ライフサイエンスコーパス: tricarboxylic acid cycle

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

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

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

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

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

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

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

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

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

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

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

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

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

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

15 aconitase (Aco1p), a [4Fe-4S] enzyme in the tricarboxylic acid cycle.

16 but no contribution of ketone bodies to the tricarboxylic acid cycle.

17 ar to have further expanded with rise of the tricarboxylic acid cycle.

18 the previously reported reductive (reverse) tricarboxylic acid cycle.

19 all of the enzymes necessary for a complete tricarboxylic acid cycle.

20 utilize lactate as an energy source via the tricarboxylic acid cycle.

21 e cleavage system and acetyl-CoA feeding the tricarboxylic acid cycle.

22 of both the electron transport chain and the tricarboxylic acid cycle.

23 e gene (mqo), which encodes an enzyme of the tricarboxylic acid cycle.

24 ose catabolism through glycolysis versus the tricarboxylic acid cycle.

25 tifunctional protein: It is an enzyme of the tricarboxylic acid cycle.

26 olism, most notably the up-regulation of the tricarboxylic acid cycle.

27 eeds the number of PHX enzymes acting in the tricarboxylic acid cycle.

28 for succinate dehydrogenase activity in the tricarboxylic acid cycle.

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

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

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

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

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

34 ssroads of oxidative phosphorylation and the tricarboxylic acid cycle.

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

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

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

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

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

40 earts were mitochondrial dysfunction and the tricarboxylic acid cycle.

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

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

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

44 damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH,

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

46 s, which adapt the yeast cell to the loss of tricarboxylic acid cycle activity by providing alternate

47 luxes into biomass as well as an increase in tricarboxylic acid cycle activity for both mutations.

48 Thus, acute hypoglycemia reduced total brain tricarboxylic acid cycle activity in 3dRH animals (-37 +

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

50 nd the absence of differential regulation of tricarboxylic acid cycle activity, which occurs in IR-ir

51 ect between mitochondrial beta-oxidation and tricarboxylic acid cycle activity.

52 onventional scheme involving glycolysis, the tricarboxylic acid cycle and ATP-producing oxidative pho

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

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

55 However, a disproportionate reduction in tricarboxylic acid cycle and fatty acid oxidation protei

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

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

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

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

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

61 The data suggest that up-regulation of the tricarboxylic acid cycle and induced mutation facilitate

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

63 table increases occurred in flux through the tricarboxylic acid cycle and its efflux to the fatty aci

64 participating in pyrimidine metabolism, the tricarboxylic acid cycle and its upstream contributors,

65 Flux through tricarboxylic acid cycle and mitochondrial fatty acid be

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

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

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

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

70 The expression of multiple genes encoding tricarboxylic acid cycle and oxidative phosphorylation e

71 Palmitate also (a) reduced expression of tricarboxylic acid cycle and oxidative phosphorylation m

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

73 and instead favor ATP production through the tricarboxylic acid cycle and oxidative phosphorylation.

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

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

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

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

78 ase (PC)-catalyzed anaplerotic flux into the tricarboxylic acid cycle and stimulation of pyruvate cyc

79 nzymes involved in fatty acid oxidation, the tricarboxylic acid cycle and the electron transport chai

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

81 t with reduced glucose flux through both the tricarboxylic acid cycle and the oxidative arm of the pe

82 on and flux of 13C-labeled acetyl-CoA in the tricarboxylic acid cycle and to increased utilization of

83 o acetyl-CoA, an important precursor for the tricarboxylic acid cycle and type II fatty acid synthesi

84 o acetyl-CoA, an important precursor for the tricarboxylic acid cycle and type II fatty acid synthesi

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

86 heme assembly, pyrimidine biosynthesis, the tricarboxylic acid cycle, and apoptosis.

87 iratory chain and of H. influenzae's partial tricarboxylic acid cycle, and decreased anaerobic expres

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

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

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

91 cid catabolism, not gluconeogenesis, not the tricarboxylic acid cycle, and not the pentose phosphate

92 xpression of enzymes involved in glycolysis, tricarboxylic acid cycle, and oxidative phosphorylation

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

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

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

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

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

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

99 ids, all intermediates of glycolysis and the tricarboxylic acid cycle, are shown here to activate E.

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

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

102 ompounds appears to be due to the incomplete tricarboxylic acid cycle, as no genes potentially encodi

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

104 bations in pathways of interest, such as the tricarboxylic acid cycle, as well as unbiased characteri

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

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

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

108 tivities of the key enzymes of the reductive tricarboxylic acid cycle, ATP citrate lyase, 2-oxoglutar

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

110 er of major metabolic pathways including the tricarboxylic acid cycle, but retains sufficient electro

111 tb H37Rv predicts the presence of a complete tricarboxylic acid cycle, but we recently found that alp

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

113 the other enzymes involved in the reductive tricarboxylic acid cycle could be measured.

114 t the roles of NAD and ADP in regulating the tricarboxylic acid cycle dehydrogenase fluxes, demonstra

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

116 n fatty acids and catalyzes carbon flow from tricarboxylic acid cycle-derived metabolites to gluconeo

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

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

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

120 the presence of glutamine, signaling via the tricarboxylic acid cycle/electron transport chain, an in

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

122 The activity of a second matrix protein, the tricarboxylic acid cycle enzyme aconitase, was similarly

123 The tricarboxylic acid cycle enzyme fumarate hydratase (FH)

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

125 llelic inactivation of the gene encoding the tricarboxylic acid cycle enzyme fumarate hydratase (FH).

126 Mutations of the tricarboxylic acid cycle enzyme fumarate hydratase cause

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

128 lastocystis succinyl-CoA synthetase (SCS), a tricarboxylic acid cycle enzyme that conserves energy by

129 ogenase (IDH) is an allosterically regulated tricarboxylic acid cycle enzyme that has been shown to b

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

131 Although tricarboxylic acid cycle enzymes are encoded by the geno

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

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

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

135 aperone subunit, pyruvate dehydrogenase, the tricarboxylic acid cycle enzymes, NADH oxidase enzymes,

136 components of the respiratory complexes and tricarboxylic acid cycle enzymes.

137 idative phosphorylation and functionality of tricarboxylic acid cycle enzymes.

138 show marked reductions in the activities of tricarboxylic acid cycle enzymes.

139 g the superoxide dismutase SodB and multiple tricarboxylic acid cycle enzymes.

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

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

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

143 mpensatory increases in anaplerosis maintain tricarboxylic acid cycle flux and account for a greater

144 However, tricarboxylic acid cycle flux did not change significant

145 lite pools was fast relative to the neuronal tricarboxylic acid cycle flux for all cerebral tissue ty

146 to diminished fatty acid beta-oxidation and tricarboxylic acid cycle flux rather than abnormalities

147 potential compensatory mechanisms to sustain tricarboxylic acid cycle flux that resolve the apparent

148 esponding increases in fatty acid oxidation, tricarboxylic acid cycle flux, and gluconeogenesis witho

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

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

151 ransmitter cycling and 18% of total neuronal tricarboxylic acid cycle flux.

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

153 The neuronal tricarboxylic acid cycle fluxes in cerebral gray matter,

154 evidence for the operation of the reductive tricarboxylic acid cycle for autotrophic CO(2) fixation

155 te, which is further catabolized through the tricarboxylic acid cycle for the production of ATP or se

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

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

158 1alpha induced oxidative phosphorylation and tricarboxylic acid cycle gene expression, we also observ

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

160 involved postglycolytically and include many tricarboxylic acid cycle genes and those involved in the

161 de novo lipogenesis (cytosolic pool), in the tricarboxylic acid cycle (glutamate pool), and in chain

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

163 n metabolic intermediate before entering the tricarboxylic acid cycle have been characterized.

164 itochondria electron transport chain and the tricarboxylic acid cycle have been identified as potenti

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

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

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

168 enzymes involved in lipid metabolism and the tricarboxylic acid cycle in colonic epithelial cells bef

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

170 ate (GABA) and succinate before entering the tricarboxylic acid cycle in support of cell growth, as t

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

172 IDH) is believed to control flux through the tricarboxylic acid cycle in vivo.

173 ln and GABA/Gln cycling and their respective tricarboxylic acid cycles in the rat cortex under condit

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

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

176 Glutamine conversion into the tricarboxylic acid cycle intermediate alpha-ketoglutarat

177 re, we provide biochemical evidence that the tricarboxylic acid cycle intermediate L-malic acid (MA)

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

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

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

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

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

183 Seven tricarboxylic acid cycle intermediates (citrate, isocitr

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

185 onsequence of hypoxia is the accumulation of tricarboxylic acid cycle intermediates (TCAIs).

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

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

188 DeltapckA mutant, which is unable to utilize tricarboxylic acid cycle intermediates and gluconeogenic

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

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

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

192 Tricarboxylic acid cycle intermediates are decreased dur

193 nd a defect in growth on some amino acid and tricarboxylic acid cycle intermediates as sole carbon so

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

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

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

197 te cycling" activity (pyruvate exchange with tricarboxylic acid cycle intermediates measured by (13)C

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

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

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

201 es, including acylcarnitines, organic acids (tricarboxylic acid cycle intermediates), amino acids, an

202 f 13C-labeled acetyl-CoA into ketone bodies, tricarboxylic acid cycle intermediates, amino acids, and

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

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

205 sis, as a source of glutamate, arginine, and tricarboxylic acid cycle intermediates, and for particip

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

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

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

209 hypothesize that capsule synthesis requires tricarboxylic acid cycle intermediates.

210 zymes for the degradation of anthranilate to tricarboxylic acid cycle intermediates.

211 r decreases in pyruvate cycling activity and tricarboxylic acid cycle intermediates.

212 8 production is attributable to depletion of tricarboxylic acid cycle intermediates.

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

214 in most other organisms: (i) flux around the tricarboxylic acid cycle is absent and the small fluxes

215 ynthesis of sugars from intermediates of the tricarboxylic acid cycle is essential for growth.

216 The tricarboxylic acid cycle is expected to yield precursors

217 rbohydrate metabolism via glycolysis and the tricarboxylic acid cycle is pivotal for cancer growth, a

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

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

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

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

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

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

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

225 strates, namely pyruvate, glutamate, and the tricarboxylic acid cycle metabolites.

226 .1-33 fmol were achieved for glycoloytic and tricarboxylic acid cycle metabolites.

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

228 autotrophic CO(2) fixation via the reductive tricarboxylic acid cycle might be more important than pr

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

230 Consistent with this hypothesis, S. aureus tricarboxylic acid cycle mutants fail to make capsule.

231 The tricarboxylic acid cycle NAD+-specific isocitrate dehydr

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

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

234 Second, the tricarboxylic acid cycle of strain 195 is confirmed to b

235 nals for glutamine C4, C3 and C2, indicating tricarboxylic acid cycle operation followed by conversio

236 ha-keto acids originating from the reductive tricarboxylic acid cycle or reductive acetate pathway.

237 Of the 51 members of the glycolytic, tricarboxylic acid cycle, oxidative phosphorylation, and

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

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

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

241 an 83% increase in anaplerotic flux into the tricarboxylic acid cycle (P<0.03) that was supported by

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

243 tic gluconeogenic, fatty acid oxidation, and tricarboxylic acid cycle pathways.

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

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

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

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

248 y, disrupting metabolic pathways such as the tricarboxylic acid cycle, purine biosynthesis, and oxida

249 At similar tricarboxylic acid cycle rates, flux through carnitine p

250 Despite similar tricarboxylic acid cycle rates, palmitate oxidation rate

251 Finally, it was observed that the tricarboxylic acid cycle reactions operated in a rather

252 chaperones, glutathione-S-transferases, the tricarboxylic acid cycle, reductions in Z-line-associate

253 evisiae revealed genetic modules involved in tricarboxylic acid cycle regulation (RTG1, RTG2, RTG3),

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

255 Moreover, ineffective tricarboxylic acid cycle replenishment, disturbed carboh

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

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

258 dehydrogenase, both proteins involved in the tricarboxylic acid cycle, significantly decreased expres

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

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

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

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

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

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

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

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

267 cellular fates, a cell permeable analog of a tricarboxylic acid cycle (TCA) intermediate, alpha-ketog

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

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

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

271 omplex catalyses a rate-limiting step of the tricarboxylic acid cycle (TCA) of aerobically respiring

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

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

274 e steps in the pentose phosphate pathway and tricarboxylic acid cycle that are associated with the ge

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

276 several pathways, including glycolysis, the tricarboxylic acid cycle, the pentose phosphate pathway,

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

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

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

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

281 nd pentose phosphate pathways, and increased tricarboxylic acid cycle turnover at the expense of anap

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

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

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

285 versely, if the number of PHX enzymes of the tricarboxylic acid cycle well exceeds the PHX enzymes of

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

287 genes encoding enzymes of every step of the tricarboxylic acid cycle were downregulated in the crypt

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

289 n of latent pathways and flux changes in the tricarboxylic acid cycle were found to correlate well wi

290 enes involved in aerobic respiration and the tricarboxylic acid cycle were repressed as expected.

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

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

293 through the (incomplete) reductive (reverse) tricarboxylic acid cycle, whereas the lack of CO(2)-enha

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

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

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

297 A central hub of carbon metabolism is the tricarboxylic acid cycle, which serves to connect the pr

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

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

300 ways used to deliver glutamine carbon to the tricarboxylic acid cycle, with a large increase in the a