ライフサイエンスコーパス: acetyl-CoA

1 atory element-binding protein 1c (SREBP-1c), acetyl-CoA carboxylase, and fatty-acid synthase, three k

2 data are explained by conversion of the M+2 acetyl-CoA to M+2 malonyl-CoA, which serves as the accep

3 egulatory element-binding proteins 1c and 2, acetyl-CoA carboxylase, and HMG-CoA reductase mRNAs/prot

4 for glucose oxidation to acetyl coenzyme A (acetyl-CoA) and CO2, NADH for the reduction of acetyl-Co

5 on of acetyl phosphate to acetyl-coenzyme A (acetyl-CoA) and posttranscriptionally regulated by CsrAB

6 Acetyl coenzyme A (acetyl-CoA) generated from glucose and acetate uptake is

7 Acetyl coenzyme A (acetyl-CoA) is a key metabolite at the crossroads of met

8 Metabolic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acetylation and gene re

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

10 on source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

11 in a manner dependent on acetyl coenzyme A (acetyl-CoA) production by the enzyme ATP-citrate lyase (

12 ressing the expression of acetyl coenzyme A (acetyl-CoA) synthetase (Acss), leading to decreased acet

13 ve to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for metabolic regula

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

15 biosynthesis of cytosolic acetyl coenzyme A (acetyl-CoA, the two-carbon isoprenoid precursor) with a

16 that artificial perturbation of the acetate/acetyl-CoA balance alters the acetyl-lysine occupancy of

17 esulting structural features in AMP- and ADP-acetyl-CoA synthetase proteins in this study expand the

18 rates revealed the greatest activity against acetyl-CoA, and structure-guided mutagenesis of putative

19 inds prior to agmatine to generate an AgmNAT*acetyl-CoA*agmatine ternary complex prior to catalysis.

20 e/citrate ratio is changed due to an altered acetyl-CoA to citrate conversion, and demonstrate that r

21 s, and biochemical analysis revealed altered acetyl-CoA metabolism.

22 and fatty acid oxidation, activated the AMPK-acetyl-CoA carboxylase pathway, and promoted inefficient

23 M (S-adenosylmethionine) synthetases, and an acetyl-CoA synthetase.

24 rted P. falciparum drug resistance genes, an acetyl-CoA transporter (pfact) and a UDP-galactose trans

25 bolism mediated by the SREBP-SCD pathway, an acetyl-CoA carboxylase (ACC) and certain nuclear hormone

26 spite nutrient excess, induced both AMPK and acetyl-CoA carboxylase (ACC) phosphorylation.

27 increased levels of phosphorylated AMPK and acetyl-CoA carboxylase (ACC).

28 lectrophoresis, and the depletion of ATP and acetyl-CoA as well as the production of ADP and malonyl-

29 ural conformations in succinyl-CoA-bound and acetyl-CoA-bound forms.

30 -CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable intermediates.

31 droxyhexanoyl-CoA, 3-hydroxybutyryl-CoA, and acetyl-CoA.

32 , 4-hydroxypentanoyl-CoA, propionyl-CoA, and acetyl-CoA.

33 mRNA levels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Acc1).

34 ing SREBP-1c, fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) gene expression.

35 mide adenine dinucleotide, reduced form) and acetyl-CoA levels.

36 ase (PFL) converting pyruvate to formate and acetyl-CoA.

37 nutrients including glucose, glutamine, and acetyl-CoA.

38 ylmalate synthase, converting glyoxylate and acetyl-CoA to malate, or glyoxylate and propionyl-CoA to

39 to serious metabolic diseases in humans, and acetyl-CoA carboxylase is a target for drug discovery in

40 s well as a protease subunit (clpP)-like and acetyl-CoA carboxylase subunit D (accD)-like open readin

41 included higher levels of neutral lipid and acetyl-CoA in WT tumors.

42 largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1 ) at the molecular level play such

43 called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation rep

44 t indicate that each of the oxaloacetate and acetyl-CoA substrates is bound to an independent site ne

45 metabolism to generate both oxaloacetate and acetyl-CoA, enabling persistent tricarboxylic acid (TCA)

46 he overexpression of genes encoding PEX7 and acetyl-CoA carboxylase further improved fatty alcohol pr

47 evels of CsrABb and the acetyl phosphate and acetyl-CoA balance contribute to the activation of the R

48 me A yielding dihydroxyacetone phosphate and acetyl-CoA, two key central metabolites.

49 In biochemical production, pyruvate and acetyl-CoA are primary building blocks.

50 PKM2 directs the synthesis of pyruvate and acetyl-CoA, the latter of which is transported to mitoch

51 cose carbon flow via OAA-malate-pyruvate and acetyl-CoA-fatty acid pathways in TRCs.

52 ion, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of

53 proteins, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing TPT were cruci

54 related to N2O reduction, PHA synthesis and acetyl-CoA formation.

55 ers the ethylmalonyl-CoA pathway directly as acetyl-CoA, bypassing pathways for formaldehyde oxidatio

56 ural plasticity and establish a link between acetyl-CoA generation 'on-site' at chromatin for histone

57 diauxic shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2 We conclude th

58 for membrane lipid synthesis is catalyzed by acetyl-CoA carboxylase, a large complex composed of four

59 oA biosynthesis and is feedback-inhibited by acetyl-CoA.

60 CLY) from mitochondria-derived citrate or by acetyl-CoA synthetase short-chain family member 2 (ACSS2

61 e allosteric inhibition of beta-oxidation by acetyl-CoA.

62 3)C2-isotopologues was indicative of [(13)C2]acetyl-CoA being the precursor units in the formation of

63 auses a significant decrease in the cellular acetyl-CoA pool, leading to reduction in circadian chang

64 Surprisingly, this pathway cleaves acetyl-CoA to donate a methyl group for production of me

65 of human MEC-17 in complex with its cofactor acetyl-CoA at 1.7A resolution.

66 s governed by the circadian clock to control acetyl-CoA levels and fatty acid synthesis.

67 precursor for lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (A

68 oA generating system provided by a cytosolic acetyl-CoA carboxylase, the mitochondrial AAE13 protein

69 Manipulation of alternative cytosolic acetyl-CoA pathways partially decoupled lipogenesis from

70 ACLY produces cytosolic acetyl-CoA from mitochondrially derived citrate.

71 lism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes.

72 he citrate-malate shuttle supplies cytosolic acetyl-CoA and plastidic glycolysis and malic enzyme sup

73 ular acetate levels resulting from decreased acetyl-CoA synthetase activity.

74 source exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels r

75 between decreased phosphorylation, decreased acetyl-CoA carboxylase Acc1 phosphorylation, and sterol

76 enzyme complex carbon monoxide dehydrogenase/acetyl-CoA synthase (CODH/ACS).

77 at these processes require acetate-dependent acetyl CoA synthetase 2 (ACSS2).

78 ndria suppresses GDH and glutamine-dependent acetyl-CoA formation.

79 by substituting for the depleted FAO-derived acetyl-CoA) or a nucleoside mix rescued the phenotype of

80 PDH-like pathway contributes glucose-derived acetyl-CoA to the TCA cycle in a stage-independent proce

81 te a significant decrease in glucose-derived acetyl-CoA.

82 cetyl-CoA relative to beta-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulate

83 oxylic acid cycle influx of pyruvate-derived acetyl-CoA relative to beta-oxidation-derived acetyl-CoA

84 evidence that these cells attempt to direct acetyl-CoA into the tricarboxylic acid (TCA) cycle for A

85 ent increased AMPK activation and downstream acetyl-CoA carboxylase phosphorylation and glucose uptak

86 However, pyruvate decarboxylation during acetyl-CoA formation limits the theoretical maximum carb

87 Mxr1p is a key regulator of ACS1 encoding acetyl-CoA synthetase in cells cultured in YPA.

88 ss is controlled by the rate-limiting enzyme acetyl-CoA carboxylase (ACC), an attractive but traditio

89 le including Acc1p, the rate-limiting enzyme acetyl-CoA carboxylase.

90 Here we show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) directly regulates histo

91 A novel target is the multifunctional enzyme acetyl-CoA carboxylase (ACC), which catalyzes the first

92 and its primary downstream targeting enzyme, acetyl-CoA carboxylase, up-regulated gene expression of

93 ssion measurements of key lipogenic enzymes [acetyl CoA carboxylase 1 (ACC1), fatty acid synthase (FA

94 ctivating factor (PAF) biosynthetic enzymes, acetyl-CoA:lyso-PAF acetyltransferase (lyso-PAF-AT) and

95 reasing the activity of the anabolic factors acetyl-CoA carboxylase and ribosomal protein S6 and inhi

96 nthesis enzymes [fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACLY)].

97 s, potentially relevant to pathogen fitness, acetyl-CoA/propionyl-CoA intracellular balance and secon

98 first four characterized proteins: BEAT [for acetyl CoA:benzylalcohol acetyltransferase], AHCT [for a

99 Pyruvate and butyrate competed for acetyl-CoA production, as evidenced by significant chang

100 the cells adapt by reducing their demand for acetyl-CoA by importing rather than synthesizing fatty a

101 rather than citrate lyase, is essential for acetyl-CoA synthesis in fission yeast.

102 ovo lipogenesis, and thus, both the need for acetyl-CoA and the oxygen-dependent SCD1-reaction, by sc

103 e for the first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient

104 yltransferase protein and is responsible for acetyl-CoA synthetase acetylation.

105 tion of CO, CoA, and a methyl-cation to form acetyl-CoA at a unique Ni,Ni-[4Fe4S] cluster (the A-clus

106 lyzes the formation of N-acetylagmatine from acetyl-CoA and agmatine.

107 l enzymes that commonly produce ethanol from acetyl-CoA with acetaldehyde as intermediate and play a

108 talyzes the transfer of an acetyl group from acetyl-CoA to the sn-3 position of diacylglycerol to for

109 lyzing the transfer of an acetyl moiety from acetyl-CoA to the C-4 amino group of UDP-d-viosamine.

110 he formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate.

111 -limiting conditions, but how cells generate acetyl-CoA under starvation stress is less understood.

112 ic enzymes, which either utilize or generate acetyl-CoA, and proteins involved in transcriptional and

113 sult, expression of the mSREBP1 target genes acetyl-CoA carboxylase and fatty-acid synthase was suppr

114 her, these data identify WAT-derived hepatic acetyl CoA as the main regulator of HGP by insulin and l

115 presses HGP is through reductions in hepatic acetyl CoA by suppression of lipolysis in white adipose

116 e HPA axis and ensuing reductions in hepatic acetyl CoA content as a common mechanism responsible for

117 asure rates of whole-body lipolysis, hepatic acetyl CoA content, pyruvate carboxylase activity and he

118 ction in hepatic glucose production, hepatic acetyl CoA content and whole-body lipolysis, which resul

119 Insulin's ability to suppress hepatic acetyl CoA, PC activity, and lipolysis was lost in high-

120 pyruvate to glucose through greater hepatic acetyl-CoA allosteric activation of pyruvate carboxylase

121 he liver, which results in increased hepatic acetyl-CoA content, a potent activator of pyruvate carbo

122 However, how acetyl-CoA is produced under nutritional stress is uncle

123 tudy expand the ASKHA superfamily to include acetyl-CoA synthetase.

124 ns with dynamic acetylation sites, including acetyl-CoA acetyltransferase 1 (Acat1), an enzyme centra

125 involved in fatty acid synthesis, including acetyl-CoA carboxylase, and three out of five putative t

126 In B cells, SCFAs increase acetyl-CoA and regulate metabolic sensors to increase ox

127 ion, elevating glucose uptake, and increased acetyl-CoA levels, leading to more ROS generation in hyp

128 Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with e

129 ich increased fatty acid oxidation increases acetyl-CoA concentrations, thereby inactivating PDH and

130 P-1(32-36)amide activated AMPK and inhibited acetyl-CoA carboxylase, suggesting activation of fat met

131 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylat

132 C) catalyzes the conversion of pyruvate into acetyl-CoA, a critical step in metabolism.

133 be susceptible to novel therapies that limit acetyl-CoA availability.

134 tein content of adipose triglyceride lipase, acetyl-CoA carboxylase 2 and AMP-activated protein kinas

135 ation were observed with a HFD despite lower acetyl-CoA levels.

136 ]glucose or [1,2-(13)C2]palmitate) or/and M1 acetyl-CoA (e.g. [1-(13)C]octanoate).

137 or two labeled substrates, which generate M2 acetyl-CoA (e.g. [(13)C6]glucose or [1,2-(13)C2]palmitat

138 3)C2,(2)H3]acetate, which forms M5 + M4 + M3 acetyl-CoA.

139 s with varying chain lengths helped maintain acetyl-CoA levels.

140 Despite these efforts to maximize acetyl-CoA for energy-generating purposes, its levels re

141 atine using an ordered sequential mechanism; acetyl-CoA binds prior to agmatine to generate an AgmNAT

142 AMP-activated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphorylation at S659,

143 abeling rate ( 0.03 h(-1)) of key metabolite acetyl-CoA reached to P7 strain's metabolism limitation

144 Mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1) regulates pyruvat

145 n isotopic technique to assess mitochondrial acetyl-CoA turnover ( approximately citric acid flux) in

146 ndeed, the (13)C enrichment in mitochondrial acetyl-CoA (18.9%) and malonyl-CoA (19.9%) are identical

147 s, and (iii) the channeling of mitochondrial acetyl-CoA from pyruvate dehydrogenase to carnitine acet

148 not proxies of the labeling of mitochondrial acetyl-CoA.

149 several fatty acid synthesis genes, namely, acetyl-CoA carboxylase, fatty acid synthase, SREBP1c, ch

150 Instead of producing large amounts of net acetyl-CoA reductively, the cells adapt by reducing thei

151 o the nucleus provides a pathway for nuclear acetyl-CoA synthesis required for histone acetylation an

152 A decrease in ACSS2 lowers nuclear acetyl-CoA levels, histone acetylation, and responsive e

153 eacetylation by increasing nucleocytoplasmic acetyl-CoA levels impairs Wnt3a-induced osteoblast diffe

154 egulates the availability of nucleocytosolic acetyl-CoA for protein acetylation and that AMPK activat

155 timizing the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the

156 Here, we show that the nucleocytosolic acetyl-CoA synthetase enzyme, ACSS2, supplies a key sour

157 lase (Aspa), which facilitates generation of acetyl CoA.

158 etion and early pharmaceutical inhibition of acetyl CoA carboxylase 1, the rate limiting step of FAS,

159 n chronic infection, a specific inhibitor of acetyl CoA carboxylase 1, 5-(tetradecyloxy)-2-furoic aci

160 no significant change in phosphorylation of acetyl CoA carboxylase.

161 pon glucose, the epigenomic reprogramming of acetyl CoA synthesis, the plasticity of aging mechanisms

162 inistration is associated with activation of acetyl-CoA carboxylase and changes in the expression pro

163 CrbRS controls transcriptional activation of acetyl-CoA synthase-1 (ACS-1) and thus regulates the ace

164 rsus C18 FAs is regulated by the activity of acetyl-CoA carboxylase (Acc1), the first and rate-limiti

165 -CoA by modulating the enzymatic activity of acetyl-CoA Synthetase 1 (AceCS1).

166 genomics study revealed that the activity of acetyl-CoA synthetase 2 (ACSS2) contributes to cancer ce

167 esults reveal a previously unknown aspect of acetyl-CoA metabolism that affects the immune and nervou

168 hen attacks the thioester carbonyl carbon of acetyl-CoA to yield a tetrahedral adduct between the two

169 mitochondria, and although carboxylation of acetyl-CoA is the known mechanism for generating the dis

170 lase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting r

171 Nucleocytosolic concentration of acetyl-CoA affects histone acetylation and links metabol

172 cle, whereas the myocardial concentration of acetyl-CoA was significantly increased in end-stage hear

173 by increasing the cellular concentration of acetyl-CoA, indicating that the regulation of acetyl-CoA

174 Thus, the spatial and temporal control of acetyl-CoA production by ACLY participates in the mechan

175 ation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein

176 strate for the first time that deficiency of acetyl-CoA: alpha-glucosaminide N-acetyltransferase caus

177 in the HGSNAT gene leading to deficiency of acetyl-CoA: alpha-glucosaminide N-acetyltransferase invo

178 glycolytic genes and a significant delay of acetyl-CoA accumulation and reentry into growth from qui

179 The development of acetyl-CoA carboxylase (ACC) inhibitors for the treatmen

180 modimers in the ER membrane and is devoid of acetyl-CoA transport activity.

181 acer and the mass isotopomer distribution of acetyl-CoA.

182 glucose uptake with consequent diversion of acetyl-CoA into ketogenesis.

183 atic steatosis, as well as the expression of acetyl-CoA carboxylase and fatty acid synthase.

184 tients and was correlated with expression of acetyl-CoA synthetase enzyme 2, ACSS2.

185 AMPK thus regulates homeostasis of acetyl-CoA, a key metabolite at the crossroads of metabo

186 The import of acetyl-CoA into the ER lumen by AT-1/SLC33A1 is essentia

187 The import of acetyl-CoA into the lumen of the endoplasmic reticulum (

188 The reduced influx of acetyl-CoA into the ER lumen results in reduced acetylat

189 nergy-sensing enzyme AMPK, and inhibition of acetyl-CoA carboxylase and mammalian target of rapamycin

190 tissue and increased UCP-3 and inhibition of acetyl-CoA carboxylase in skeletal muscle, findings cons

191 reversible NADH-mediated interconversions of acetyl-CoA, acetaldehyde, and ethanol but seemed to be p

192 enesis in mice by liver-specific knockout of acetyl-CoA carboxylase (ACC) genes and treat the mice wi

193 tivities but, rather, decreases the level of acetyl-CoA in the nucleus.

194 mice consuming a HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

195 bacterial cell responds to lowered levels of acetyl-CoA by inducing RpoS, allowing reprogramming of E

196 clock regulates the intracellular levels of acetyl-CoA by modulating the enzymatic activity of acety

197 s accompanied by decreased protein levels of acetyl-CoA carboxylase, a key regulator of both lipid ox

198 The absolute levels of acetyl-CoA were found to be maintained despite a signifi

199 The method was applied to measurements of acetyl-CoA turnover under different conditions (glucose

200 ed by the WLP to generate three molecules of acetyl-CoA from glucose, rather than the two molecules t

201 Eleven spontaneous mutations of acetyl-CoA carboxylase have been identified in many herb

202 f mitochondria, UCP2 limits the oxidation of acetyl-CoA-producing substrates such as glucose and enha

203 m was gathered from the labeling patterns of acetyl-CoA proxies, i.e. total acetyl-CoA, the acetyl mo

204 t cells and that required phosphorylation of acetyl-CoA carboxylase (ACC) 1 and/or ACC2 at the AMPK s

205 n augmenting AMPK-induced phosphorylation of acetyl-CoA carboxylase and in activating the PI3K/AKT pa

206 o up-regulated, leading to the production of acetyl-CoA, which can feed TAG accumulation upon exposur

207 ance for nuclear ACLY-mediated production of acetyl-CoA, which promotes histone acetylation, BRCA1 re

208 or cost-effective, large-scale production of acetyl-CoA-derived molecules.

209 atment increased ACC levels and the ratio of acetyl-CoA to free CoA in these animals, indicating incr

210 hat catalyzes the second partial reaction of acetyl-CoA carboxylase.

211 A sharp reduction of acetyl-CoA and ATP levels in NCTC cells indicated reduce

212 etyl-CoA) and CO2, NADH for the reduction of acetyl-CoA to ethanol, and NADH and reduced ferredoxin f

213 se (AMPK), plays a role in the regulation of acetyl-CoA homeostasis and global histone acetylation.

214 cetyl-CoA, indicating that the regulation of acetyl-CoA homeostasis represents another mechanism in t

215 response to acetyl-CoA and the regulation of acetyl-CoA synthetase activity by the acetylation level.

216 of AceCS1 contributes to the rhythmicity of acetyl-CoA levels both in vivo and in cultured cells.

217 Here we review the roles of acetyl-CoA and S-adenosylmethionine (SAM), donor substra

218 ffect of six mutations on the sensitivity of acetyl-CoA carboxylase to nine herbicides representing t

219 tase enzyme, ACSS2, supplies a key source of acetyl-CoA for tumors by capturing acetate as a carbon s

220 al nuclei decreased the de novo synthesis of acetyl-CoA and acetylation of core histones.

221 The synthesis of acetyl-CoA depends primarily on the PDH-catalyzed conver

222 haea, catalyzing the reversible synthesis of acetyl-CoA from CO and a methyl group through a series o

223 adipose and liver, but the impact of diet on acetyl-CoA and histone acetylation in these tissues rema

224 HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

225 o the lipid biosynthetic precursors NADPH or acetyl-CoA.

226 t methanol to higher-chain alcohols or other acetyl-CoA derivatives using enzymatic reactions in a ca

227 n the selective binding of succinyl-CoA over acetyl-CoA.

228 and increased phosphorylated (p-)AMPK and p-acetyl CoA carboxylase.

229 Comparison of the human PANK3.acetyl-CoA complex to the structures of PANK3 in four ca

230 ACOT12, the primary acetyl-CoA thioesterase in the liver of human, mouse, an

231 tone acetylation turnover to locally produce acetyl-CoA for histone H3 acetylation in these regions a

232 thelial cells oxidize fatty acids to produce acetyl-CoA for epigenetic modifications critical to lymp

233 Acetate is utilized to produce acetyl-CoA without carbon loss or redox imbalance.

234 decarboxylase (MCD), an enzyme that produces acetyl CoA from malonyl CoA.

235 ATP citrate-lyase produces acetyl-CoA in the nucleus and cytosol and regulates hist

236 m the mitochondria to the nucleus to provide acetyl-CoA necessary for histone acetylation, suggesting

237 s reduced with CO, catalyzed by the purified acetyl-CoA synthase/CO dehydrogenase from A. woodii.

238 nase, which results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen spe

239 s enzymatically acetylated with radiolabeled acetyl CoA by the SAGA complex from Saccharomyces cerevi

240 atty acid hydroxylase alleviated the reduced acetyl-CoA carboxylase activity, restored the rate of fa

241 a not-yet-reported Factor420-free reductive acetyl-CoA pathway, confirmed by stable carbon isotopic

242 etate production as well as in the reductive acetyl-CoA pathway were detected in all four genomes inf

243 We also found that AT-1 activity regulates acetyl-CoA flux, causing epigenetic modulation of the hi

244 ty acid-responsive factor Oaf1 in regulating acetyl-CoA production in glucose grown cells.

245 We used the dexamethasone system to silence acetyl-CoA carboxylase gene and observed prolific root g

246 Besides the conventional carbon sources, acetyl-CoA has recently been shown to be generated from

247 is used as the sole biosynthetic substrate, acetyl-CoA is commonly generated by pyruvate decarboxyla

248 K to phosphorylate its endogenous substrates acetyl CoA carboxylase and Raptor, and provokes mitochon

249 Acly in cultured adipocytes also suppressed acetyl-CoA and histone acetylation levels.

250 nvolved in lipogenesis: fatty acid synthase, acetyl-CoA carboxylase 1, and glycerol-3-phosphate acylt

251 ls of SREBP1-c, SREBP2, fatty-acid synthase, acetyl-CoA carboxylase, ATP citrate lyase, and Glut-1 we

252 upplementation allows the cell to synthesize acetyl-CoA by an alternative, less favored pathway, in p

253 PDH synthesizes acetyl-CoA; acetate supplementation allows the cell to s

254 PDH bypass in the cytosol, which synthesizes acetyl-CoA from acetate.

255 AMP-activated protein kinase and its target acetyl-CoA carboxylase.

256 -CoA and histone acetylation levels and that acetyl-CoA abundance correlates with acetylation of spec

257 Our results also demonstrated that acetyl-CoA or acetyl-phosphate could acetylate MDH chemi

258 We show that acetyl-CoA synthase, rather than citrate lyase, is essen

259 ry of ancient autotrophic cells, notably the acetyl CoA pathway in archaea and bacteria.

260 The acetyl-CoA "Wood-Ljungdahl" pathway couples the folate-m

261 The acetyl-CoA-dependent enzyme YvoF is a close relative of

262 central carbon metabolism and augmenting the acetyl-CoA pool.

263 ccumulate as an obligate by-product from the acetyl-CoA cleavage because of the lack of a CO dehydrog

264 Additional suppressor mutations in the acetyl-CoA binding site of pyruvate carboxylase (PycA) r

265 monoxide dehydrogenase, a key enzyme in the acetyl-CoA pathway, was compared in biofilm and plankton

266 form inhibition (a specific inhibitor of the acetyl-CoA pathway) were conducted on biofilm and plankt

267 -bound p300 HAT complexes and shows that the acetyl-CoA binding site is stably formed in the absence

268 tributes less than 50% of the carbons to the acetyl-CoA pool.

269 se metabolism appreciably contributes to the acetyl-CoA pools required for tricarboxylic acid metabol

270 It not only uses the acetyl-CoA derived from glycolysis but also uses breakdo

271 several histone lysines correlated with the acetyl-CoA: (iso)butyryl-CoA ratio in liver.

272 PDH levels, potentially limiting pyruvate to acetyl CoA conversion.

273 e as activated forms of acetate analogous to acetyl-CoA.

274 that PDH does not appreciably contribute to acetyl-CoA synthesis, tricarboxylic acid metabolism, or

275 re, IDH flux may not be a net contributor to acetyl-CoA production, although we cannot rule out net r

276 pionyl-CoA degradation and its conversion to acetyl-CoA.

277 A turnover and the contributions of fuels to acetyl-CoA are calculated from the uptake of the acetate

278 T genes and reduced conversion of glucose to acetyl-CoA, a substrate for HATs.

279 Acetate (metabolized to acetyl-CoA, thereby substituting for the depleted FAO-de

280 O2 due to the decarboxylation of pyruvate to acetyl-CoA and limitations in the reducing power of the

281 (PDHc) catalyzing conversion of pyruvate to acetyl-CoA comprises three components: E1p, E2p, and E3.

282 PDH, which converts pyruvate to acetyl-CoA, has been known to be primarily regulated by

283 the overall reaction converting pyruvate to acetyl-CoA.

284 ized to ensure the conversion of pyruvate to acetyl-CoA.

285 ondrial matrix where it converts pyruvate to acetyl-CoA.

286 hich catalyzes the conversion of pyruvate to acetyl-CoA.

287 d PatZ-positive cooperativity in response to acetyl-CoA and the regulation of acetyl-CoA synthetase a

288 c catalytic activity and is not sensitive to acetyl-CoA activation, in contrast to other PC enzymes.

289 athway that converts glutamine ultimately to acetyl-CoA for biosynthetic processes.

290 g patterns of acetyl-CoA proxies, i.e. total acetyl-CoA, the acetyl moiety of citrate, C-1 + 2 of bet

291 The total acetyl-CoA turnover and the contributions of fuels to ac

292 phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl

293 A1, a membrane transporter that translocates acetyl-CoA from the cytosol into the endoplasmic reticul

294 uctase (rPFOR), which incorporates CO2 using acetyl-CoA as a substrate and generates pyruvate, and py

295 The Burkholderia species utilize acetyl-CoA and oxaloacetate, substrates for citrate synt

296 ither CO2 reduction or acetate oxidation via acetyl-CoA.

297 ylase-expressing seeds indicated the in vivo acetyl-CoA carboxylase activity was reduced to approxima

298 e-1 were increased in their tissues, whereas acetyl-CoA concentration was decreased.

299 se deprivation stimulated a pathway in which acetyl-CoA was formed from glutamine downstream of gluta

300 d in all species and catalyse reactions with acetyl-CoA or propionyl-CoA.

301 le for cleavage of the thioester bond within acetyl-CoA, producing acetate and coenzyme A for a range