ライフサイエンスコーパス: tricarboxylic acid

1 oxylic acids (citric acid and homologs), and tricarboxylic acids.

2 Tricarboxylic acid acetyl coenzyme A production and ATP

3 iate metabolism, especially reactions in the tricarboxylic acid and the urea cycles.

4 Tricarboxylic acid and urea cycle fluxes were also reduc

5 and regulate various enzymes involved in the tricarboxylic acid and urea cycles, oxidative phosphoryl

6 o acids (pyruvic acid and homologs), hydroxy tricarboxylic acids (citric acid and homologs), and tric

7 and upregulation of molecules linked to the tricarboxylic acid cycle (eg, aspartate aminotransferase

8 ) efflux can be attributed to enzymes of the tricarboxylic acid cycle (oxoglutarate dehydrogenase, is

9 The tricarboxylic acid cycle (TCA cycle) is a central metabo

10 Fumarate hydratase (FH) is an enzyme of the tricarboxylic acid cycle (TCA cycle) that catalyses the

11 ssumed to be burned fully by tissues via the tricarboxylic acid cycle (TCA cycle) to carbon dioxide.

12 Decreased activities of key tricarboxylic acid cycle (TCA) cycle enzymes may underli

13 etabolism; e.g., amino acid degradation, the tricarboxylic acid cycle (TCA) cycle, and fatty acid met

14 lerotic source to provide metabolites to the tricarboxylic acid cycle (TCA) for biosynthesis.

15 uptake and incorporation into glutamate and tricarboxylic acid cycle (TCA) intermediates in part via

16 The Krebs tricarboxylic acid cycle (TCA) is central to metabolic e

17 IRT3 deacetylase activates the rate-limiting tricarboxylic acid cycle (TCA) isocitrate dehydrogenase

18 ynthase (Ccar_06155) was a key enzyme in its tricarboxylic acid cycle (TCA) pathway.

19 ic pollutants into benign metabolites of the tricarboxylic acid cycle (TCA), lipogenesis, and other a

20 hese compounds involving deregulation of the tricarboxylic acid cycle activity and suppression of mit

21 abolism, photosynthesis, remobilization, and tricarboxylic acid cycle activity) allow to refix 79% of

22 In mitochondria, it oxidizes NADH from the tricarboxylic acid cycle and beta-oxidation, reduces ubi

23 flux of glutamine-derived carbon through the tricarboxylic acid cycle and by concurrently activating

24 hondrial substrate supply pathways (i.e. the tricarboxylic acid cycle and fatty acid oxidation).

25 vels, directing glucose carbon away from the tricarboxylic acid cycle and fatty-acid synthesis.

26 mine to alpha-ketoglutarate to replenish the tricarboxylic acid cycle and generate ATP.

27 ling of glucose-derived metabolites into the tricarboxylic acid cycle and glutathione biosynthesis, r

28 that genes encoding proteins involved in the tricarboxylic acid cycle and glycolysis pathways were hi

29 complex connects the glycolytic flux to the tricarboxylic acid cycle and is central to the regulatio

30 , this limits glutamate availability for the tricarboxylic acid cycle and other biosynthetic reaction

31 atively more prominent at the expense of the tricarboxylic acid cycle and oxidative metabolism in gen

32 y mitochondria to fuel ATP production by the tricarboxylic acid cycle and oxidative phosphorylation (

33 ysfunctions that included impairments to the tricarboxylic acid cycle and oxidative phosphorylation (

34 ally, mitochondrial energy metabolism (e.g., tricarboxylic acid cycle and oxidative phosphorylation)

35 wnregulation of enzymes participating in the tricarboxylic acid cycle and oxidative phosphorylation.

36 lack major metabolic pathways including the tricarboxylic acid cycle and oxygen-evolving photosystem

37 s the rate of carbohydrate oxidation via the tricarboxylic acid cycle and pentose-phosphate pathway.

38 o mitochondria is also known to activate the tricarboxylic acid cycle and seems to be crucial for mat

39 are particularly depleted and that both the tricarboxylic acid cycle and the glutamine synthetase/gl

40 olism via an altered rate of cataplerosis of tricarboxylic acid cycle anions.

41 he contribution of exogenous pyruvate to the tricarboxylic acid cycle as acetyl-CoA is increased in S

42 converted to glutamate by GLS, entering the tricarboxylic acid cycle as an important energy source.

43 The marked accumulation of tricarboxylic acid cycle derivatives and amino acids dem

44 characterize the activity of M. tuberculosis tricarboxylic acid cycle during adaptation to and recove

45 ubunit I relative to actin; in cortex, lower tricarboxylic acid cycle enzyme aconitase and higher pro

46 ctivating mutations of the gene encoding the tricarboxylic acid cycle enzyme fumarate hydratase (FH)

47 The tricarboxylic acid cycle enzyme fumarate hydratase (FH)

48 Mutations of the tricarboxylic acid cycle enzyme fumarate hydratase cause

49 labeling data suggest the inhibition of the tricarboxylic acid cycle enzyme succinate dehydrogenase,

50 te dehydrogenase complex, a rate-controlling tricarboxylic acid cycle enzyme.

51 pericarp discs or the catalytic capacity of tricarboxylic acid cycle enzymes measured in isolated mi

52 ne monophosphate, polysaccharide production, tricarboxylic acid cycle enzymes, global transcription,

53 ctokinase, glucokinase, pyruvate kinase, and tricarboxylic acid cycle enzymes, indicating ATP product

54 o different metabolites and to calculate the tricarboxylic acid cycle flux (VTCA) by a one-compartmen

55 However, tricarboxylic acid cycle flux did not change significant

56 ude a rapid increase in ATP/ADP, anaplerotic tricarboxylic acid cycle flux, and increases in the malo

57 lutamine uptake was approximately 50% of the tricarboxylic acid cycle flux, the rate of ATP productio

58 acid production was approximately 6% of the tricarboxylic acid cycle flux.

59 d FH, a gene on chromosome 1q43 encoding the tricarboxylic acid cycle fumarate hydratase enzyme.

60 strocytes, and alternations in mitochondrial tricarboxylic acid cycle function.

61 s of TRIM24 iHMECs revealed a glycolytic and tricarboxylic acid cycle gene signature, alongside incre

62 in cohesive operation of glycolysis and the tricarboxylic acid cycle in a normal glucose-replete mil

63 m through the IRG1/itaconate axis within the tricarboxylic acid cycle in activated macrophages.

64 involvement of the increased activity of the tricarboxylic acid cycle in carbon repartitioning.

65 arbon metabolism, sucrose synthesis, and the tricarboxylic acid cycle in leaves and oil synthesis in

66 The differences in key metabolites of the tricarboxylic acid cycle in the triple mutant versus the

67 ssion and covalent regulation, and hence the tricarboxylic acid cycle influx of pyruvate-derived acet

68 Iron efflux via an iron-chelating tricarboxylic acid cycle intermediate provides a direct

69 ize heme from the amino acid glycine and the tricarboxylic acid cycle intermediate succinyl CoA for i

70 show that alpha-ketoglutarate (alpha-KG), a tricarboxylic acid cycle intermediate, extends the lifes

71 ough the decarboxylation of cis-aconitate, a tricarboxylic acid cycle intermediate.

72 esting that glutamine's ability to replenish tricarboxylic acid cycle intermediates (anaplerosis) is

73 Seven tricarboxylic acid cycle intermediates (citrate, isocitr

74 (N2,N2-dimethylguanosine, N1-methylinosine), tricarboxylic acid cycle intermediates (malate, fumarate

75 tal nitrogen added as N2O and large pools of tricarboxylic acid cycle intermediates and amino acids.

76 ts of perfusion and (11)C incorporation into tricarboxylic acid cycle intermediates and bicarbonate a

77 red metabolic profiles, including changes in tricarboxylic acid cycle intermediates and in the majori

78 The kinetics of acetate incorporation into tricarboxylic acid cycle intermediates and into lipids s

79 response is concurrent with rapid changes in tricarboxylic acid cycle intermediates and large changes

80 Tricarboxylic acid cycle intermediates are decreased dur

81 d for the conversion of 4-hydroxybenzoate to tricarboxylic acid cycle intermediates as well as the ma

82 Amino acids, beta-hydroxybutyrate, and tricarboxylic acid cycle intermediates decreased after O

83 xpression increased anaplerotic refilling of tricarboxylic acid cycle intermediates in mouse brain du

84 anthranilate, which is further degraded into tricarboxylic acid cycle intermediates or utilized to ma

85 thermore, the spatiotemporal distribution of tricarboxylic acid cycle intermediates was already chang

86 Glucose-induced increases in tricarboxylic acid cycle intermediates were attenuated b

87 re metabolism, leading to elevated levels of tricarboxylic acid cycle intermediates, amino acids, sug

88 respiration rates, changes in the levels of tricarboxylic acid cycle intermediates, and accumulation

89 d oxidation, and in cellular accumulation of tricarboxylic acid cycle intermediates, ATP and reactive

90 oenergetics as measured by altered levels of tricarboxylic acid cycle intermediates, NAD(+)/NADH, and

91 8 production is attributable to depletion of tricarboxylic acid cycle intermediates.

92 n of upstream metabolites and a depletion of tricarboxylic acid cycle intermediates.

93 considered incapable of de novo synthesis of tricarboxylic acid cycle intermediates; therefore they r

94 idopsis are differentially fine-regulated by tricarboxylic acid cycle metabolites (most likely depend

95 lipophilic methyl-conjugates of pyruvate and tricarboxylic acid cycle metabolites bypassed the gateke

96 nd the global declines in the glycolytic and tricarboxylic acid cycle metabolites characteristic of n

97 s controlling the levels of Met, sugars, and tricarboxylic acid cycle metabolites were also significa

98 diture were associated with PC6, PC9 (AA and tricarboxylic acid cycle metabolites), and PC10.

99 dance of dipeptide metabolites, depleted key tricarboxylic acid cycle metabolites, and slowed progres

100 decreased cellular ATP and depleted critical tricarboxylic acid cycle metabolites, leading to suppres

101 ed photosynthesis, hormone biosynthesis, and tricarboxylic acid cycle metabolites.

102 ntermediates derived from the glycolysis and tricarboxylic acid cycle pathways.

103 and metabolism of [U-(13)C3]glycerol in the tricarboxylic acid cycle prior to gluconeogenesis or gly

104 Despite similar tricarboxylic acid cycle rates, palmitate oxidation rate

105 Moreover, ineffective tricarboxylic acid cycle replenishment, disturbed carboh

106 s chosen for further studies for its role in tricarboxylic acid cycle replenishment.

107 of mitochondrially localized enzymes of the tricarboxylic acid cycle resulted in enhanced transitory

108 HFD-fed SIRT3 knockout (KO) mice showed that tricarboxylic acid cycle substrate-based respiration is

109 eviously suggested that, during hypoxia, the tricarboxylic acid cycle switches to a noncyclic operati

110 adapts to hypoxia, it slows and remodels its tricarboxylic acid cycle to increase production of succi

111 at mediates pyruvate oxidation and fuels the tricarboxylic acid cycle to meet energy demand.

112 ng cells shifted their metabolism to use the tricarboxylic acid cycle to metabolize acetate in contra

113 nate:ubiquinone oxidoreductase) connects the tricarboxylic acid cycle to the electron transport chain

114 otoxic extracellular Glu through a truncated tricarboxylic acid cycle under hypoglycemic conditions.

115 Levels of the intermediates of the tricarboxylic acid cycle were altered, and increases in

116 in ndufv1, fluxes through glycolysis and the tricarboxylic acid cycle were dramatically increased com

117 iling suggested that both glycolysis and the tricarboxylic acid cycle were suppressed in a similar ma

118 gy metabolism pathways (e.g., glycolysis and tricarboxylic acid cycle).

119 ive pentose phosphate pathway, Calvin cycle, tricarboxylic acid cycle, and amino acid biosynthetic pa

120 but decreasing transcription of genes in the tricarboxylic acid cycle, and genes that regulate the ce

121 oration of nutrient-derived carbons into the tricarboxylic acid cycle, and increased glutathione leve

122 abolic changes, affecting glycolysis and the tricarboxylic acid cycle, and led to a successive induct

123 metabolic processes, such as glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation.

124 , and proline), sugars, intermediates of the tricarboxylic acid cycle, and polyamines and lower level

125 components of the electron transport chain, tricarboxylic acid cycle, and protein import apparatus.

126 lant metabolism by affecting glycolysis, the tricarboxylic acid cycle, and the biosynthesis of amino

127 sis and tighter matching between FAO and the tricarboxylic acid cycle, apelin treatment could contrib

128 ut also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclea

129 unt generates catabolites that may enter the tricarboxylic acid cycle, but it is unknown whether cata

130 rofiling revealed an altered activity of the tricarboxylic acid cycle, changes in amino acid levels,

131 nses a blockage at the aconitase step of the tricarboxylic acid cycle, either through elevated citrat

132 id metabolic pathways, including glycolysis, tricarboxylic acid cycle, fatty-acid activation and synt

133 performed to compare metabolism through the tricarboxylic acid cycle, fermentation, alanine metaboli

134 ate dehydrogenase (MDH), a key enzyme in the tricarboxylic acid cycle, has been identified to be acet

135 lytic pathway and decreased flux through the tricarboxylic acid cycle, in order to decrease mitochond

136 ral key mitochondrial functions, such as the tricarboxylic acid cycle, mitochondrial electron transfe

137 ed in fermentation, hydrogen production, the tricarboxylic acid cycle, NAD biosynthesis, nitrate and

138 that were only regulated by citrate included tricarboxylic acid cycle, nitrogen metabolism, sulfur me

139 meostasis, regulating ATP production via the tricarboxylic acid cycle, OXPHOS, and fatty acid oxidati

140 etoglutarate in the mitochondria to fuel the tricarboxylic acid cycle, PDAC relies on a distinct path

141 oxygen levels and certain byproducts of the tricarboxylic acid cycle, PHDs act as sensors of the cel

142 photosynthetic light and dark reactions, the tricarboxylic acid cycle, protein metabolism, and redox

143 ases can be related to changing modes of the tricarboxylic acid cycle, reorganizing the usage of orga

144 ong been known to act as an inhibitor of the tricarboxylic acid cycle, the fate of the amino acid flu

145 erse reaction, supporting anaplerosis of the tricarboxylic acid cycle, under conditions leading to sl

146 mic branching of the S. oneidensis anaerobic tricarboxylic acid cycle, unreported in any other organi

147 ites decreases citrate oxidation through the tricarboxylic acid cycle, whereas increased glutamine up

148 etone body production and breakdown, and the tricarboxylic acid cycle, which inversely correlated wit

149 Ketoglutarate (AKG) is a key intermediate of tricarboxylic acid cycle, which is generated during endu

150 cal for cellular energetics as a part of the tricarboxylic acid cycle, which produces reducing equiva

151 ck of oxygen-evolving photosystem II and the tricarboxylic acid cycle, which suggested partnership in

152 ase fatty acid uptake and oxidation into the tricarboxylic acid cycle, while reducing glucose and lac

153 dies within the vessels using an alternative tricarboxylic acid cycle-associated pathway, ultimately

154 te dehydrogenase) and pyruvate flux into the tricarboxylic acid cycle.

155 ate pathway, and gluconeogenesis through the tricarboxylic acid cycle.

156 rs of an enzyme involved in the operation of tricarboxylic acid cycle.

157 nicotine, oxidative phosphorylation, and the tricarboxylic acid cycle.

158 ase complex is missing in the cyanobacterial tricarboxylic acid cycle.

159 earts were mitochondrial dysfunction and the tricarboxylic acid cycle.

160 (CcpE) that functions as a regulator of the tricarboxylic acid cycle.

161 ns involved in the respiratory chain and the tricarboxylic acid cycle.

162 uctions in enzymes of beta-oxidation and the tricarboxylic acid cycle.

163 Carbon may be fixed via the reductive tricarboxylic acid cycle.

164 y acids as well as increased activity of the tricarboxylic acid cycle.

165 leotide and fatty acid biosynthesis, and the tricarboxylic acid cycle.

166 d represses the metabolism of glutamine into tricarboxylic acid cycle.

167 growth on two-carbon substrates) or the full tricarboxylic acid cycle.

168 lysis, resulting in an increased flux to the tricarboxylic acid cycle.

169 ADH-GDH is to provide 2-oxoglutarate for the tricarboxylic acid cycle.

170 y acid synthesis and pyruvate entry into the tricarboxylic acid cycle.

171 nent of the electron transport chain and the tricarboxylic acid cycle.

172 g alpha-ketoglutarate-oxidizing steps in the tricarboxylic acid cycle.

173 ate synthase activity, the first step in the tricarboxylic acid cycle.

174 omega-amidase links sulfur metabolism to the tricarboxylic acid cycle.

175 ctate into pyruvate and thus replenishes the tricarboxylic acid cycle.

176 ose catabolism through glycolysis versus the tricarboxylic acid cycle.

177 olved in cell growth, RNA metabolism and the tricarboxylic acid cycle.

178 ith suppression of glucose metabolism in the tricarboxylic acid cycle.

179 undance in controlling the flux-modus of the tricarboxylic acid cycle.

180 conversion of malate and oxaloacetate in the tricarboxylic acid cycle.

181 ce defenses to substrates that can enter the tricarboxylic acid cycle.

182 ssroads of oxidative phosphorylation and the tricarboxylic acid cycle.

183 d by a decreased glycolysis and an increased tricarboxylic acid cycle/oxidative pathway, preceded the

184 how that p53 represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 an

185 sis, amino acid catabolism, and the urea and tricarboxylic acid cycles, as well as mitochondrial regu

186 R-beta-selective ligand increased markers of tricarboxylic acid-dependent and -independent energy bio

187 n the expression levels of mitochondrial and tricarboxylic acid genes.

188 rioxo-2, 5,11,13-tetraazahexadecane-10,14,16-tricarboxylic acid)), have demonstrated promising result

189 2 (also known as HKUST-1; BTC, benzene-1,3,5-tricarboxylic acid) infiltrated with the molecule 7,7,8,

190 was associated with decreased levels of some tricarboxylic acid intermediates and amino acids, wherea

191 IDO)-dependent tryptophan metabolites (TMs), tricarboxylic acid intermediates, and purine metabolites

192 ributes to the acetyl-CoA pools required for tricarboxylic acid metabolism (TCA) cycle and fatty acid

193 1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reduc

194 expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase

195 reciably contribute to acetyl-CoA synthesis, tricarboxylic acid metabolism, or fatty acid synthesis i

196 In the presence of slow reacting di- and tricarboxylic acids (oxalic, malonic, succinic, and citr

197 quantify the melanin biomarker pyrrole-2,3,5-tricarboxylic acid (PTCA) was evaluated as a means of no

198 rdial metabolic networks such as the reverse tricarboxylic acid (rTCA) cycle and clay mineral catalys

199 imordial nature of the non-enzymatic reverse tricarboxylic acid (rTCA) cycle and describe a modeling

200 The reverse tricarboxylic acid (rTCA) cycle has been explored from v

201 ne, associated to accumulation of glutamate, tricarboxylic acid (TCA) anaplerotic intermediates and G

202 n and iron limitation dramatically decreased tricarboxylic acid (TCA) cycle activity, creating a meta

203 d oxidation, an effect linked to a defect in tricarboxylic acid (TCA) cycle activity.

204 Tricarboxylic acid (TCA) cycle anaplerosis is maintained

205 did not cause energy distress, but impaired tricarboxylic acid (TCA) cycle anaplerosis, macromolecul

206 ncover a previously unknown link between the tricarboxylic acid (TCA) cycle and cell cycle progressio

207 stimulates glutamine catabolism through the tricarboxylic acid (TCA) cycle and consequently lowers i

208 (Fh1), a key component of the mitochondrial tricarboxylic acid (TCA) cycle and cytosolic fumarate me

209 e cells and by reducing carbon flux into the tricarboxylic acid (TCA) cycle and de novo lipid biosynt

210 cose deprivation stimulated re-wiring of the tricarboxylic acid (TCA) cycle and early steps of glucon

211 include mitochondrial genes involved in the tricarboxylic acid (TCA) cycle and other nuclear-encoded

212 expression of genes encoding enzymes of the tricarboxylic acid (TCA) cycle and oxidative phosphoryla

213 hird, the relative flux through the complete tricarboxylic acid (TCA) cycle and succinate dehydrogena

214 Certain enzymes of the tricarboxylic acid (TCA) cycle are modified or accumulat

215 y regulated in BMSCs from T2D mice, with the tricarboxylic acid (TCA) cycle being one of the primary

216 glycolysis enzyme abundance and decreases in tricarboxylic acid (TCA) cycle enzyme abundance with inc

217 Mutations in the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase

218 Germ line mutations of the gene encoding the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase

219 ars, inherited and acquired mutations in the tricarboxylic acid (TCA) cycle enzymes have been reporte

220 cation of cancer-associated mutations in the tricarboxylic acid (TCA) cycle enzymes isocitrate dehydr

221 e mutations in nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle enzymes that produce onco

222 ate metabolism enzymes, and a portion of the tricarboxylic acid (TCA) cycle enzymes.

223 n (pyruvate and oxaloacetate) must enter the tricarboxylic acid (TCA) cycle first and then use phosph

224 approach, we found the mean rates of hepatic tricarboxylic acid (TCA) cycle flux (VTCA) and anaplerot

225 ial changes in overall respiration rates and tricarboxylic acid (TCA) cycle flux.

226 (leuZ) prevents sRNA-dependent remodeling of tricarboxylic acid (TCA) cycle fluxes and decreases anti

227 cells attempt to direct acetyl-CoA into the tricarboxylic acid (TCA) cycle for ATP production rather

228 carbon is not completely broken down by the tricarboxylic acid (TCA) cycle for energy; instead, it i

229 oacetate and acetyl-CoA, enabling persistent tricarboxylic acid (TCA) cycle function.

230 creases in glycolytic capacity, and improved tricarboxylic acid (TCA) cycle function.

231 Typhimurium undergoes an incomplete tricarboxylic acid (TCA) cycle in the anaerobic mammalia

232 ynthetic) failure such as that consequent to tricarboxylic acid (TCA) cycle intermediate depletion.

233 c pathway product phosphoenolpyruvate to the tricarboxylic acid (TCA) cycle intermediate oxaloacetic

234 abolyzed to alpha-ketoglutarate (alphaKG), a tricarboxylic acid (TCA) cycle intermediate, through two

235 utarate, another output of the pathway and a tricarboxylic acid (TCA) cycle intermediate.

236 significant alterations in the levels of key tricarboxylic acid (TCA) cycle intermediates and amino a

237 Altered levels of tricarboxylic acid (TCA) cycle intermediates and the ass

238 ding to less glucose carbons contributing to tricarboxylic acid (TCA) cycle intermediates and the pen

239 sed anabolic demands, wherein glycolytic and tricarboxylic acid (TCA) cycle intermediates are shunted

240 le into a "dead end" pathway that sequesters tricarboxylic acid (TCA) cycle intermediates into methyl

241 Several glycolysis/gluconeogenesis and tricarboxylic acid (TCA) cycle intermediates showed incr

242 thione metabolites, choline derivatives, and tricarboxylic acid (TCA) cycle intermediates were altere

243 ve oxygen species with oxidative stress, and tricarboxylic acid (TCA) cycle intermediates were quanti

244 riation in lipid and amino acid metabolites, tricarboxylic acid (TCA) cycle intermediates, and acylca

245 ng amino acids, polyamines, fatty acids, and tricarboxylic acid (TCA) cycle intermediates, were teste

246 nitine (a leucine catabolite), and decreased tricarboxylic acid (TCA) cycle intermediates--generated

247 ge of the pathway and coordinately decreases tricarboxylic acid (TCA) cycle intermediates.

248 mulation of organic acids that are primarily tricarboxylic acid (TCA) cycle intermediates.

249 ly assumed to be involved in replenishing of tricarboxylic acid (TCA) cycle intermediates.

250 could be rescued by the addition of multiple tricarboxylic acid (TCA) cycle intermediates.

251 icularly pentose phosphate pathway (PPP) and tricarboxylic acid (TCA) cycle intermediates.

252 The tricarboxylic acid (TCA) cycle is a central metabolic pa

253 The tricarboxylic acid (TCA) cycle is an interface among gly

254 The tricarboxylic acid (TCA) cycle is central to energy prod

255 The tricarboxylic acid (TCA) cycle is involved in the comple

256 ing glucose and glutamine utilization in the tricarboxylic acid (TCA) cycle is not well understood, w

257 ial superoxide damage to Fe-S enzymes in the tricarboxylic acid (TCA) cycle leads to acetate buildup

258 Malate, the tricarboxylic acid (TCA) cycle metabolite, increased lif

259 epigenetic changes directed by mitochondrial tricarboxylic acid (TCA) cycle metabolites.

260 were highly expressed intracellularly, while tricarboxylic acid (TCA) cycle oxidoreductive enzymes an

261 d to changes in the levels of glycolysis and tricarboxylic acid (TCA) cycle pathway intermediates.

262 s for respiratory chain flavoproteins or for tricarboxylic acid (TCA) cycle resulted in increased res

263 sed longevity suggesting that anaplerosis of tricarboxylic acid (TCA) cycle substrates likely plays a

264 Plant mitochondria have a fully operational tricarboxylic acid (TCA) cycle that plays a central role

265 Tumor cells utilize Gln in the tricarboxylic acid (TCA) cycle to maintain sufficient po

266 multiple anaplerotic routes into a canonical tricarboxylic acid (TCA) cycle to satisfy their energy r

267 must make a sudden switch from utilizing the tricarboxylic acid (TCA) cycle to using the ethylmalonyl

268 tabolism was not strictly glycolytic, as the tricarboxylic acid (TCA) cycle was functional in all mel

269 m of hyperpolarized [1-(13)C]pyruvate in the tricarboxylic acid (TCA) cycle was monitored in the isol

270 s, including important intermediaries of the tricarboxylic acid (TCA) cycle, amino acids including pr

271 s, including conspicuous cristae, mtDNA, the tricarboxylic acid (TCA) cycle, and ATP synthesis powere

272 L-malic acid in mitochondria as part of the tricarboxylic acid (TCA) cycle, and in the cytosol/nucle

273 e components of mitochondrialbeta-oxidation, tricarboxylic acid (TCA) cycle, and respiratory chain.

274 ycolysis, the pentose phosphate pathway, the tricarboxylic acid (TCA) cycle, and serine biosynthesis

275 at the level of pyruvate metabolism and the tricarboxylic acid (TCA) cycle, and these perturbations

276 ent assimilation of these compounds into the tricarboxylic acid (TCA) cycle, and, correspondingly, th

277 scription of HAP4 and genes required for the tricarboxylic acid (TCA) cycle, electron transport chain

278 rboxykinase (PCK2), the hub molecule linking tricarboxylic acid (TCA) cycle, glycolysis and gluconeog

279 marate hydratase, an essential enzyme in the tricarboxylic acid (TCA) cycle, has been identified as o

280 Enzymes of the tricarboxylic acid (TCA) cycle, including aconitase and

281 ine-derived metabolic intermediates into the Tricarboxylic Acid (TCA) cycle, leading to reduced citra

282 several multienzyme systems involved in the tricarboxylic acid (TCA) cycle, photorespiration, and th

283 the pentose phosphate pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose me

284 in kinase in coordinating glycolysis and the tricarboxylic acid (TCA) cycle, which is instrumental in

285 s glycolysis and regulates the expression of tricarboxylic acid (TCA) cycle-related genes.

286 lyses from these mouse studies revealed that tricarboxylic acid (TCA) cycle-related urinary metabolit

287 , the pentose phosphate (PP) pathway and the tricarboxylic acid (TCA) cycle.

288 a drop in glutaminolysis and filling of the tricarboxylic acid (TCA) cycle.

289 lung cancers (NSCLCs) oxidize glucose in the tricarboxylic acid (TCA) cycle.

290 carbon flux through both glycolysis and the tricarboxylic acid (TCA) cycle.

291 y regulating entry of carbohydrates into the tricarboxylic acid (TCA) cycle.

292 ysis, the pentose phosphate pathway, and the tricarboxylic acid (TCA) cycle.

293 or synthesis, and decreased flux through the tricarboxylic acid (TCA) cycle.

294 te and disrupted metabolites involved in the tricarboxylic acid (TCA) cycle.

295 tions of the proteins constituting the plant tricarboxylic acid (TCA) cycle.

296 nd Plasmodium mitochondria operate canonical tricarboxylic acid (TCA) cycles and electron transport c

297 dation, cell growth, oxygen consumption, and tricarboxylic acid (TCA) metabolism were surprisingly ma

298 obal change from an oxidative to a reductive tricarboxylic acid (TCA) program.

299 oglutarate, an important intermediate in the tricarboxylic acid (TCA, Krebs) cycle and a promising th

300 the reaction of the dianion of pyrrole-1,2,5-tricarboxylic acid tert-butyl ester dimethyl ester with