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1 commodates nevanimibe and an endogenous acyl-coenzyme A.
2 d to be essential for PvrA to bind palmitoyl coenzyme A.
3 ulation of citrate, the precursor for acetyl coenzyme A.
4 is from lysophosphatidic acid (LPA) and acyl-coenzyme A.
6 s conversion of acetyl coenzyme A to malonyl coenzyme A, a carbon donor for long-chain FA synthesis,
8 DIP2A) is known to be involved in acetylated coenzyme A (Ac-CoA) synthesis and is primarily expressed
9 the transfer of an acetyl group from acetyl-coenzyme A (Ac-CoA) to the amine of a wide range of subs
10 with inositol hexaphosphate (InsP6), acetyl-coenzyme A (AcCoA) and/or substrate Resistance to Ralsto
12 at catalyzes pyruvate's conversion to acetyl coenzyme A (AcCoA), thereby connecting these two pathway
13 ne residues by employing the cofactor acetyl-coenzyme A (AcCoA), thereby providing a dynamic control
15 ased levels of acetyl phosphate, acetoacetyl coenzyme A (acetoacetyl-CoA), butyryl CoA, acetoacetate,
16 d ferredoxin for glucose oxidation to acetyl coenzyme A (acetyl-CoA) and CO2, NADH for the reduction
17 in conversion of acetyl phosphate to acetyl-coenzyme A (acetyl-CoA) and posttranscriptionally regula
19 Acetate and the related metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic functi
21 t can also catalyze the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an arylamine s
26 rnative carbon source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.
27 ferentiation in a manner dependent on acetyl coenzyme A (acetyl-CoA) production by the enzyme ATP-cit
29 esis by suppressing the expression of acetyl coenzyme A (acetyl-CoA) synthetase (Acss), leading to de
30 s cycle, glyoxylate is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes
31 te lyase (ACLY) synthesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular building
32 d is sensitive to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for meta
34 e, enabling biosynthesis of cytosolic acetyl coenzyme A (acetyl-CoA, the two-carbon isoprenoid precur
35 e oxidation to fuel the production of acetyl coenzyme A, acetylation of histones and induction of gen
36 n architecturally distinct subfamily of acyl coenzyme A (acyl-CoA) dehydrogenase (ACAD) enzymes that
38 the transport of cytoplasmic long chain acyl-coenzyme A (acyl-CoA) into the mitochondrial matrix, whi
41 activity of the long-chain cytoplasmic acyl coenzyme A (acyl-CoA) thioesterase 7 (ACOT7) to regulate
42 nd di-, poly-, and persulfide derivatives of coenzyme A, although polysulfide itself is also efficien
43 PqsBC catalyzes the condensation of octanoyl-coenzyme A and 2-aminobenzoylacetate (2-ABA) to form the
44 best inhibitors are competitive with acetyl coenzyme A and an X-ray cocrystal structure reveals that
46 amide synthase that uses C16 fatty acid acyl-coenzyme A and dihydroxy LCB substrates but increased ac
47 e enzyme phosphotransacylase (PTAC) recycles Coenzyme A and generates an acyl phosphate that can serv
50 he downstream metabolites, including malonyl-coenzyme A and palmitic acid, completely restored the in
56 imidine, isoprenoid, methionine, riboflavin, coenzyme A, and folate, as well as other biosynthetic pa
57 th 3,5-dihydroxybenzoic acid, ATP, malonate, coenzyme A, and the malonyl-CoA ligase MatB, venemycin p
59 s the polymerization of 3-(R)-hydroxybutyryl-coenzyme A as a means of carbon storage in many bacteria
62 eracting partner, Golgi adaptor protein acyl-coenzyme A binding domain containing protein 3 (ACBD3).
63 uncover that the Golgi resident protein acyl-coenzyme A binding domain-containing 3 (ACBD3) serves as
64 emperature as the different variants of acyl-coenzyme A binding protein have similar m-values when th
66 re, we identify the PO membrane protein acyl-coenzyme A-binding domain protein 5 (ACBD5) as a binding
67 Low-molecular mass (10 kD) cytosolic acyl-coenzyme A-binding protein (ACBP) has a substantial infl
69 SAR-related proteins THIOREDOXIN h3, ACYL-COENZYME A-BINDING PROTEIN6, and PATHOGENESIS-RELATED1 w
73 ctivated protein kinase activation of acetyl-coenzyme A carboxylase (ACC) and increased lipid content
77 ort into mitochondria via deletion of acetyl coenzyme A carboxylase 2 (ACC2) does not cause cardiomyo
78 tural environments, where heteromeric acetyl-coenzyme A carboxylase encoded in part by the chloroplas
79 d nuclear gene that targets homomeric acetyl-coenzyme A carboxylase to plastids, where the multidomai
81 in ACC2, encoding a plastid-targeted acetyl-coenzyme A carboxylase, cause hypersensitivity to specti
82 DI-010976, an allosteric inhibitor of acetyl-coenzyme A carboxylases (ACC) ACC1 and ACC2, reduces hep
84 3) Direct acetyl transfer between LD and coenzyme A catalyzed by E2pCD was observed with a rate c
86 physical interaction of the major SOAT, acyl-coenzyme A:cholesterol acyltransferase (ACAT)-related en
87 ress the cholesterol-esterifying enzyme acyl-coenzyme A:cholesterol acyltransferase (ACAT1), but not
88 sterol O-acyltransferase 1 (also named acyl-coenzyme A:cholesterol acyltransferase, ACAT1) transfers
89 -acyltransferase (MBOAT) enzyme family, acyl-coenzyme A:cholesterol acyltransferases (ACATs) catalyse
93 ched-chain amino acid metabolism, isovaleryl-Coenzyme A (CoA) and isobutyryl-CoA, with three molecule
94 N-acyltransferase reaction using fatty acyl-coenzyme A (CoA) and long-chain base (LCB) substrates to
97 olution crystal structure of AF-Est2 reveals Coenzyme A (CoA) bound in the vicinity of the active sit
99 roduce mm flux through the key fluoromalonyl coenzyme A (CoA) building block, thereby offering the po
101 (OG) is a small molecule inhibitor of acetyl coenzyme A (CoA) carboxylase (ACC), the enzyme that cont
102 kinase (AMPK) levels, and diminished acetyl coenzyme A (CoA) carboxylase phosphorylation than in the
105 The Arabidopsis (Arabidopsis thaliana) acyl-coenzyme A (CoA) desaturase-like (ADS) gene family conta
106 ly conserved ER protein FIT2 as a fatty acyl-coenzyme A (CoA) diphosphatase that hydrolyzes fatty acy
107 catalyzes the reduction of hydroxycinnamoyl-coenzyme A (CoA) esters using NADPH to produce hydroxyci
108 metabolic machinery for the biosynthesis of Coenzyme A (CoA) from exogenous pantothenic acid (Vitami
109 directed metabolic fluxes to generate acetyl-Coenzyme A (CoA) from glucose resulting in augmented his
110 nome of MLL-rearranged AML by linking acetyl-coenzyme A (CoA) homeostasis to Bromodomain and Extra-Te
111 eport the identification of a putative enoyl-coenzyme A (CoA) hydratase/isomerase that is required fo
113 ty of SPT, allowing utilization of myristoyl-coenzyme A (CoA) in addition to its canonical substrate
116 zyme DmdB, a methylmercaptopropionate (MMPA)-coenzyme A (CoA) ligase, catalyzes the second step in th
117 DmdB, a 3-methylmercaptopropionate (MMPA)-coenzyme A (CoA) ligase, undergoes two sequential confor
119 o enzymes, Ptr4CL3 and Ptr4CL5, catalyze the coenzyme A (CoA) ligation of 4-coumaric acid to 4-coumar
121 ation of the meta-hydroxyl group of caffeoyl-coenzyme A (CoA) on the pathway to monolignols, with the
122 ity were correlated with changes in the acyl-coenzyme A (CoA) pool in developing seeds of transgenic
123 cate that YacG is frequently associated with coenzyme A (CoA) production enzymes, linking the protein
124 levels of intermediate and anaplerotic acyl-coenzyme A (CoA) species incorporated into the Krebs cyc
126 carbon-carbon bond forming step between acyl coenzyme A (CoA) substrates offer a versatile route for
128 essive missense mutations in COASY, encoding coenzyme A (CoA) synthase in one NBIA-affected subject.
129 rase superfamily member 2 (Them2) is an acyl-coenzyme A (CoA) thioesterase that catalyzes the hydroly
130 tochondrion-associated long-chain fatty acyl coenzyme A (CoA) thioesterase that is highly expressed i
132 the ATP-dependent conversion of citrate and coenzyme A (CoA) to oxaloacetate and acetyl-CoA(1-5).
134 lysophosphatidylethanolamine (LPE) with acyl-coenzyme A (CoA), designated LYSOPHOSPHATIDYLETHANOLAMIN
137 ate generated during synthesis of fatty acyl-coenzyme A (CoA), the reaction catalyzed by an enzyme in
139 ing the final and committed step in the acyl-coenzyme A (CoA)-dependent biosynthesis of triacylglycer
140 metabolites into 4-methyl-pentanol (4MP) via coenzyme A (CoA)-dependent chemistry were taken from nin
149 ative abundance of the gene encoding butyryl-coenzyme A (CoA):acetate-CoA-transferase, a major enzyme
150 eneration (PKAN) and result in low levels of coenzyme-A (CoA) in the CNS due to impaired production o
152 ecreased the expression of medium-chain acyl coenzyme A dehydrogenase (MCAD) and short-chain acyl coe
153 A dehydrogenase (MCAD) and short-chain acyl coenzyme A dehydrogenase (SCAD), involved in the regulat
154 h (enoyl-coenzyme A, hydratase/3-hydroxyacyl coenzyme A dehydrogenase)], and a marker of proximal tub
155 mical analyses showed lower beta-hydroxyacyl coenzyme-A dehydrogenase activity and higher lactate deh
157 rrier protein) synthase (ACPS) catalyzes the coenzyme A-dependent activation of apo-ACPP to generate
158 wo separable mechanisms: dampening of acetyl-coenzyme A-dependent carbon metabolism through histone h
159 unable to convert free fatty acids to their coenzyme A derivatives, accumulates free fatty acids dur
162 es, we conducted a mouse trial of a stearoyl-coenzyme A desaturase (SCD) inhibitor ("5b") that preven
164 0 (P = 1.6 x 10(-8)) as a marker of stearoyl coenzyme A desaturase 1 activity, and the ratio of 20:3n
165 abolism genes (fatty acid synthase, stearoyl-coenzyme A desaturase 1, and perilipin 2) was drasticall
166 This review provides an overview of stearoyl-coenzyme A desaturase-1 (SCD1) as a novel therapeutic ta
168 ate (P-HPD, an isomer of AI-2-phosphate) and coenzyme A, determine the crystal structure of an LsrF c
169 of increased or decreased expression of ACYL-COENZYME A:DIACYLGLYCEROL ACYLTRANSFERASE1 (DGAT1) or PH
170 one (line CL37) or together with castor acyl:coenzyme A:diacylglycerol acyltransferase2 reduced HFA a
171 ex (PDHc), which converts pyruvate to acetyl coenzyme A, enables E. coli to resist these antimicrobia
172 uided mutational analyses suggests that acyl-coenzyme A enters the active site through the cytosolic
174 es high carbon flux through the ethylmalonyl coenzyme A (ethylmalonyl-CoA) pathway (EMC pathway).
176 lism; this limits the availability of acetyl coenzyme A for histone acetylation at genes encoding inf
177 group of N(10)-formyl-THF to produce formyl-coenzyme A (formyl-CoA) as a central reaction intermedia
178 The biosynthesis of the major acyl carrier Coenzyme A from pantothenic acid (PA) is critical for su
180 interestingly, we also identified endogenous coenzyme A glutathione disulfide (CoA-S-S-G) in tissue f
181 tein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) has been linked t
182 ts under regular 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatm
183 Until recently, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have
184 e shown that the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors known as stati
188 The mevalonate [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase] pathway synthesizes lipi
189 y acid-binding protein 1), and Ehhadh (enoyl-coenzyme A, hydratase/3-hydroxyacyl coenzyme A dehydroge
190 razinamide (PZA), interrupts biosynthesis of coenzyme A in Mycobacterium tuberculosis by binding to a
192 degradation through hydration of the dienoyl-coenzyme A intermediate as observed in Geobacter metalli
198 o and activated the promoters of 4-coumarate:coenzyme A ligase genes (Os4CL3 and Os4CL5) resulting in
199 that the gene encoding a specific cinnamate coenzyme A ligase likely obtained its new function follo
200 n Escherichia coli, synthesis of the malonyl coenzyme A (malonyl-CoA) required for membrane lipid syn
205 tion, we cloned and characterized a caffeoyl-coenzyme A O-methyltransferase (PhCCoAOMT1) from the pet
206 ed protein (Adrp), whereas it augmented acyl-coenzyme A oxidase 1 (Acox-1), proliferator-activated re
207 lytic transport involving sliders (including coenzyme A) picking up, transporting and selectively del
208 s and in vivo rescue potential of the acetyl-Coenzyme A precursor S-acetyl-4'-phosphopantetheine as a
209 One therapeutic strategy is to generate Coenzyme A precursors downstream of the defective step i
211 spectrometric sequencing: a hydroxycinnamoyl-Coenzyme A:quinate hydroxycinnamoyl transferase (HQT) wa
214 olesterol, in the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) activity, and in the in vit
216 ombination with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) inhibitor (statin), will re
217 in Npc1a weakens the ability of ectopic HMG Coenzyme A reductase (Hmgcr) to induce germ cell migrati
218 the formation of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), a main regulator of choles
219 thway upstream of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the target of statins.
220 ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), which catalyzes a rate-lim
224 ncoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR; the target of statins) as i
225 interfering with 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGR) activity, a key player in is
226 tylase (HDAC) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) by having a hydroxamate grou
228 Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) can modulate inflammatory
229 Inhibitors of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase and isoprenylation attenuated, wher
231 AHA/ACC) changed 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) eligibility crit
232 indications for 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) therapy than mid
233 es of the influence of hydroxymethylglutaryl-coenzyme A reductase inhibitors (also known as statins)
236 ering properties, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have broad ant
240 ted with elevated 3-hydroxy-3-methylglutaryl-coenzyme A reductase mRNA levels and anti-Src-Tyr416 imm
241 inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway to protect against infectio
242 osynthetic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase results from its sterol-induced bin
243 non-initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase therapy in patients with cirrhosis
244 roxylase) and ccr1g (deficient for cinnamoyl-coenzyme A reductase) lines, albeit to a lower extent.
245 protein 2, human 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and human low-density lipoprotein
246 e-limiting enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and increased plasma membrane chol
247 by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are among the most widely prescrib
248 family B member 1, peroxisomal trans-2-enoyl-coenzyme A reductase, phospholipase A2 receptor, protein
249 emia, inhibit the 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme of de nov
250 ically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which is a rate-limiting enzyme fo
252 rget of pitavastatin, hydroxymethylglutarate coenzyme-A reductase (HMGCR), was found to be over-expre
253 tins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors, are drugs with multipl
256 he genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1) and MAKIBISHI1, the rate-l
257 1) and CER3 catalyzes the conversion of acyl-Coenzyme A's to alkanes with strict substrate specificit
258 ctly dependent on metabolites such as acetyl-coenzyme A, S-adenosylmethionine, and NAD+, among others
259 olignol biosynthetic enzyme hydroxycinnamoyl coenzyme A:shikimate hydroxycinnamoyl transferase (HCT)
264 onfirmed the role of a hydroxymethylglutaryl-coenzyme A synthase cassette, three flavin-dependent tai
265 ein-based model for the NiP center of acetyl coenzyme A synthase using a nickel-substituted azurin pr
266 nic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty acid synthase, and stearoyl-C
269 this study is to explore parasite fatty acyl-coenzyme A synthetase (ACS) as a novel drug target.
274 Although many Archaea have AMP-Acs (acetyl-coenzyme A synthetase) and ADP-Acs, the extant methanoge
276 ctroscopy, the cutin mutants long-chain acyl-coenzyme A synthetase2 (lacs2), permeable cuticle1 (pec1
277 enin polyketide biosynthetic metabolon (ACYL COENZYME A SYNTHETASE5, POLYKETIDE SYNTHASE A [PKSA], PK
278 is activation is mediated by long-chain acyl-coenzyme A synthetases (LACSs), which are encoded by a f
280 cycle for the generation of cytosolic acetyl-coenzyme A that can be used for fatty acid and cholester
281 need to be converted to their corresponding coenzyme A thioesters to become metabolically available.
283 talyze the sequential esterification of acyl-coenzyme A thioesters to the R4, R3, R3', and R2 positio
286 lyse the transfer of an acyl group from acyl-coenzyme A to cholesterol to generate cholesteryl ester,
287 LDHA maintains high concentrations of acetyl-coenzyme A to enhance histone acetylation and transcript
288 n enzyme that catalyzes conversion of acetyl coenzyme A to malonyl coenzyme A, a carbon donor for lon
289 the transfer of an acetyl group from acetyl coenzyme A to polyamines such as spermidine and spermine
292 ons suggested that SvBAHD05 is a p-coumaroyl coenzyme A transferase (PAT) mainly involved in the addi
294 ith the high carbon efficiency drive, acetyl-coenzyme A was entirely produced using the carbon-effici
295 the synthesis of nicotinate, NAD+, NADP+ and coenzyme A were detected among the essential vitamins an
296 for their mission: E1 and E2 generate acetyl-coenzyme A, whereas the FAD/NAD(+)-dependent E3 performs
297 onverted to the central intermediate benzoyl-coenzyme A, which is enzymatically reduced to cyclohexa-
298 used cysteine to synthesize glutathione and coenzyme A, which, together, down-regulated ferroptosis.
299 ich decarboxylates pyruvate and forms acetyl-coenzyme A with concomitant reduction of low-potential f
300 he transfer of an acetyl group from P-HPD to coenzyme A yielding dihydroxyacetone phosphate and acety