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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 lability of glycerol-3-phosphate (Gro3P) and fatty acyl-CoA.
5 and a final reduction to form the elongated fatty acyl-CoA.
6 tional activation is prevented by long chain fatty acyl-CoA.
7 or, triacsin C, evidence of its mediation by fatty acyl-CoA.
8 inhibited by ACPSH but not by fatty acid or fatty-acyl CoA.
9 s that catalyze the hydrolysis of long chain fatty acyl CoAs.
10 atalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs.
11 t activity toward the long chain unsaturated fatty acyl-CoAs.
12 no change in the concentration of any other fatty acyl-CoAs.
13 roduces the first double bond into saturated 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 odimerize and form peroxisomal importers for fatty acyl-CoAs.
17 st both saturated and unsaturated long-chain fatty acyl-CoAs.
18 erase activity which catalyzes hydrolysis of fatty acyl-CoAs.
24 tion results in an increase in intracellular fatty acyl-CoA and DAG concentrations, which results in
25 T2 activity was dependent on the presence of fatty acyl-CoA and diacylglycerol, indicating that this
26 transporters, led accumulation of long-chain fatty acyl-coA and triacylglycerol in insulin-resistant
27 coded ceramide synthases use very-long-chain fatty acyl-CoA and trihydroxy LCB substrates, and LOH2 (
28 rsors for phosphatidic acid (PA) (long-chain fatty acyl-CoAs and lysophosphatidic acid [LPA]) were no
29 ted clear preference to long chain saturated fatty acyl-CoAs and oleoyl-CoA as acyl donors, which is
30 ve with both medium-and long-chain saturated fatty acyl-CoAs and showed maximal activity with C14-CoA
31 low micromolar concentrations of long chain fatty acyl-CoAs and the non-hydrolyzable thioether analo
32 gands are in the nanomolar range, long chain fatty acyl-CoAs and unsaturated fatty acids may both rep
33 to the similar affinities of PPAR alpha for fatty acyl-CoAs and unsaturated fatty acids, CoA thioest
35 nizes a broad range of medium and long chain fatty acyl-CoA, and its activity was not affected by Ca(
36 CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid int
41 r fatty acid-acyl carrier protein (ACP) over fatty acyl-CoA as the acyl substrate for signal synthesi
42 4 nM K(d) values) for unsaturated long chain fatty acyl-CoAs as well as unsaturated long chain fatty
44 rict control of the metabolism of long-chain fatty acyl-CoAs because of the multiplicity of their cel
48 2-6His hydrolyzes both medium and long chain fatty acyl-CoAs but has highest activity toward the long
49 oA thioesterase (Acot) gene family hydrolyze fatty acyl-CoAs, but their biological functions remain i
50 Acot) gene family catalyze the hydrolysis of fatty acyl-CoAs, but their biological functions remain u
51 ming; EC 6.2.1.3) catalyzes the formation of fatty acyl-CoA by a two-step process that proceeds throu
52 (ACBP) stimulates utilization of long-chain fatty acyl-CoA by a variety of membrane-bound enzymes, i
53 atalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs by branched-chain acyl-CoA oxidase (pris
57 the time trends in activities depend on the fatty-acyl CoA chain lengths of the different ceramide s
60 the catalytic alpha,beta-dehydrogenation of fatty acyl-CoAs consists of two C-H bond dissociation pr
61 old increase in liver triglyceride and total fatty acyl-CoA content without any significant increase
62 iated with 30% increases in triglyceride and fatty acyl-CoA contents in the liver of rosiglitazone-tr
63 iated with 50% decreases in triglyceride and fatty acyl-CoA contents in the skeletal muscle of rosigl
64 ed to a significant reduction in heart total fatty acyl-CoA (control, 99.5 +/- 3.8; hLpL0, 36.2 +/- 3
65 -1) (P < 0.05) after acipimox; intramuscular fatty acyl CoA decreased from 10.3 +/- 1.9 to 4.54 +/- 0
67 te dehydrogenase kinase, medium-chain length fatty acyl-CoA dehydrogenase, ubiquinone-cytochrome c re
68 broad range of substrate specificity toward fatty acyl-CoA derivatives and monoacylglycerols, among
69 in (ACBP) has high affinity for medium chain fatty acyl-CoAs, direct interaction of ACBP with >14-car
70 ed 10-18-carbon and unsaturated 14-20-carbon fatty acyl-CoAs displaced SCP-2-bound fluorescent ligand
73 HNF-4alphaLBD intrinsic Trp fluorescence by fatty acyl-CoAs (e.g. pamitoyl-, stearoyl-, linoleoyl-,
74 action is the initial step of the microsomal fatty acyl-CoA elongation pathway responsible for format
75 fatty acids and the subsequent reduction of fatty acyl-CoAs enabled the efficient synthesis of fatty
76 ated fatty acids (e.g. arachidonic acid) and fatty acyl-CoA esters (e.g. arachidonoyl-CoA) has been r
78 dely expressed protein that binds long-chain fatty acyl-CoA esters and plays a role in fatty acyl-CoA
79 concentrations of five individual long-chain fatty acyl-CoA esters extracted from muscle tissue sampl
84 of the peroxisome to hijack the medium chain fatty acyl-CoA generated from the beta-oxidation pathway
85 e activity of iPLA 2beta can lead to reduced fatty acyl-CoA generation and impair fatty acid oxidatio
89 effect on cholesterol transfer, and 5 mol % fatty acyl-CoAs increased transfer rates, demonstrating
90 yme catalyzes the synthesis of omega-hydroxy fatty acyl-CoA intermediates in the pathway to cutin syn
91 esaturase, an enzyme that converts saturated fatty acyl-CoAs into cis-Delta-9 unsaturated fatty acids
92 Escherichia coli catalyzed the oxidation of fatty acyl-CoAs into trans-2-enoyl-CoA and produced H2 O
95 Increases in intramyocellular long-chain fatty acyl-CoAs (LCACoA) have been implicated in the pat
96 chain fatty acid (LCFA) but also long chain fatty acyl CoA (LCFA-CoA), the physiological significanc
97 Although it is hypothesized that long-chain fatty acyl CoAs (LCFA-CoAs) and long-chain fatty acids (
98 long chain fatty acid (LCFA) and long chain fatty acyl-CoA (LCFA-CoA) binding site(s) remains to be
99 binding protein ACBP may modulate long-chain fatty acyl-CoA (LCFA-CoA) distribution, its physiologica
100 high affinity (Kd=0.06-12 nm) for long chain fatty acyl-CoAs (LCFA-CoA) and low affinity (Kd=58-296 n
101 estore the hypothalamic levels of long-chain fatty acyl-CoAs (LCFA-CoAs) and to normalize food intake
104 om K(d) values) obtained with a radiolabeled fatty acyl-CoA ligand binding assay raised questions reg
107 -related lipopeptide, was mis-annotated as a fatty acyl-CoA ligase; however, it is in fact a FAAL tha
109 ycle proteins and co-transfected with either fatty acyl:CoA ligases (ACSLs) 1, 3, or 6 or the SLC27A
112 ed the levels of triacylglycerol, long-chain fatty acyl-coA, malonyl-CoA, fatty acid oxidation, AMP-a
113 m iPLA(2)gamma(-/-) mice were insensitive to fatty acyl-CoA-mediated augmentation of calcium-induced
115 Collectively, these results demonstrate that fatty acyl-CoA modulates phosphofructokinase activity th
116 A binding protein (ACBP) maintains a pool of fatty acyl-CoA molecules in the cell and plays a role in
117 in the endoplasmic reticulum, where each use fatty acyl-CoAs of defined chain length for ceramide syn
118 e cytochrome P450 enzyme CYP86A22 is the key fatty acyl-CoA omega-hydroxylase essential for the produ
119 tochrome P450 gene CYP86A22, which encodes a fatty acyl-CoA omega-hydroxylase involved in estolide bi
120 effects of saturated versus polyunsaturated fatty acyl-CoAs on HNF-4alpha LBD secondary structure co
123 ion system, which consists of three enzymes: fatty acyl-CoA oxidase (ACOX), enoyl-CoA hydratase/3-hyd
126 t in PPARalpha (PPARalpha(-/-)), peroxisomal fatty acyl-CoA oxidase (AOX(-/-)), and in both PPARalpha
127 ta-oxidation pathway in mice at the level of fatty acyl-CoA oxidase (AOX), the first and rate-limitin
129 oxisome proliferators, whereas those lacking fatty acyl-CoA oxidase (AOX-/-), the first enzyme of the
131 n phytanoyl-CoA alpha hydroxylase (PAHX) and fatty acyl-CoA oxidase (FACO) mRNA levels during differe
132 efective in ACX1, ACX3, or ACX4 have reduced fatty acyl-CoA oxidase activity on specific substrates.
134 transfected with H2O2-generating peroxisomal fatty acyl-CoA oxidase cDNA, which encodes the first and
137 PPAR alpha and of the classical peroxisomal fatty acyl-CoA oxidase in energy metabolism, and in the
139 om mice deficient in PPAR alpha, peroxisomal fatty acyl-CoA oxidase, and some of the other enzymes of
140 ased expression of mRNAs for the peroxisomal fatty acyl-CoA oxidase, bifunctional enzyme, or thiolase
141 le of catalyzing straight-chain acyl-CoAs by fatty acyl-CoA oxidase, L-bifunctional protein, and thio
143 catalyzed hydrolysis of saturated long-chain fatty acyl-CoAs (palmitoyl-CoA approximately myristoyl-C
144 arboxylase 2 [ACC2], a critical regulator of fatty acyl-CoA partitioning between cytosol and mitochon
145 responsible for the biosynthesis of the 16:3 fatty acyl-CoA precursor, we identified and cloned three
148 ited broad starter-unit specificities toward fatty acyl-CoAs ranging in sizes between C6 and C16 and
151 ion in jojoba requires, in addition to WS, a fatty acyl-CoA reductase (FAR) and an efficient fatty ac
152 oduced in yeast via targeted expression of a fatty acyl-CoA reductase (TaFAR) in the peroxisome of Sa
154 in another gene in plasmalogen biosynthesis, fatty acyl-CoA reductase 1 (FAR1), in two families affec
156 A 23mer His-based peptide derived from human fatty acyl-CoA reductase 1 in complex with heme exhibite
158 synthesis in mammals is accomplished by two fatty acyl-CoA reductase isozymes that are expressed at
159 of CER4-6, which encodes an alcohol-forming fatty acyl-CoA reductase, was elevated 120-fold in iw1Iw
162 bited high affinity for saturated long chain fatty acyl-CoAs, regardless of chain length (1-13 nM K(d
163 er axis involving accumulation of long-chain fatty acyl-CoA, release of cholecystokinin, and subseque
166 chain acyl-CoA synthetase-1 and its product fatty acyl-CoA, shown previously to be required for budd
167 hase activity that utilizes an atypical 16:3 fatty acyl-CoA starter unit, resulting in the formation
169 RS enzymes capable of accepting a variety of fatty acyl-CoA starter units in recombinant enzyme studi
170 -alkylresorcinols using medium to long-chain fatty acyl-CoA starter units via iterative condensations
171 ch increased the SPT affinity toward the C18 fatty acyl-CoA substrate by twofold and significantly el
172 i 2,4-dienoyl-CoA reductase with NADP+ and a fatty acyl-CoA substrate reveals a possible mechanism fo
175 a higher specific activity toward long-chain fatty acyl-CoA substrates (palmitoyl-CoA and eicosapenta
178 purified protein was shown to be active with fatty acyl-CoA substrates that ranged from C(8) to C(16)
179 iolase superfamily enzyme that condenses two fatty acyl-CoA substrates to produce a beta-ketoacid pro
181 instead produced triketide alkylpyrones from fatty acyl-CoA substrates with shorter chain lengths.
187 y acid transport related proteins as well as fatty acyl CoA synthase are expressed in keratinocytes a
188 ome proliferator response element-containing fatty acyl CoA synthase gene, although it cannot be rule
189 ve fatty acid transport related proteins and fatty acyl CoA synthase, an enzyme that facilitates the
190 ases (ACSLs) 1, 3, or 6 or the SLC27A family fatty acyl-CoA synthase FATP2/SLCA27A2 to test their eff
191 GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related pr
192 apidly converted to 5HD-CoA by mitochondrial fatty acyl CoA synthetase and acted as a weak substrate
193 mportant lysine residue in a number of FadD (fatty acyl CoA synthetase) enzymes is acetylated by KATm
194 ochondrial HMG-CoA synthase and increases in fatty acyl-CoA synthetase (3-8-fold) and carnitine palmi
199 uced function of peroxisomal very long chain fatty acyl-CoA synthetase (VLCS) that leads to severe an
201 the fatty acid transport and very long-chain fatty acyl-CoA synthetase activities were distinguishabl
202 of fatty acid accumulation, very long-chain fatty acyl-CoA synthetase activities, and the fatty acid
203 lted in either wild-type or nearly wild-type fatty acyl-CoA synthetase activity profiles; 2) those th
205 d vacuolar morphology through the long-chain fatty acyl-CoA synthetase Faa1, independently of the RNA
208 s, suppression was completely blocked by the fatty acyl-CoA synthetase inhibitor, triacsin C, evidenc
209 We propose that this sequence represents the fatty acyl-CoA synthetase signature motif (FACS signatur
210 ing the ATP/AMP binding domain and the 25-aa fatty acyl-CoA synthetase signature motif, but displays
211 Eighteen site-directed mutations within the fatty acyl-CoA synthetase structural gene (fadD) corresp
212 Fatty acid transport protein 4 (FATP4) is a fatty acyl-CoA synthetase that preferentially activates
215 were reversed by triacsin C, an inhibitor of fatty acyl-CoA synthetase, the enzyme that generates LC-
219 ce, DGWLHTGDIGXWXPXGXLKIIDRKK, common to all fatty acyl-CoA synthetases for which sequence informatio
221 he family of both prokaryotic and eukaryotic fatty acyl-CoA synthetases, indicating a common ancestry
223 ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in ins
225 d that membranes from infected cells possess fatty acyl-CoA thioesterase activity, which is stimulate
226 em2) is a mitochondria-associated long-chain fatty acyl-CoA thioesterase that is activated upon bindi
227 fat inducible thioesterase) is a long-chain fatty acyl-CoA thioesterase that is highly expressed in
228 odel and experimental analysis indicate that fatty acyl CoA thioesters, the proposed HNF4alpha ligand
230 esterase activity directed toward long chain fatty acyl-CoA thioesters, thus distinguishing the catal
232 an indirect route of provision of ER luminal fatty acyl-CoA through a luminal carnitine acyltransfera
235 tilizes lysophosphatidylcholine (LysoPC) and fatty acyl-CoA to produce various phosphatidylcholine (P
236 ected ion monitoring was used to analyze the fatty acyl-CoAs to achieve reliable quantification of th
237 PT) I catalyzes the conversion of long-chain fatty acyl-CoAs to acyl carnitines in the presence of l-
239 CPTI) catalyzes the conversion of long-chain fatty acyl-CoAs to acylcarnitines in the presence of l-c
240 nd CPT1b catalyze acyl transfer from various fatty acyl-CoAs to carnitine, whereas CPT1c does not.
241 esterases (Acots) catalyze the hydrolysis of fatty acyl-CoAs to form free fatty acids plus CoA, but t
242 catalyzes the flavin-dependent oxidation of fatty acyl-CoAs to the corresponding trans-2-enoyl-CoAs.
245 rated that high affinity ligands (long chain fatty acyl-CoAs, unsaturated fatty acids), but not weak
248 h catalyzes the conversion of fatty acids to fatty acyl-CoA, was inhibited with triacsin C, the incre
251 ence of elevated tissue levels of long-chain fatty acyl CoA, which can impair beta-cell cell function
253 -binding cassette (ABC) half-transporters of fatty acyl-CoAs with both distinct and overlapping subst
254 Thus, native liver ACBP binds >14-carbon fatty acyl-CoAs with nanomolar affinity at a single bind
255 resistance and intramuscular accumulation of fatty acyl-CoA without alteration in whole-body adiposit
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