ライフサイエンスコーパス: coenzyme

1 to l-idonic acid and uses NADPH as preferred coenzyme.

2 drogenase to generate alanine with NADH as a coenzyme.

3 ith the 5'-deoxyadenosyl moiety of the B(12) coenzyme.

4 biosynthesis of this universally distributed coenzyme.

5 romatic dehalogenase that does not require a coenzyme.

6 forms, and in complex with the nicotinamide coenzyme.

7 DIP2A) is known to be involved in acetylated coenzyme A (Ac-CoA) synthesis and is primarily expressed

8 with inositol hexaphosphate (InsP6), acetyl-coenzyme A (AcCoA) and/or substrate Resistance to Ralsto

9 at catalyzes pyruvate's conversion to acetyl coenzyme A (AcCoA), thereby connecting these two pathway

10 ne residues by employing the cofactor acetyl-coenzyme A (AcCoA), thereby providing a dynamic control

11 gosome biogenesis via its metabolite, acetyl-coenzyme A (AcCoA).

12 ased levels of acetyl phosphate, acetoacetyl coenzyme A (acetoacetyl-CoA), butyryl CoA, acetoacetate,

13 Coenzyme A (CoA) and acetyl-coenzyme A (acetyl-CoA) are ubiquitous cellular molecule

14 Acetate and the related metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic functi

15 Acetyl coenzyme A (acetyl-CoA) generated from glucose and aceta

16 t can also catalyze the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an arylamine s

17 Metabolic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acetylation

18 riglycerides, suggesting an increased acetyl coenzyme A (acetyl-CoA) load.

19 tochondrial homeostasis by regulating acetyl-coenzyme A (acetyl-CoA) metabolism.

20 rnative carbon source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

21 The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element f

22 s cycle, glyoxylate is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes

23 te lyase (ACLY) synthesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular building

24 d is sensitive to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for meta

25 demonstrate that A-485 competes with acetyl coenzyme A (acetyl-CoA).

26 e, enabling biosynthesis of cytosolic acetyl coenzyme A (acetyl-CoA, the two-carbon isoprenoid precur

27 tion process is the recognition of free acyl coenzyme A (acyl-CoA) from the lipid bilayer.

28 the transport of cytoplasmic long chain acyl-coenzyme A (acyl-CoA) into the mitochondrial matrix, whi

29 tion of enzymes regulating long-chain acetyl-coenzyme A (Acyl-CoA) metabolism.

30 Acetate, a precursor of acetyl coenzyme A (CoA) (a product of fatty acid beta-oxidation

31 Coenzyme A (CoA) and acetyl-coenzyme A (acetyl-CoA) are

32 abundance of the low molecular weight thiols coenzyme A (CoA) and glutathione in S47 cells.

33 Cofactors such as NAD, AMP, and Coenzyme A (CoA) are essential for a diverse set of reac

34 roduce mm flux through the key fluoromalonyl coenzyme A (CoA) building block, thereby offering the po

35 (OG) is a small molecule inhibitor of acetyl coenzyme A (CoA) carboxylase (ACC), the enzyme that cont

36 Its coenzyme A (CoA) derivative, itaconyl-CoA, inhibits B(12

37 ly conserved ER protein FIT2 as a fatty acyl-coenzyme A (CoA) diphosphatase that hydrolyzes fatty acy

38 catalyzes the reduction of hydroxycinnamoyl-coenzyme A (CoA) esters using NADPH to produce hydroxyci

39 directed metabolic fluxes to generate acetyl-Coenzyme A (CoA) from glucose resulting in augmented his

40 nome of MLL-rearranged AML by linking acetyl-coenzyme A (CoA) homeostasis to Bromodomain and Extra-Te

41 brida) flowers have the precursor 4-coumaryl coenzyme A (CoA) in common.

42 DmdB, a 3-methylmercaptopropionate (MMPA)-coenzyme A (CoA) ligase, undergoes two sequential confor

43 ation of the meta-hydroxyl group of caffeoyl-coenzyme A (CoA) on the pathway to monolignols, with the

44 levels of intermediate and anaplerotic acyl-coenzyme A (CoA) species incorporated into the Krebs cyc

45 tauri extraplastidial lipids, while the 16:4-coenzyme A (CoA) species was not detected.

46 carbon-carbon bond forming step between acyl coenzyme A (CoA) substrates offer a versatile route for

47 rase superfamily member 2 (Them2) is an acyl-coenzyme A (CoA) thioesterase that catalyzes the hydroly

48 t transfers 4'-phosphopantetheine (Ppt) from coenzyme A (CoA) to diverse acyl carrier proteins.

49 the ATP-dependent conversion of citrate and coenzyme A (CoA) to oxaloacetate and acetyl-CoA(1-5).

50 lysophosphatidylethanolamine (LPE) with acyl-coenzyme A (CoA), designated LYSOPHOSPHATIDYLETHANOLAMIN

51 fatty acid (LCFA) uptake and activation with coenzyme A (CoA), mediating the fate of LCFA.

52 ate generated during synthesis of fatty acyl-coenzyme A (CoA), the reaction catalyzed by an enzyme in

53 gand binding on the energy landscape of acyl-coenzyme A (CoA)-binding protein (ACBP).

54 ing the final and committed step in the acyl-coenzyme A (CoA)-dependent biosynthesis of triacylglycer

55 LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).

56 ative abundance of the gene encoding butyryl-coenzyme A (CoA):acetate-CoA-transferase, a major enzyme

57 group of N(10)-formyl-THF to produce formyl-coenzyme A (formyl-CoA) as a central reaction intermedia

58 ts under regular 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) treatm

59 Until recently, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have

60 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are

61 The mevalonate [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase] pathway synthesizes lipi

62 We show that succinyl-coenzyme A (succinyl-CoA) binds to KAT2A.

63 Caffeoyl-coenzyme A 3-O-methyltransferase (CCoAOMT) is an S-adeno

64 best inhibitors are competitive with acetyl coenzyme A and an X-ray cocrystal structure reveals that

65 -acetyltransferase (gene: Nat8l) from acetyl-coenzyme A and aspartate.

66 amide synthase that uses C16 fatty acid acyl-coenzyme A and dihydroxy LCB substrates but increased ac

67 e enzyme phosphotransacylase (PTAC) recycles Coenzyme A and generates an acyl phosphate that can serv

68 irement for growth and specifically inhibits coenzyme A and isoleucine biosynthesis.

69 he downstream metabolites, including malonyl-coenzyme A and palmitic acid, completely restored the in

70 to depletion of the energy substrate acetyl coenzyme A and the antioxidant glutathione.

71 ynthases that use very-long-chain fatty acyl-coenzyme A and trihydroxy LCB substrates.

72 s the polymerization of 3-(R)-hydroxybutyryl-coenzyme A as a means of carbon storage in many bacteria

73 eracting partner, Golgi adaptor protein acyl-coenzyme A binding domain containing protein 3 (ACBD3).

74 uncover that the Golgi resident protein acyl-coenzyme A binding domain-containing 3 (ACBD3) serves as

75 emperature as the different variants of acyl-coenzyme A binding protein have similar m-values when th

76 enzyme kinetics, suggesting decreased acetyl coenzyme A binding.

77 it was uncovered that PZA inhibits bacterial Coenzyme A biosynthesis.

78 mulates the conversion of pyruvate to acetyl-coenzyme A by the pyruvate dehydrogenase complex.

79 ctivated protein kinase activation of acetyl-coenzyme A carboxylase (ACC) and increased lipid content

80 ar gene (ACC2) that targets homomeric acetyl-coenzyme A carboxylase (ACCase) to plastids.

81 ort into mitochondria via deletion of acetyl coenzyme A carboxylase 2 (ACC2) does not cause cardiomyo

82 l regulatory element-binding protein, acetyl coenzyme A carboxylase, and fatty acid synthase.

83 in ACC2, encoding a plastid-targeted acetyl-coenzyme A carboxylase, cause hypersensitivity to specti

84 DI-010976, an allosteric inhibitor of acetyl-coenzyme A carboxylases (ACC) ACC1 and ACC2, reduces hep

85 h (enoyl-coenzyme A, hydratase/3-hydroxyacyl coenzyme A dehydrogenase)], and a marker of proximal tub

86 rom palmitic acid (PA) catalyzed by stearoyl-coenzyme A desaturase (SCD) activity.

87 Changes in stearoyl-coenzyme A desaturase (SCD) expression and activity were

88 es, we conducted a mouse trial of a stearoyl-coenzyme A desaturase (SCD) inhibitor ("5b") that preven

89 e cellular lipid reprogramming upon stearoyl-coenzyme A desaturase 1 (SCD1) inhibition.

90 abolism genes (fatty acid synthase, stearoyl-coenzyme A desaturase 1, and perilipin 2) was drasticall

91 uided mutational analyses suggests that acyl-coenzyme A enters the active site through the cytosolic

92 level on the non-heme diiron enzyme benzoyl coenzyme A epoxidase, BoxB.

93 lism; this limits the availability of acetyl coenzyme A for histone acetylation at genes encoding inf

94 The biosynthesis of the major acyl carrier Coenzyme A from pantothenic acid (PA) is critical for su

95 boxylic acid (TCA) cycle by producing acetyl coenzyme A from pyruvate.

96 interestingly, we also identified endogenous coenzyme A glutathione disulfide (CoA-S-S-G) in tissue f

97 razinamide (PZA), interrupts biosynthesis of coenzyme A in Mycobacterium tuberculosis by binding to a

98 We further demonstrated that palmitoyl coenzyme A is a ligand for the PvrA, enhancing the bindi

99 Coenzyme A is an essential metabolite known for its cent

100 In cells, Coenzyme A is synthesized de novo in five enzymatic step

101 ciated domain and coenriches with fatty acyl-coenzyme A ligase Faa1 at LD bud sites.

102 o and activated the promoters of 4-coumarate:coenzyme A ligase genes (Os4CL3 and Os4CL5) resulting in

103 that the gene encoding a specific cinnamate coenzyme A ligase likely obtained its new function follo

104 nolignols under the catalysis of p-coumaroyl-coenzyme A monolignol transferase (PMT).

105 eficiency of the mitochondrial methylmalonyl-coenzyme A mutase (MMUT).

106 tion, we cloned and characterized a caffeoyl-coenzyme A O-methyltransferase (PhCCoAOMT1) from the pet

107 ed protein (Adrp), whereas it augmented acyl-coenzyme A oxidase 1 (Acox-1), proliferator-activated re

108 s and in vivo rescue potential of the acetyl-Coenzyme A precursor S-acetyl-4'-phosphopantetheine as a

109 One therapeutic strategy is to generate Coenzyme A precursors downstream of the defective step i

110 Cinnamoyl-coenzyme A reductase (CCR) catalyzes the reduction of hy

111 in Npc1a weakens the ability of ectopic HMG Coenzyme A reductase (Hmgcr) to induce germ cell migrati

112 thway upstream of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), the target of statins.

113 ubiquitination of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), which catalyzes a rate-lim

114 synthesis called 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR).

115 tic inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).

116 ncoding PCSK9 and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR; the target of statins) as i

117 AHA/ACC) changed 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) eligibility crit

118 indications for 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor (statin) therapy than mid

119 es of the influence of hydroxymethylglutaryl-coenzyme A reductase inhibitors (also known as statins)

120 ering properties, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have broad ant

121 Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors have been shown to impro

122 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are an important group

123 Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors), commonly prescribed in

124 inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway to protect against infectio

125 non-initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase therapy in patients with cirrhosis

126 roxylase) and ccr1g (deficient for cinnamoyl-coenzyme A reductase) lines, albeit to a lower extent.

127 by inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are among the most widely prescrib

128 family B member 1, peroxisomal trans-2-enoyl-coenzyme A reductase, phospholipase A2 receptor, protein

129 emia, inhibit the 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme of de nov

130 ically inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, which is a rate-limiting enzyme fo

131 Here, we reintroduced CINNAMOYL-COENZYME A REDUCTASE1 (CCR1) expression specifically in

132 he genes encoding 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE1 (HMGR1) and MAKIBISHI1, the rate-l

133 Mitochondrial acyl-coenzyme A species are emerging as important sources of

134 The acetyl coenzyme A synthase (ACS) enzyme plays a central role in

135 Here, we identified a novel biomarker, coenzyme A synthase (COASY), whose mRNA expression was c

136 ein-based model for the NiP center of acetyl coenzyme A synthase using a nickel-substituted azurin pr

137 nic genes such as 3-hydroxy-3-methylglutaryl-coenzyme A synthase, fatty acid synthase, and stearoyl-C

138 6K1 in insulin-stimulated adipocytes-namely, coenzyme A synthase, lipocalin 2, and cortactin.

139 The 3-hydroxy-3-methylglutaryl coenzyme A synthases (HCSs) are responsible for beta-alk

140 lysine acylation in metabolism is the acetyl-coenzyme A synthetase (Acs) enzyme.

141 Succinyl Coenzyme A synthetase (SCS) is a key mitochondrial enzym

142 Here, we show that loss of the VLCFA-coenzyme A synthetase Fat1, which is essential for VLCFA

143 Acyl coenzyme A synthetase-1 (ACSL1) facilitates long-chain f

144 ctroscopy, the cutin mutants long-chain acyl-coenzyme A synthetase2 (lacs2), permeable cuticle1 (pec1

145 talyze the sequential esterification of acyl-coenzyme A thioesters to the R4, R3, R3', and R2 positio

146 lyse the transfer of an acyl group from acyl-coenzyme A to cholesterol to generate cholesteryl ester,

147 ons suggested that SvBAHD05 is a p-coumaroyl coenzyme A transferase (PAT) mainly involved in the addi

148 Inspired by acetyl-coenzyme A transporting and delivering acetyl groups in

149 ith the high carbon efficiency drive, acetyl-coenzyme A was entirely produced using the carbon-effici

150 1) and CER3 catalyzes the conversion of acyl-Coenzyme A's to alkanes with strict substrate specificit

151 lytic transport involving sliders (including coenzyme A) picking up, transporting and selectively del

152 tins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors, are drugs with multipl

153 e oxidation to fuel the production of acetyl coenzyme A, acetylation of histones and induction of gen

154 in vitro assay requiring only isolated LDs, Coenzyme A, and ATP to drive lipid synthesis.

155 th 3,5-dihydroxybenzoic acid, ATP, malonate, coenzyme A, and the malonyl-CoA ligase MatB, venemycin p

156 y acid-binding protein 1), and Ehhadh (enoyl-coenzyme A, hydratase/3-hydroxyacyl coenzyme A dehydroge

157 ctly dependent on metabolites such as acetyl-coenzyme A, S-adenosylmethionine, and NAD+, among others

158 onverted to the central intermediate benzoyl-coenzyme A, which is enzymatically reduced to cyclohexa-

159 used cysteine to synthesize glutathione and coenzyme A, which, together, down-regulated ferroptosis.

160 re, we identify the PO membrane protein acyl-coenzyme A-binding domain protein 5 (ACBD5) as a binding

161 Here we show that acyl-coenzyme A-binding protein (ACBP) potently facilitates v

162 rrier protein) synthase (ACPS) catalyzes the coenzyme A-dependent activation of apo-ACPP to generate

163 wo separable mechanisms: dampening of acetyl-coenzyme A-dependent carbon metabolism through histone h

164 ECR encoding the mitochondrial trans-2-enoyl-coenzyme A-reductase involved in human mtFAS.

165 ulation of citrate, the precursor for acetyl coenzyme A.

166 is from lysophosphatidic acid (LPA) and acyl-coenzyme A.

167 commodates nevanimibe and an endogenous acyl-coenzyme A.

168 d to be essential for PvrA to bind palmitoyl coenzyme A.

169 ress the cholesterol-esterifying enzyme acyl-coenzyme A:cholesterol acyltransferase (ACAT1), but not

170 sterol O-acyltransferase 1 (also named acyl-coenzyme A:cholesterol acyltransferase, ACAT1) transfers

171 -acyltransferase (MBOAT) enzyme family, acyl-coenzyme A:cholesterol acyltransferases (ACATs) catalyse

172 of increased or decreased expression of ACYL-COENZYME A:DIACYLGLYCEROL ACYLTRANSFERASE1 (DGAT1) or PH

173 one (line CL37) or together with castor acyl:coenzyme A:diacylglycerol acyltransferase2 reduced HFA a

174 eneration (PKAN) and result in low levels of coenzyme-A (CoA) in the CNS due to impaired production o

175 rget of pitavastatin, hydroxymethylglutarate coenzyme-A reductase (HMGCR), was found to be over-expre

176 Aramchol, an oral stearoyl-coenzyme-A-desaturase-1 inhibitor, has been shown to red

177 We describe, for example, a putative coenzyme-A-induced-fit substrate binding mechanism media

178 structures reveals that upon binding to the coenzyme and substrate, the active pocket of BmLDH under

179 tabolites in tissue and blood including many coenzymes and antioxidants ( Anal.

180 irst study to report identification of major coenzymes and antioxidants and quantify them, simultaneo

181 The identities of coenzymes and antioxidants in blood NMR spectra were est

182 )H NMR experiment can simultaneously measure coenzymes and antioxidants in extracts of whole human bl

183 Considering that the levels of coenzymes and antioxidants represent a sensitive measure

184 e and evaluate important metabolites such as coenzymes and antioxidants that are present at high conc

185 methionine and in a large range of essential coenzymes and cofactors and is therefore essential for a

186 for major macromolecules are calculated, 2) coenzymes and inorganic ions are identified and their st

187 attachment of NAD(+)-glycerol dehydrogenase coenzyme-apoenzyme complex onto supporting gold electrod

188 e find that blocking the entry of fatty acyl coenzyme As (CoAs) into peroxisomal beta-oxidation in th

189 zymes (NAD(+), NADH, NADP(+), NADPH), energy coenzymes (ATP, ADP, AMP), antioxidants (GSH, GSSG), and

190 l for human metabolism, the organocobalamins coenzyme B12 and methylcobalamin, are highly photolabile

191 mation of an inactive dimer, alter substrate/coenzyme binding, or impair structural stability of HSD1

192 This study demonstrates coenzyme engineering of a hyperthermophilic 6PGDH and it

193 icotinamide adenine dinucleotide (NAD(+)), a coenzyme essential for DNA repair, glycolysis, and oxida

194 ybdopterin-based two-electron reduction, two coenzyme F(420)-based hydride transfers, and one coenzym

195 siroheme, corrins (including vitamin B(12)), coenzyme F(430), heme d (1), and bilins.

196 zyme F(420)-based hydride transfers, and one coenzyme F(430)-based radical process.

197 PH-binding site and was dependent on reduced coenzyme F420 (F420H2), a stronger reductant with a mid-

198 t amino acids as well as rare cofactors like coenzyme F420 The latter likely accounts for the strong

199 These data show that coenzyme F430 can be synthesized from sirohydrochlorin u

200 e proteins that catalyse the biosynthesis of coenzyme F430 from sirohydrochlorin, termed CfbA-CfbE, a

201 However, it is unclear how coenzyme F430 is synthesized from the common primogenito

202 The enzyme uses an ancillary factor called coenzyme F430, a nickel-containing modified tetrapyrrole

203 adenine dinucleotide (NAD(+)) is a critical coenzyme for cellular energy metabolism.

204 NAD is an essential coenzyme for numerous cellular processes.

205 Flavin mononucleotide (FMN) is a coenzyme for numerous proteins involved in key cellular

206 otinamide adenine dinucleotide (NAD(+)) is a coenzyme for redox reactions, making it central to energ

207 ispensible for all organisms, notably as the coenzyme form pyridoxal 5'-phosphate.

208 The ability to visualize the ubiquitous coenzymes fundamental to cellular functions, simultaneou

209 Although its action as a coenzyme has been well documented, the roles of TPP in p

210 und data, reliable peak identities for these coenzymes have been established.

211 As the major coenzyme in fuel oxidation and oxidative phosphorylation

212 ide adenine dinucleotide (NADH)-an important coenzyme in living cells-generating NAD(*) radicals with

213 er-soluble B-complex vitamin, functions as a coenzyme in macronutrient oxidation and in the productio

214 B(1) is well-characterized for its role as a coenzyme in metabolic pathways, particularly those invol

215 Adenine Dinucleotide (NADH) is an important coenzyme in the human body that participates in many met

216 in adenine dinucleotide, which are essential coenzymes in all free-living organisms.

217 on, where her work on the role of folic acid coenzymes in one-carbon metabolism revealed the mechanis

218 ow immobilization of anionic nucleotides and coenzymes, in addition to charge- and size-selective cap

219 of Phe 34 can influence the position of the coenzyme, indicating a new regulatory mechanism involvin

220 macromolecules (DNA, RNA, proteins), lipids, coenzymes, inorganic ions and species-specific component

221 Stoichiometric use of natural coenzymes is not viable economically, and the instabilit

222 ide adenine dinucleotide (NAD), a ubiquitous coenzyme, is required for many physiological reactions a

223 Accordingly, ethyl-coenzyme M (ethyl-CoM) was identified as an intermediate

224 s methanofuran, tetrahydromethanopterin, and coenzyme M at different oxidation states.

225 2-ketopropyl-coenzyme M oxidoreductase/carboxylase (2-KPCC) is a bact

226 A) use enzymes homologous to MCR named alkyl-coenzyme M reductase (ACR).

227 Methyl coenzyme M reductase (MCR) catalyzes the last step in th

228 Methyl-coenzyme M reductase (MCR) has been originally identifie

229 ry of the methanogenesis gene cluster methyl-coenzyme M reductase (Mcr) in the Bathyarchaeota, and th

230 rding to the well-accepted mechanism, methyl-coenzyme M reductase (MCR) involves Ni-mediated thiolate

231 Methyl-coenzyme M reductase (MCR) is the key enzyme of methanog

232 The enzyme methyl-coenzyme M reductase (MCR) plays an important role in me

233 Methyl-coenzyme M reductase (MCR), found in strictly anaerobic

234 h archaeal methane/alkane metabolism, methyl-coenzyme M reductase (Mcr), in metagenome-assembled geno

235 ailable metagenomes for homologues of methyl-coenzyme M reductase complex (MCR), we have obtained ten

236 engineered archaeal strain to produce methyl-coenzyme M reductase from unculturable anaerobic methano

237 genesis in methanogens is mediated by methyl-coenzyme M reductase, an enzyme that is also responsible

238 s that are necessary for a functional methyl-coenzyme M reductase, and all subunits were detected in

239 s that are necessary for a functional methyl-coenzyme M reductase, and all subunits were detected in

240 ated in the methylation of Arg-285 in methyl coenzyme M reductase, binds a methylcobalamin cofactor r

241 Methyl-coenzyme M reductase, the rate-limiting enzyme in methan

242 genes involved in carbohydrate transport or coenzyme metabolism were duplicated, likely facilitating

243 substrates with extended carbon chains and a coenzyme moiety-unusual for a thiolase-are unknown.

244 an-made synthetic biomimetics of the natural coenzymes NAD(P)H in redox biocatalysis.

245 A, and endogenous CoA-S-S-G along with redox coenzymes (NAD(+), NADH, NADP(+), NADPH), energy coenzym

246 We show that the binding of the coenzyme NADH alone or in concert with GTP results in a

247 cture of Bsp5 in complex with d-arginine and coenzyme NADPH.

248 cells exhibited elevated levels of the redox coenzyme nicotine adenine dinucleotide (NAD+), elevated

249 dinucleotide phosphate (NADP(+) and NADPH); coenzymes of energy including adenosine triphosphate (AT

250 Coenzymes of redox reactions: oxidized/reduced nicotinam

251 slational modification or the recruitment of coenzymes or metal ions to achieve catalytic function.

252 on, and aromatization, all in the absence of coenzymes or recruitment of specialized domains.

253 istinct enzymatic functions and an essential coenzyme phosphoprotein (P).

254 are involved in metabolism of oxidoreduction coenzymes, purine ribonucleoside triphosphate, ATP and p

255 d that individuals with mutations in COQ6, a coenzyme Q (also called CoQ(10), CoQ, or ubiquinone) bio

256 d its human homolog ALDH3A1 to mitochondrial coenzyme Q (CoQ) biosynthesis, an essential pathway disr

257 d by defects in Complex III (CIII) activity, coenzyme Q (CoQ) biosynthesis, and mitochondrial calcium

258 mitochondrial matrix octapeptidase Oct1p and coenzyme Q (CoQ) biosynthesis-a pathway essential for mi

259 roton leak in Fmr1 KO mitochondria caused by coenzyme Q (CoQ) deficiency and an open cyclosporine-sen

260 Coenzyme Q (CoQ) lipids are ancient electron carriers th

261 man PDAC cell lines require this pathway for coenzyme Q (CoQ) synthesis and redox homeostasis.

262 ring flavoprotein that shuttles electrons to coenzyme Q (CoQ).

263 Coenzyme Q (Q (n) ) is a vital lipid component of the el

264 n which the intra-mitochondrial synthesis of coenzyme Q (ubiquinone, Q) and Q levels are profoundly d

265 The biosynthesis of coenzyme Q presents a paradigm for how cells surmount hy

266 lfide clearance, coupling H(2)S oxidation to coenzyme Q reduction.

267 S to a persulfide and transfers electrons to coenzyme Q via a flavin cofactor.

268 functions as an oxidoreductase that reduces coenzyme Q(10) (CoQ) (also known as ubiquinone-10), whic

269 fying diseases displaying chronic low plasma Coenzyme Q(10) (CoQ) values may be important to prevent

270 n and a consequent increase in the levels of coenzyme Q(10), an endogenous lipophilic antioxidant.

271 SP1 is mediated by ubiquinone (also known as coenzyme Q(10), CoQ(10)): the reduced form, ubiquinol, t

272 s an important role in bacterial ubiquinone (coenzyme Q) biosynthesis.

273 product, the mitochondrial electron carrier coenzyme Q, both in cultured cancer cells and tumors.

274 Ubiquinone (UQ), also referred to as coenzyme Q, is a widespread lipophilic molecule in both

275 econd step of the final reaction sequence of Coenzyme Q10 (CoQ) biosynthesis.

276 We focused on the coenzyme Q10 (CoQ10) biosynthesis gene Coq2, the silenci

277 showed that sulfide oxidation is impaired in Coenzyme Q10 (CoQ10) deficiency.

278 Coenzyme Q10 (CoQ10) may represent a safe therapeutic op

279 nts (dexamethasone (DX), melatonin (MEL) and coenzyme Q10 (CoQ10)) in a single formulation (DMQ-MSs)

280 olet, has been used for the determination of coenzyme Q10 (CoQ10).

281 Hereditary defects of coenzyme Q10 biosynthesis cause steroid-resistant nephro

282 one, coenzyme Q10, or idebenone (a synthetic coenzyme Q10 homolog), as well as inhibition of oxidativ

283 The co-loading of Coenzyme Q10 into surfactant-stripped CyFaP (ss-CyFaP) m

284 pplement (vitamins A, C, and E; carotenoids; coenzyme Q10) both before and during treatment was assoc

285 , including conjugated fatty acids, sterols, coenzyme Q10, and lipophilic vitamins, such as vitamins

286 eactive oxygen species, such as glutathione, coenzyme Q10, or idebenone (a synthetic coenzyme Q10 hom

287 is of glutathione, phospholipids, NADPH, and coenzyme Q10.

288 ial phosphatase regulator of biosynthesis of coenzyme Q6 (ubiquinone or CoQ6) and a mitochondrial red

289 Ubiquinone 8 (coenzyme Q8 or Q8) mediates electron transfer within the

290 ules hinders catalytic processes that employ coenzyme recycling.

291 energy exploitation including photocatalytic coenzyme regeneration, templating, and carbon nitride ba

292 etics are excellent analogues of the natural coenzymes, revealed also in crystal structures of the en

293 xhibited a ~6.4 x 10(4)-fold reversal of the coenzyme selectivity from NADP(+) to NAD(+).

294 cterium Moorella thermoacetica with reversed coenzyme selectivity from NADP(+) to NAD(+).

295 Engineering the coenzyme specificity of redox enzymes plays an important

296 ve a dose-dependent response to nicotinamide coenzymes, such as the reduced form of nicotinamide aden

297 The B vitamins give rise to vital coenzymes that are indispensable for growth and developm

298 rely on unstable and expensive nicotinamide coenzymes that have prevented their widespread exploitat

299 th HET-P ultimately to form the final active coenzyme thiamin pyrophosphate (TPP).

300 ter-soluble molecules act as, or as part of, coenzymes within the cell.