) and long-chain acyl-CoA esters (LC-CoA).

83 ggest that, in contrast to yeast cells, very long-chain acyl-CoA esters are transported into peroxiso

84 The capacity of ACOT7 to hydrolyze long-chain acyl-CoA esters suggests potential roles in b

85 Inhibition of mitoKATP by long-chain acyl-CoA esters, like that of ATP, exhibited

86 The precise role of phosphoinositides and long-chain acyl-CoA esters, which are capable of modulat

87 ACBP binds very-long-chain acyl-CoA esters, which is required for its ab

88 relative cytosolic concentrations of GTP and long-chain acyl-CoA esters.

89 he current study, we have re-evaluated this "long-chain acyl-CoA hypothesis" by using molecular and p

90 gamma activation was completely inhibited by long-chain acyl-CoA (IC(50) approximately 20 mum) as wel

91 rom), and PanK3 was stringently regulated by long-chain acyl-CoA (IC50 = 2 microm), whereas PanK1beta

92 pport the importance of phospholipids and/or long chain acyl-CoAs in setting the physiological activi

93 10:0 CoA during seed development compared to long-chain acyl CoAs isolated from the same tissues, sug

94 C, which inhibits the conversion of FFAs to long-chain acyl CoA (LC-CoA), enhanced basal FFA efflux

95 has been proposed that de novo synthesis of long-chain acyl-CoA (LC-CoA) is a signal for glucose-sti

96 pothesized that accumulation of amphipathic, long-chain acyl-CoA (LC-CoA) metabolites stimulates lipo

97 The long-chain acyl-CoA (LC-CoA) model of glucose-stimulated

98 e metabolic events, elevated malonyl-CoA and long-chain acyl-CoA (LC-CoA), in various tissues mediate

99 skeletal muscle, levels of triglyceride and long-chain acyl-CoA (LC-CoA)-two candidate mediators of

100 tion and promoting accumulation of cytosolic long-chain acyl-CoA (LC-CoA).

101 Long-chain acyl-CoAs (LC-acyl-CoAs) are important interm

102 csl4 knockdown did not alter FA oxidation or long chain acyl-CoA levels.

103 These results suggest that long chain acyl-CoA mediates the rise in PFK activity, w

104 he affinity of FadR for DNA is controlled by long chain acyl-CoA molecules, which bind to the protein

105 nutrients involves the proposed malonyl-CoA/long-chain acyl-CoA pathway with specificity for myristo

106 Interestingly, when primed with long chain acyl-CoAs, PhlD catalyzed extra polyketide el

107 In mycobacteria, long chain acyl-CoA products (C(14)-C(26)) generated by

108 CPTs that are very active toward medium- and long-chain acyl-CoAs, respectively, CrAT and ChAT displa

109 of iPLA2beta with oleoyl-CoA, but not other long-chain acyl-CoAs, resulted in robust stoichiometric

110 and demonstrated a 10-fold increase in very long chain acyl-CoA specific activity (C24:0/C16:0).

111 effect of fatty acid with respect to MGAT's long-chain acyl-CoA substrate in Triton X-100 mixed mice

112 ereby altering the enzyme's affinity for its long-chain acyl-CoA substrate.

113 ay a role in the binding and dissociation of long chain acyl-CoA substrates and products and poses qu

114 catalyze a Claisen-type condensation between long chain acyl-CoA substrates such as myristoyl-CoA (C(

115 d storage lipid was catabolized more slowly, long-chain acyl-CoA substrates accumulated and there was

116 urified recombinant mtFabH clearly preferred long-chain acyl-CoA substrates rather than acyl-ACP prim

117 It has preference for long-chain acyl-CoA substrates, although it is also acti

118 sistance to proteolysis, and specificity for long-chain acyl-CoA substrates.

119 ed markedly decreased expression of the very long chain acyl-CoA synthase-related gene (VLACSR), a mo

120 to its nuclear export, where it deacetylates long-chain acyl-CoA synthase 5 (ACSL5), thereby facilita

121 smic SIRT6, which deacetylates and activates long-chain acyl-CoA synthase 5 (ACSL5).

122 T activity and 50% of both CPT-I, as well as long-chain acyl-CoA synthase activity, the latter two su

123 delivery of nascent FFA from the stroma for long chain acyl-CoA synthesis (LACS) occurs via simple d

124 yl-CoA synthetase ACSL1 and ACSL3 to promote long-chain acyl-CoA synthesis and channeling into the ER

125 extracts suggested that FATP1 exhibits very long chain acyl-CoA synthetase (ACS) activity and that s

126 Long chain acyl-CoA synthetase (ACS) and diacylglycerol

127 lexes that contained not only CPT1a but also long chain acyl-CoA synthetase (ACSL) and the voltage-de

128 Long chain acyl-CoA synthetase (ACSL) catalyzes the init

129 ACSL3 is a member of the long chain acyl-CoA synthetase (ACSL) family that plays

130 ers of the fatty acid transport protein/very long chain acyl-CoA synthetase (FATP/Acsvl) family are e

131 eviously unidentified gonadotropin-regulated long chain acyl-CoA synthetase (GR-LACS) was cloned and

132 Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial

133 The very long chain acyl-CoA synthetase activity of the two enzym

134 es in specific activities of the key enzymes long chain acyl-CoA synthetase and diacylglycerol acyltr

135 These results indicate that FATP1 is a very long chain acyl-CoA synthetase and suggest that a potent

136 -MCD Delta 5 and triacsin C, an inhibitor of long chain acyl-CoA synthetase that reduces LC-CoA level

137 er carnitine palmitoyl-CoA transferase, very long chain acyl-CoA synthetase, very long chain acyl-CoA

138 that sequesters GLUT4 in fat cells contains long chain acyl-CoA synthetase-1 and its product fatty a

139 rap mass spectrometry of a p75 protein band, long chain acyl-CoA synthetase-1, specifically present i

140 ally blocked by an inhibitor (triacsin C) of long chain acyl-CoA synthetase.

141 degree of similarity to the Escherichia coli long chain acyl-CoA synthetase.

142 genous long-chain fatty acids, and have very long-chain acyl CoA synthetase activities that were 40%

143 The depression in very long-chain acyl CoA synthetase activities were not appar

144 family 27 member 4, fatty acid synthase, and long-chain acyl-CoA synthetase (3), and glucose transpor

145 ets, such as directly inhibiting recombinant long-chain acyl-CoA synthetase (ACSL)-4 activity.

146 es, including myelin, requires activation by long-chain acyl-CoA synthetase (ACSL).

147 ith a skeletal muscle-specific deficiency of long-chain acyl-CoA synthetase (ACSL)1.

148 Long-chain acyl-CoA synthetase (LACS) activities are enc

149 haliana, LACS6 and LACS7, encode peroxisomal long-chain acyl-CoA synthetase (LACS) isozymes.

150 ns carnitine palmitoyltransferase-I (CPT-I), long-chain acyl-CoA synthetase (LCAS), and voltage-depen

151 n associated with decreased peroxisomal very long-chain acyl-CoA synthetase (VLCS) activity and decre

152 ed VLCFA beta-oxidation and peroxisomal very long-chain acyl-CoA synthetase (VLCS) activity.

153 e reported previously that homolog 2 of very long-chain acyl-CoA synthetase (VLCS) can activate chola

154 adrenoleukodystrophy, are activated by very long-chain acyl-CoA synthetase (VLCS) normally found in

155 vestigate the potential relationship between long-chain acyl-CoA synthetase 1 (ACSL1) and lipid metab

156 Long-chain acyl-CoA synthetase 1 (ACSL1) plays a key rol

157 type associates with increased expression of long-chain acyl-CoA synthetase 1 (ACSL1), an enzyme that

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

159 f cardiac lipotoxicity overexpressing ACSL1 (long-chain acyl-CoA synthetase 1) in cardiomyocytes, we

160 Long-chain acyl-CoA synthetase 4 (ACSL4) catalyzes the c

161 of very long-chain fatty acid 5 (ELOVL5) and long-chain acyl-CoA synthetase 4 (ACSL4).

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

163 KEY POINTS: Long-chain acyl-CoA synthetase 6 (ACSL6) mRNA is present

164 Long-chain acyl-CoA synthetase 6 (ACSL6) mRNA is present

165 sport long-chain fatty acids and has reduced long-chain acyl-CoA synthetase activity (fat1Delta faa1D

166 n studies showed that VLCS activity, but not long-chain acyl-CoA synthetase activity, was reduced to

167 t exerted a dominant negative effect against long-chain acyl-CoA synthetase activity.

168 cids and contributes the majority of cardiac long-chain acyl-CoA synthetase activity.

169 hibit synthesis of TAGs and CEs by targeting long-chain acyl-CoA synthetase and acyl-CoA:cholesterol

170 Because CPT-I and long-chain acyl-CoA synthetase appear to be associated w

171 tably, RpPat did not acetylate the wild-type long-chain acyl-CoA synthetase B (RpLcsB; formerly Rpa27

172 ated transgenic mouse lines that overexpress long-chain acyl-CoA synthetase in the heart (MHC-ACS).

173 LACS1 thus appears to function as a very long-chain acyl-CoA synthetase in wax metabolism.

174 The long-chain acyl-CoA synthetase inhibitor triacsin C comp

175 Thus, long-chain acyl-CoA synthetase isoform 1 (ACSL1) deficie

176 Loss of long-chain acyl-CoA synthetase isoform-1 (ACSL1) in mous

177 s the activation of fatty acids by one of 13 long-chain acyl-CoA synthetase isoforms.

178 ne of the cutin pathway genes, which encodes long-chain acyl-CoA synthetase LACS2, is likely to be di

179 This study revealed a central role of the long-chain acyl-CoA synthetase LCS2 in the production of

180 ce were then crossed with animals expressing long-chain acyl-CoA synthetase via the MHC promoter (MHC

181 porter protein 2 (FATP2) (also known as very long-chain acyl-CoA synthetase) directly interacts with

182 such as diacylglycerol O-acyltransferase or long-chain acyl-CoA synthetase, effectively disrupted TA

183 A human homolog of very long-chain acyl-CoA synthetase, hVLCS-H2, has two requis

184 Addition of Triacsin-C, an inhibitor of long-chain acyl-CoA synthetase, to AdCMV-GlpK-treated IN

185 s a prodrug that requires activation by very long-chain acyl-CoA synthetase-1 (ACSVL1) to modulate bo

186 metabolism was to use triacsin C to inhibit long-chain acyl-CoA synthetase.

187 r9 showed mostly additive effects with cer6, long-chain acyl-CoA synthetase1 (lacs1), and lacs2 and r

188 oot formation because of a point mutation in Long Chain Acyl-CoA Synthetase2, a gene essential for cu

189 (CYPs) of the CYP77A and CYP86A subfamilies, LONG-CHAIN ACYL-COA SYNTHETASE2, GLYCEROL-3-PHOSPHATE SN

190 Long chain acyl-CoA synthetases (ACSL) activate fatty ac

191 Long chain acyl-CoA synthetases (ACSL) and fatty acid tr

192 cellular FA is the conversion to acyl-CoA by long chain acyl-CoA synthetases (Acsls).

193 ween the ABC transporter and the peroxisomal long chain acyl-CoA synthetases (LACS)6 and -7.

194 NGF treatment increased the activities of long chain acyl-CoA synthetases (LCASs), including oleoy

195 ase activity (C16:0), characteristic of very long chain acyl-CoA synthetases, whereas both mutant M1

196 olipid biosynthesis, as an inhibitor of host long-chain acyl CoA synthetases, key enzymes for glycero

197 ABSTRACT: Long-chain acyl-CoA synthetases (ACSL 1 to 6) are key en

198 Long-chain acyl-CoA synthetases (ACSL 1 to 6) are key en

199 Long-chain acyl-CoA synthetases (ACSLs) are key host-cel

200 The family of proteins that includes very long-chain acyl-CoA synthetases (ACSVL) consists of six

201 Long-chain acyl-CoA synthetases (LACS) play diverse and

202 acid transport proteins (FATP) and the very long-chain acyl-CoA synthetases (VLACS).

203 most recently identified family is the very long-chain acyl-CoA synthetases (VLCS).

204 AAE15 has sequence similarity to long-chain acyl-CoA synthetases and a predicted N-termin

205 ation of CER8/LACS1, one of nine Arabidopsis long-chain acyl-CoA synthetases thought to activate acyl

206 Other long- and very long-chain acyl-CoA synthetases were incapable of activa

207 Recent findings indicate that inhibition of long-chain acyl-CoA synthetases with triacsin C, a fatty

208 ealed that it encodes LACS2, a member of the long-chain acyl-CoA synthetases.

209 ling showed a fatty acid-induced increase in long chain acyl-CoAs that were rapidly esterified with g

210 , for example, by altering protein levels of long-chain acyl-CoA thioester hydrolase and adipophilin

211 Thioesterase III was shown to be a long-chain acyl-CoA thioesterase that is most active wit

212 responsive genes and operons is inhibited by long chain acyl-CoA thioesters but not free fatty acids

213 eased from the promoter upon the addition of long-chain acyl-CoA thioesters.

214 sis of the hydrolysis of cytosolic medium-to-long-chain acyl-CoA thioesters.

215 ial oxidative energy metabolism by restoring long-chain acyl CoA through ASCL1 activation and mechani

216 ve subunit cooperativity enhances binding of long chain acyl-CoAs to this sulfotransferase.

217 step in beta oxidation is the conversion of long-chain acyl-CoA to acylcarnitine, a reaction catalyz

218 oyltransferase I catalyzes the conversion of long-chain acyl-CoA to acylcarnitines in the presence of

219 ABCD2 (D2) is a peroxisomal long-chain acyl-CoA transporter that is highly induced b

220 el response to membrane phospholipids and/or long chain acyl-CoAs underlies the low intrinsic open pr

221 Long-chain acyl CoA was similarly reduced in human faili

222 ent is 3.8 for lauroyl-CoA, but decrease for long chain acyl-CoAs, where the Hill coefficient is only

223 FadE1 displays a strong preference for long-chain acyl-CoAs, whereas FadE2 exclusively utilizes

224 y to load atypical extender units, unusually long chain acyl-CoA with a predilection for carboxylated

225 As a result, we found that MftR binds to long-chain acyl-CoAs with low micromolar affinities.