ライフサイエンスコーパス: long-chain acyl-CoA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 10:0 CoA during seed development compared to long-chain acyl CoAs isolated from the same tissues, sug

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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