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

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

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

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

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

7 ssroads of oxidative phosphorylation and the tricarboxylic acid cycle.

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

9 t increase in pyruvate oxidation through the tricarboxylic acid cycle.

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

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

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

13 earts were mitochondrial dysfunction and the tricarboxylic acid cycle.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 otein 2) is required for the activity of the tricarboxylic acid cycle.

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

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

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

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

39 ycolytic intermediates and components of the tricarboxylic acid cycle.

40 tic apparatus, the ability to fix C, and the tricarboxylic acid cycle.

41 the produced acetyl-CoA channelled into the tricarboxylic acid cycle.

42 dation and carbon fixation via the reductive tricarboxylic acid cycle.

43 C), fatty acid beta-oxidation (FAO), and the tricarboxylic acid cycle.

44 ue to diminished entry of glutamate into the tricarboxylic acid cycle.

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

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

47 ose catabolism through glycolysis versus the tricarboxylic acid cycle.

48 by attenuating mitochondrial respiration and tricarboxylic acid cycling.

49 AGI-6780 combination significantly decreased tricarboxylic acid cycle activity and adenosine triphosp

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

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

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

53 We link mitochondrial tricarboxylic acid cycle activity to IDH2-mediated produ

54 P/O2 kidneys inferring relative increases in tricarboxylic acid cycle activity versus HMP/Air kidneys

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

56 amage to enzymes involved in glycolysis, the tricarboxylic acid cycle and ATP biosynthesis.

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

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

59 TFAM augmented the muscle tricarboxylic acid cycle and citrate synthase facilitati

60 MmOGOR from its native role in the reductive tricarboxylic acid cycle and drive it directly with ligh

61 chondrial functional pathways, including the tricarboxylic acid cycle and electron transport chain.

62 at impaired the routing of pyruvate into the tricarboxylic acid cycle and established a metabolic sta

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

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

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

66 flux to glutamate both from glucose via the tricarboxylic acid cycle and from glutamine were increas

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

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

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

70 examination of significant compounds in the tricarboxylic acid cycle and glycolysis reveals that tre

71 d effects, promoting pyruvate entry into the tricarboxylic acid cycle and inhibiting terminal effecto

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

73 BACH1 decreases glucose utilization in the tricarboxylic acid cycle and negatively regulates transc

74 The tricarboxylic acid cycle and nucleic acid metabolism pat

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

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

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

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

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

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

81 ycolysis, whereas M2 macrophages rely on the tricarboxylic acid cycle and oxidative phosphorylation;

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

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

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

85 enzyme complex that is involved in both the tricarboxylic acid cycle and the electron transport chai

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

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

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

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

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

91 lex (PDHc) activation to maintain TCA cycle (tricarboxylic acid cycle) and promotes cancer metastasis

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

93 ehydrogenase glutathionylation, impaired the tricarboxylic acid cycle, and depleted ATP in leukemia s

94 energy metabolism, including glycolysis, the tricarboxylic acid cycle, and electron transport chain,

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

96 esis, ascorbate and aldarate metabolism, the tricarboxylic acid cycle, and glycolysis-diverting pathw

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

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

99 rmediates of glycolysis/gluconeogenesis, the tricarboxylic acid cycle, and monosaccharide and disacch

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

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

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

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

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

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

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

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

108 tion of fatty acids to supply carbon for the tricarboxylic acid cycle as well as production of sucros

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

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

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

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

113 f the leg; and released intermediates of the tricarboxylic acid cycle, balancing anaplerosis from ami

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

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

116 abolites including amino acids, fatty acids, tricarboxylic acid cycle, carbohydrates and associated i

117 ght-modulated metabolites participate in the tricarboxylic acid cycle, carbon balance, phytohormone b

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

119 rate that is associated with reversal of the tricarboxylic acid cycle, coupled with increased ketogen

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

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

122 ic flux of benzoate-derived carbons from the tricarboxylic acid cycle did not reach the upper Embden-

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

124 is made by diverting aconitate away from the tricarboxylic acid cycle during inflammatory macrophage

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

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

127 the expression of genes encoding enzymes of tricarboxylic acid cycle, electron transport chain, oxid

128 The tricarboxylic acid cycle enzyme 2-oxoglutarate dehydroge

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

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

131 The tricarboxylic acid cycle enzyme fumarate hydratase (FH)

132 (HLRCC), a disease in which mutation of the tricarboxylic acid cycle enzyme fumarate hydratase (FH)

133 Loss of the tricarboxylic acid cycle enzyme fumarate hydratase (FH)

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

135 Mutations of the tricarboxylic acid cycle enzyme fumarate hydratase cause

136 chondrial isocitrate dehydrogenase (IDH)2, a tricarboxylic acid cycle enzyme mutated in subsets of ac

137 Interestingly, deficiency for the tricarboxylic acid cycle enzyme succinate dehydrogenase

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

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

140 Although tricarboxylic acid cycle enzymes are encoded by the geno

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

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

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

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

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

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

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

148 anced mitochondrial function and accelerated tricarboxylic acid cycle flux coupled with reduced fat c

149 However, tricarboxylic acid cycle flux did not change significant

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

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

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

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

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

155 to glucose as the carbon source to fuel the tricarboxylic acid cycle for vaccinia virus replication.

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 arbon and nitrogen metabolism, including the tricarboxylic acid cycle, glycolysis, respiration, and t

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

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

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

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

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

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

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

168 decreased flux from glycolysis entering the tricarboxylic acid cycle in Muller cells accompanied by

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

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

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

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

173 The generated tricarboxylic acid cycle intermediate alpha-ketoglutarat

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

175 A recent study shows that the tricarboxylic acid cycle intermediate alpha-ketoglutarat

176 showed that substantial accumulation of the tricarboxylic acid cycle intermediate alpha-ketoglutaric

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

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

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

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

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

182 Seven tricarboxylic acid cycle intermediates (citrate, isocitr

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

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

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

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

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

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

189 Tricarboxylic acid cycle intermediates are decreased dur

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

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

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

193 equires fatty acid oxidation and shunting of tricarboxylic acid cycle intermediates for de novo lipid

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

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

196 (13)C-Labeling of tricarboxylic acid cycle intermediates originating from

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

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

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

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

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

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

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

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

205 8 production is attributable to depletion of tricarboxylic acid cycle intermediates.

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

207 hypothesize that capsule synthesis requires tricarboxylic acid cycle intermediates.

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

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

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

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

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

213 We find that the tricarboxylic acid cycle is required for the terminal ef

214 wed enhanced glycolysis, glutaminolysis, and tricarboxylic acid cycle metabolism with high alpha-keto

215 TLR-induced hexokinase activity and perturb tricarboxylic acid cycle metabolism.

216 Fumarate is a tricarboxylic acid cycle metabolite whose intracellular

217 succinate, fumarate and total 2HG) and other tricarboxylic acid cycle metabolites (alpha-ketoglutarat

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 Glycolytic and tricarboxylic acid cycle metabolites revealed bottleneck

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

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

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

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

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

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

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

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

230 The tricarboxylic acid cycle NAD+-specific isocitrate dehydr

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

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

233 biopsies revealed a glutamate metabolism and tricarboxylic acid cycle node that was specific to prost

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 genes and pathways of immunity, glycolysis, tricarboxylic acid cycle, OX-PHOS, nicotinamide dinucleo

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

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

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

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

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

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

243 , there is a metabolic remodelling involving tricarboxylic acid cycle, polyol and pentose phosphate p

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

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

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

247 Despite similar tricarboxylic acid cycle rates, palmitate oxidation rate

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

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

250 Moreover, ineffective tricarboxylic acid cycle replenishment, disturbed carboh

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

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

253 bundance plots of selected analytes from the tricarboxylic acid cycle revealed differences between he

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

255 oxoglutarate dehydrogenase-an enzyme of the tricarboxylic acid cycle-specifically results in increas

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

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

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

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

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

261 sis of organic acids, including those of the tricarboxylic acid cycle (TCA cycle), by mixed-mode reve

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

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

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

265 rom patients with recessive mutations in the tricarboxylic acid cycle (TCA) gene succinyl-CoA ligase

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

267 sumption has been linked to replenishment of tricarboxylic acid cycle (TCA) intermediates and synthes

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

272 -accumulation of metabolites involved in the tricarboxylic acid cycle (TCA), and have abnormal mitoch

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 r- and redox-driven variant of the reductive tricarboxylic acid cycle that is capable of producing li

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

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

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

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

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

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

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

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

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

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

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

287 Nucleotide metabolism and the tricarboxylic acid cycle were among the pathways perturb

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

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

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

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

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

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

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

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

296 reased expression of genes that regulate the tricarboxylic acid cycle, which resulted from microbe pr

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