ライフサイエンスコーパス: TCA cycle

1 zymes with large iron requirements, like the TCA cycle).

2 MTHFD2, and MTHFD2 knockdown suppresses the TCA cycle.

3 sed glutamine uptake serves to replenish the TCA cycle.

4 cells could be rescued by supplementing the TCA cycle.

5 diverting glucose-derived pyruvate into the TCA cycle.

6 oxylase, Wood-Ljungdahl pathway or reductive TCA cycle.

7 ydrogenase activity, and glucose flux to the TCA cycle.

8 on glutamine to anaplerotically maintain the TCA cycle.

9 e (alpha-KG), a critical intermediate in the TCA cycle.

10 ate is supplied through these enzymes to the TCA cycle.

11 carbon flow into serine biosynthesis and the TCA cycle.

12 ubstrate preference to maintain a functional TCA cycle.

13 t with a redirection of carbon away from the TCA cycle.

14 hereas it inhibits glucose catabolism in the TCA cycle.

15 metabolism, oxidative phosphorylation or the TCA cycle.

16 points for acetate: the EMC pathway and the TCA cycle.

17 with visualization of multiple steps of the TCA cycle.

18 time in vivo imaging and spectroscopy of the TCA cycle.

19 diates shuttling into and cycling within the TCA cycle.

20 acids, while COD:N of 11:1 do it through the TCA cycle.

21 t to a decreased O2 delivery by rewiring the TCA cycle.

22 decreased, which confirmed disruption of the TCA cycle.

23 s constituting the plant tricarboxylic acid (TCA) cycle.

24 ate (PP) pathway and the tricarboxylic acid (TCA) cycle.

25 lysis and filling of the tricarboxylic acid (TCA) cycle.

26 both glycolysis and the tricarboxylic acid (TCA) cycle.

27 f carbohydrates into the tricarboxylic acid (TCA) cycle.

28 ) oxidize glucose in the tricarboxylic acid (TCA) cycle.

29 creased flux through the tricarboxylic acid (TCA) cycle.

30 abolites involved in the tricarboxylic acid (TCA) cycle.

31 nal effector of the first two enzymes of the TCA cycle, aconitase (citB) and to a lesser extent citra

32 CS suppression reduced TCA cycle activity and diverted oxaloacetate, the substr

33 In Staphylococcus aureus, TCA cycle activity is controlled by several regulators (

34 t during post-exponential-phase growth, when TCA cycle activity was maximal.

35 e metabolism led to selective corrections of TCA cycle activity, membrane potential, and intrabacteri

36 ntegration of fatty acid beta-oxidation with TCA cycle activity.

37 n dramatically decreased tricarboxylic acid (TCA) cycle activity, creating a metabolic block and sign

38 ct linked to a defect in tricarboxylic acid (TCA) cycle activity.

39 es involved in amino acid metabolism and the TCA cycle affects the dietary response.

40 ed serum starvation significantly suppressed TCA cycle, altered glucose and fatty acids metabolism, a

41 mitochondrial function and metabolism in the TCA cycle, amino acids, carnitine, lipids, and bile acid

42 nt intermediaries of the tricarboxylic acid (TCA) cycle, amino acids including proline and citrulline

43 me large quantities of glutamine to maintain TCA cycle anaplerosis and support cell survival.

44 y distress, but impaired tricarboxylic acid (TCA) cycle anaplerosis, macromolecule production, and re

45 on glutamine as a major tri-carboxylic acid (TCA) cycle anaplerotic substrate to support proliferatio

46 Our study demonstrates a link between the TCA cycle and a specific cell cycle transition in the on

47 nhibits the contribution of glutamine to the TCA cycle and activates glucose catabolism in SkMel5 mel

48 ochondrial enzymes, including members of the TCA cycle and affiliated pathways, harbor thioredoxin (T

49 g metabolic stress contributes to changes in TCA cycle and amino acid metabolism, and cell death, whi

50 luated the in vitro activities of a range of TCA cycle and associated enzymes under varying redox sta

51 mitochondrial metabolic pathways, such as a TCA cycle and ETC-driven ATP synthesis, but also possess

52 promoting glutaminolysis and preserving the TCA cycle and hexosamine biosynthesis.

53 defects, highlighting the importance of the TCA cycle and lipid biosynthesis during sporulation.

54 or glutamate (both amino acids that feed the TCA cycle and nucleotide synthesis) or nucleosides.

55 e in the expression of genes involved in the TCA cycle and oxidative phosphorylation.

56 respiration by inducing transcription of the TCA cycle and OXPHOS genes carried by both nuclear and m

57 markedly decreased steady state contents of TCA cycle and photorespiratory intermediates as well as

58 direct regulator of carbon flow through the TCA cycle and providing a mechanism for the coordination

59 n of acetyl-CoA occurs predominantly via the TCA cycle and that assimilation occurs via the EMC pathw

60 te can be a primary source of carbon for the TCA cycle and thus of energy.

61 Tricarboxylic (TCA) cycle and a number of amino acid-related biological

62 unknown link between the tricarboxylic acid (TCA) cycle and cell cycle progression in the Caenorhabdi

63 e catabolism through the tricarboxylic acid (TCA) cycle and consequently lowers intracellular glutami

64 ent of the mitochondrial tricarboxylic acid (TCA) cycle and cytosolic fumarate metabolism, in normal

65 ing carbon flux into the tricarboxylic acid (TCA) cycle and de novo lipid biosynthesis.

66 mulated re-wiring of the tricarboxylic acid (TCA) cycle and early steps of gluconeogenesis to promote

67 required for tricarboxylic acid metabolism (TCA) cycle and fatty acid biosynthesis.

68 al genes involved in the tricarboxylic acid (TCA) cycle and other nuclear-encoded RNAs with mitochond

69 encoding enzymes of the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS).

70 lux through the complete tricarboxylic acid (TCA) cycle and succinate dehydrogenase is small under he

71 ondria operate canonical tricarboxylic acid (TCA) cycles and electron transport chains, although the

72 om central carbon catabolism (glycolysis and TCA cycle), and was controlled by cAMP-Crp.

73 gulation of key intermediates in glycolysis, TCA cycle, and glutaminolysis.

74 ammasome without undergoing oxidation in the TCA cycle, and independently of uncoupling protein-2 (UC

75 of metabolic capabilities that suppress the TCA cycle, and that this coupled with decreased RNAIII t

76 terotrophs rely on the transhydrogenase, the TCA cycle, and the oxidative pentose phosphate pathway t

77 cluster biosynthesis factors, members of the TCA cycle, and Type VI Secretion System components.

78 such as vitamin metabolism, the citric acid (TCA) cycle, and amino acid metabolism.

79 uous cristae, mtDNA, the tricarboxylic acid (TCA) cycle, and ATP synthesis powered by an electron tra

80 d degradation, the tricarboxylic acid cycle (TCA) cycle, and fatty acid metabolism.

81 ochondria as part of the tricarboxylic acid (TCA) cycle, and in the cytosol/nucleus as part of the DN

82 ugh glycolysis, beta-oxidation, citric acid (TCA) cycle, and oxidative phosphorylation (oxphos), ther

83 chondrialbeta-oxidation, tricarboxylic acid (TCA) cycle, and respiratory chain.

84 e phosphate pathway, the tricarboxylic acid (TCA) cycle, and serine biosynthesis in cancer cells and

85 uvate metabolism and the tricarboxylic acid (TCA) cycle, and these perturbations are accompanied by t

86 these compounds into the tricarboxylic acid (TCA) cycle, and, correspondingly, there are a variety of

87 ding is that genes in a large portion of the TCA cycle are dispensable, suggesting that S. elongatus

88 ve mitochondrial enzymes associated with the TCA cycle are essential for epigenetic remodeling and ar

89 Thus, glycolysis and the TCA cycle are uncoupled at the level of lactate, which i

90 Certain enzymes of the tricarboxylic acid (TCA) cycle are modified or accumulated, and TCA cycle by

91 glycolysis, glutaminolysis, the citric acid (TCA) cycle as well as the amino acids pools, suggesting

92 from T2D mice, with the tricarboxylic acid (TCA) cycle being one of the primary metabolic pathways i

93 dogenous fumarate accumulation and a genetic TCA cycle block reflected by decreased maximal mitochond

94 re not only able to survive with a truncated TCA cycle, but that they are also able of supporting pro

95 (TCA) cycle are modified or accumulated, and TCA cycle bypasses were repressed rather than induced.

96 biochemical link between glycolysis and the TCA cycle can be completely severed without affecting no

97 Here, we show that lactate is also a TCA cycle carbon source for NSCLC.

98 ral superposition of the SbnG active site to TCA cycle citrate synthases and site-directed mutagenesi

99 l fold of SbnG is structurally distinct from TCA cycle citrate synthases yet similar to metal-depende

100 We found that down-regulation of TCA cycle components, including citrate synthase, malate

101 This decreases Gln uptake, levels of TCA cycle components, mTOR signaling, and proliferation

102 found that following down-regulation of the TCA cycle, cyclin B levels were normal but CDK-1 remaine

103 ed that accumulation of succinate due to the TCA cycle defect could be the major connecting hub betwe

104 2 by revealing an unprecedented link between TCA cycle defects and positive modulation of mTOR functi

105 y increases the formation of both lipid- and TCA cycle-derived intermediates that augment insulin sec

106 l clpC allele, or decreased flux through the TCA cycle diminished the demand for LA and rendered SufT

107 d genes required for the tricarboxylic acid (TCA) cycle, electron transport chain, and oxidative phos

108 IK3CA but also require the expression of the TCA cycle enzyme 2-oxoglutarate dehydrogenase (OGDH).

109 al report of an inactivating mutation in the TCA cycle enzyme complex, succinate dehydrogenase (SDH)

110 tions that inhibit PDHK2 also inactivate the TCA cycle enzyme, aconitase.

111 pression of citrate synthase (CS), the first TCA cycle enzyme, prevented glutamine-withdrawal-induced

112 undance and decreases in tricarboxylic acid (TCA) cycle enzyme abundance with increasing iron limitat

113 Mutations in the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase (FH) are associated

114 of the gene encoding the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase (FH) cause a heredi

115 However, expression of genes encoding TCA cycle enzymes and mitochondria electron transport co

116 RNA sequencing reveals that a number of TCA cycle enzymes and nuclear-encoded mitochondrial gene

117 Genes encoding putative glycolytic and TCA cycle enzymes as well as components of respiratory c

118 so driven by mutations in genes encoding the TCA cycle enzymes or by activation of hypoxia signaling.

119 this nuclear localization, and a failure of TCA cycle enzymes to enter the nucleus correlates with l

120 st consistent with the disruption of two key TCA cycle enzymes, pyruvate dehydrogenase and alpha-keto

121 mutations prompted us to examine the role of TCA cycle enzymes.

122 cquired mutations in the tricarboxylic acid (TCA) cycle enzymes have been reported in diverse cancers

123 ociated mutations in the tricarboxylic acid (TCA) cycle enzymes isocitrate dehydrogenases 1 and 2 (ID

124 ar-encoded mitochondrial tricarboxylic acid (TCA) cycle enzymes that produce oncogenic metabolites, t

125 sh skeletal muscle glycogen as the source of TCA cycle expansion that normally accompanies exercise a

126 A complete TCA cycle facilitates utilization of the microbiota-deri

127 oacetate) must enter the tricarboxylic acid (TCA) cycle first and then use phosphoenolpyruvate carbox

128 accompanies exercise and imply that impaired TCA cycle flux is a central mechanism of restricted oxid

129 indices of pyruvate dehydrogenase activity, TCA cycle flux, and hepatic TAG secretion.

130 ty measurements that directly correlate with TCA cycle flux, as measured by gas chromatography mass s

131 rized by no changes in respiration rates and TCA cycle flux, which together with increases of pyruvat

132 ound TRX to be a redox-sensitive mediator of TCA cycle flux.

133 However, PEPCK is also a key regulator of TCA cycle flux.

134 lls also share an increase in glycolytic and TCA cycle flux.

135 he mean rates of hepatic tricarboxylic acid (TCA) cycle flux (VTCA) and anaplerotic flux (VANA) to be

136 ll respiration rates and tricarboxylic acid (TCA) cycle flux.

137 -dependent remodeling of tricarboxylic acid (TCA) cycle fluxes and decreases antibiotic sensitivity w

138 xit of citrate from the mitochondria and the TCA cycle for the generation of cytosolic acetyl-coenzym

139 pathways crucial to tumor growth require the TCA cycle for the processing of glucose and glutamine de

140 rect acetyl-CoA into the tricarboxylic acid (TCA) cycle for ATP production rather than utilizing it f

141 arate, providing mechanistic explanation for TCA cycle fragmentation.

142 s necessary for the maintenance of oxidative TCA cycle function and mitochondrial membrane potential.

143 acyl-CoA metabolism, glucose metabolism, and TCA cycle function in the absorptive state and suggest t

144 Genetic reconstitution only of the oxidative TCA cycle function specifically in these inducible rho(o

145 on) cells) diminished respiration, oxidative TCA cycle function, and the mitochondrial membrane poten

146 mitochondrial respiration, network dynamics, TCA cycle function, and turnover all have the potential

147 CoA, enabling persistent tricarboxylic acid (TCA) cycle function.

148 c capacity, and improved tricarboxylic acid (TCA) cycle function.

149 is a major direct positive regulator of the TCA cycle gene citB.

150 c pathways, including amino acid metabolism, TCA cycle, gluconeogenesis, glutathione metabolism, pant

151 the hub molecule linking tricarboxylic acid (TCA) cycle, glycolysis and gluconeogenesis by conversion

152 essential enzyme in the tricarboxylic acid (TCA) cycle, has been identified as one such potential th

153 ontributes glucose-derived acetyl-CoA to the TCA cycle in a stage-independent process, whereas anaple

154 ate oxidation from (13)C-glucose through the TCA cycle in mouse tissues and cultured cells.

155 ctron acceptors induce a complete, oxidative TCA cycle in S.

156 Real-time molecular imaging of the TCA cycle in vivo will be important in understanding the

157 undergoes an incomplete tricarboxylic acid (TCA) cycle in the anaerobic mammalian gut.

158 ere, we present evidence that an alternative TCA cycle, in which acetate:succinate CoA-transferase (A

159 tion; it requires the activity of a branched TCA cycle, in which glutamine-dependent reductive carbox

160 Enzymes of the tricarboxylic acid (TCA) cycle, including aconitase and succinate dehydrogen

161 The TCA cycle integrates glucose, amino acid, and lipid meta

162 tabolic routes by quantitatively drawing off TCA cycle intermediaries.

163 Last, addition of the TCA cycle intermediate alpha-ketoglutarate to the Rb TKO

164 e reversed by metabolic supplementation with TCA cycle intermediate alpha-ketoglutarate.

165 2OG is a TCA cycle intermediate and an essential cofactor for man

166 ermeable ester of alphaKG reversed the lower TCA cycle intermediate concentrations and increased ATP

167 mation, decreased glycemia, deranged hepatic TCA cycle intermediate concentrations, and impaired hepa

168 ry rates were unaltered in roots and shoots, TCA cycle intermediate organic acids were depleted in le

169 ith the antioxidant N-acetyl cysteine or the TCA cycle intermediate oxaloacetate efficiently rescues

170 mediator, the mitochondrial the citric acid(TCA) cycle intermediate alpha-ketoglutarate (alphaKG), w

171 ch as that consequent to tricarboxylic acid (TCA) cycle intermediate depletion.

172 osphoenolpyruvate to the tricarboxylic acid (TCA) cycle intermediate oxaloacetic acid.

173 toglutarate (alphaKG), a tricarboxylic acid (TCA) cycle intermediate, through two deamination reactio

174 etabolize (13)C-labeled beta-HB into various TCA cycle intermediates and amino acids.

175 mine (Q) as an anaplerotic carbon source for TCA cycle intermediates and as a nitrogen source for nuc

176 ster of alpha-ketoglutarate reversed the low TCA cycle intermediates and ATP content in myotubes duri

177 -M), encoded by the nuclear PCK2 gene, links TCA cycle intermediates and glycolytic pools through the

178 tal muscle ammonia toxicity by targeting the TCA cycle intermediates and mitochondrial ROS.

179 s in increased glutamine dependence for both TCA cycle intermediates and reactive oxygen species supp

180 id and sensitive methods for quantifying the TCA cycle intermediates and related organic acids.

181 led a reduced ability to utilize a number of TCA cycle intermediates as well as a failure to utilize

182 not retain increased levels of glycolytic or TCA cycle intermediates but nevertheless displayed incre

183 observed during hyperammonaemia with reduced TCA cycle intermediates compared to controls.

184 , the contribution of circulating lactate to TCA cycle intermediates exceeds that of glucose, with gl

185 ectrometry (LC-MS/MS) method to quantify the TCA cycle intermediates in a 96-well format after O-benz

186 asted mice, (13)C-lactate extensively labels TCA cycle intermediates in all tissues.

187 ransaminase enables anaplerotic refilling of TCA cycle intermediates in stroke-affected brain.

188 ), resulting in diminished production of the TCA cycle intermediates oxaloacetate and NADPH, and impa

189 was validated for quantitation of all common TCA cycle intermediates with good sensitivity, including

190 l and cellular studies on the interaction of TCA cycle intermediates with KDM5B, which is a current m

191 During exercise, glycolytic intermediates, TCA cycle intermediates, and pantothenate expand dramati

192 enables glucose-derived carbon to replenish TCA cycle intermediates, as a key component of anabolic

193 reveal the potential for KDM5B inhibition by TCA cycle intermediates, but suggest that in cells, such

194 nides have a modest effect on glycolytic and TCA cycle intermediates, but they strongly deplete nucle

195 enous glutamine for proliferation, supply of TCA cycle intermediates, lipid synthesis, mTOR activity,

196 llular lactate levels, and altered levels of TCA cycle intermediates, the latter of which may be rela

197 , including lactate metabolism and increased TCA cycle intermediates.

198 e metabolic process involved in replenishing TCA cycle intermediates.

199 reases incorporation of Gln carbons into the TCA cycle intermediates.

200 mine (Q) as an anaplerotic carbon source for TCA cycle intermediates.

201 levels of other nonessential amino acids or TCA cycle intermediates.

202 lactate concentration, as well as changes in TCA cycle intermediates.

203 ons in the levels of key tricarboxylic acid (TCA) cycle intermediates and amino acids.

204 Altered levels of tricarboxylic acid (TCA) cycle intermediates and the associated metabolites

205 carbons contributing to tricarboxylic acid (TCA) cycle intermediates and the pentose phosphate pathw

206 , wherein glycolytic and tricarboxylic acid (TCA) cycle intermediates are shunted away for the synthe

207 pathway that sequesters tricarboxylic acid (TCA) cycle intermediates into methylcitrate cycle interm

208 ysis/gluconeogenesis and tricarboxylic acid (TCA) cycle intermediates showed increased abundance at 1

209 th oxidative stress, and tricarboxylic acid (TCA) cycle intermediates were quantified.

210 amino acid metabolites, tricarboxylic acid (TCA) cycle intermediates, and acylcarnitines between the

211 amines, fatty acids, and tricarboxylic acid (TCA) cycle intermediates, were tested for the ability to

212 tabolite), and decreased tricarboxylic acid (TCA) cycle intermediates--generated hypotheses that were

213 d coordinately decreases tricarboxylic acid (TCA) cycle intermediates.

214 acids that are primarily tricarboxylic acid (TCA) cycle intermediates.

215 olved in replenishing of tricarboxylic acid (TCA) cycle intermediates.

216 the addition of multiple tricarboxylic acid (TCA) cycle intermediates.

217 sphate pathway (PPP) and tricarboxylic acid (TCA) cycle intermediates.

218 abolites, including amino acids, lipids, and TCA-cycle intermediates that are avidly utilized by canc

219 Therefore, the TCA cycle involves numerous carbon fluxes through centra

220 via an accelerated oxidation of fuels in the TCA cycle is involved in life span regulation; this mech

221 The tricarboxylic acid (TCA) cycle is a central metabolic pathway responsible fo

222 The tricarboxylic acid (TCA) cycle is an interface among glycolysis, lipid metab

223 The tricarboxylic acid (TCA) cycle is central to energy production and biosynthe

224 The tricarboxylic acid (TCA) cycle is involved in the complete oxidation of orga

225 amine utilization in the tricarboxylic acid (TCA) cycle is not well understood, with the source(s) of

226 The tricarboxylic acid cycle (TCA cycle) is a central metabolic pathway that provides

227 The latter, also formed by the TCA cycle, is converted to phosphoglycerate by a reactio

228 succinate, an intermediate metabolite in the TCA cycle, is increased by 24-fold in BMSCs from T2D mic

229 ce of the glyoxylate cycle, a variant of the TCA cycle, is still poorly documented in cyanobacteria.

230 ating PCK2 hindered fumarate carbon flows in TCA cycle, leading to attenuated oxidative phosphorylati

231 c intermediates into the Tricarboxylic Acid (TCA) cycle, leading to reduced citrate production and de

232 e to Fe-S enzymes in the tricarboxylic acid (TCA) cycle leads to acetate buildup by Ald4p.

233 ppears to be caused by altered mitochondrial TCA cycle metabolism and respiratory substrate utilizati

234 irely new regime wherein the local status of TCA cycle metabolism is interrogated on the time scale o

235 Multiple genes involved in TCA cycle metabolism were also significantly reduced in

236 tion that results in the accumulation of the TCA cycle metabolite fumarate.

237 rexpressing KDM5B in response to dosing with TCA cycle metabolite pro-drug esters, suggesting that th

238 Malate, the tricarboxylic acid (TCA) cycle metabolite, increased lifespan and thermotole

239 reases in the steady-state concentrations of TCA cycle metabolites including alpha-KG, succinate, fum

240 chondrion depended on which transporters for TCA cycle metabolites were included in the model.

241 in oxidative phosphorylation and changes in TCA cycle metabolites, as well as decreased mitochondria

242 tions between various microbiota members and TCA cycle metabolites, as well as some microbial-specifi

243 ing in AMP/ATP ratio, the release of ROS and TCA cycle metabolites, as well as the localization of im

244 (13)C-lactate revealed extensive labeling of TCA cycle metabolites.

245 irected by mitochondrial tricarboxylic acid (TCA) cycle metabolites.

246 behavior to a metabolic imbalance: levels of TCA-cycle metabolites including alpha-ketoglutarate are

247 se results provide evidence for a functional TCA cycle metabolon in plants, which we discuss in the c

248 hesis, heat shock, calvin cycle, glycolysis, TCA cycle, mitochondrial electron transport, and starch

249 In summary, our work identifies the pyruvate-TCA cycle node as a focal point for controlling the host

250 e majority of carbons in the tricyclic acid (TCA) cycle of ECs and contributes to lipid biosynthesis

251 d intracellularly, while tricarboxylic acid (TCA) cycle oxidoreductive enzymes and most electron tran

252 levels of glycolysis and tricarboxylic acid (TCA) cycle pathway intermediates.

253 ent extents of combination of glycolysis and TCA cycle pathways for anaerobic reducing power and ener

254 s in the levels of enzymes of glycolysis and TCA cycle pathways, which were reflective of an imbalanc

255 systems involved in the tricarboxylic acid (TCA) cycle, photorespiration, and the degradation of bra

256 Although the TCA cycle plays a crucial role in aerobic organisms and

257 indicated that lactate's contribution to the TCA cycle predominates.

258 of the cell, and that down-regulation of the TCA cycle prevents the removal of CDK-1 inhibitory phosp

259 glutarate to generate citrate via retrograde TCA cycling, promoting lipogenesis and reprogramming of

260 P7's Wood-Ljungdahl pathway, right branch of TCA cycle, pyruvate synthesis, and sugar phosphate pathw

261 nversely, inhibiting metabolic flux into the TCA cycle reduced cellular heme levels and HAP4 transcri

262 AZD3965 also increased the levels of TCA cycle-related metabolites and (13)C-glucose mitochon

263 ulates the expression of tricarboxylic acid (TCA) cycle-related genes.

264 se studies revealed that tricarboxylic acid (TCA) cycle-related urinary metabolites were increased in

265 Only the combination of TCA cycle replenishment plus asparagine supplementation

266 te pathway (PPP) and the tricarboxylic acid (TCA) cycle, reprogramming glucose metabolism.

267 and connects the glycolytic pathway with the TCA cycle, restored CFA to rne deaD mutant bacteria cult

268 ain flavoproteins or for tricarboxylic acid (TCA) cycle resulted in increased resistance of E. coli t

269 Analysis of the proteins in TCA cycle showed succinate dehydrogenase subunit B (SDHB

270 nd it is possible that some PAOs may rely on TCA cycle solely without glycolysis.

271 ation, including glycolysis/gluconeogenesis, TCA cycle, starch biosynthesis, lipid metabolism, protei

272 ting that anaplerosis of tricarboxylic acid (TCA) cycle substrates likely plays a role in lifespan ex

273 on at the intersection of glycolysis and the TCA cycle, such as pyruvate, acetate, oxaloacetate and c

274 An oxygen-tolerant TCA cycle supporting anaerobic manganese reduction is th

275 iations in the complete dehydrogenase-driven TCA cycle that could support anaerobic acetate oxidation

276 have a fully operational tricarboxylic acid (TCA) cycle that plays a central role in generating ATP a

277 e and glutamine, by supplying carbons to the TCA cycle to produce ATP, positively feed back to mTORC1

278 the metabolic flux to be redirected from the TCA cycle to the glyoxylate shunt, which was also activa

279 nd pyruvate oxidation via the tricarboxylic (TCA) cycle to aerobic glycolysis, thereby increasing dep

280 cells utilize Gln in the tricarboxylic acid (TCA) cycle to maintain sufficient pools of biosynthetic

281 routes into a canonical tricarboxylic acid (TCA) cycle to satisfy their energy requirements.

282 witch from utilizing the tricarboxylic acid (TCA) cycle to using the ethylmalonyl-CoA pathway for ass

283 by tissues via the tricarboxylic acid cycle (TCA cycle) to carbon dioxide.

284 tate, substrates for citrate synthase in the TCA cycle, to produce oxalic acid in response to bacteri

285 t role for OAT1 in metabolism involving: the TCA cycle, tryptophan and other amino acids, fatty acids

286 )C labeling in organic acids involved in the TCA cycle using scheduled multiple reaction monitoring a

287 nverted to aspartate and reintroduced in the TCA cycle via 2-oxoglutarate/glutamate.

288 cess, whereas anapleurotic carbon enters the TCA cycle via a stage-dependent phosphoenolpyruvate carb

289 te the anaplerotic entry of glutamine to the TCA cycle via GDH.

290 yoxylate shunt (via isocitrate lyase) or the TCA cycle (via isocitrate dehydrogenase (ICDH) activity)

291 ing that the newly discovered cyanobacterial TCA cycle (via the gamma-aminobutyric acid pathway or al

292 h the highest frequency, whereas the reverse TCA cycle was little used.

293 The TCA cycle was previously shown to be necessary for the d

294 dehydrogenase, which links glycolysis to the TCA cycle, was also maximized to ensure the conversion o

295 at fatty acid signaling and flux through the TCA cycle were enhanced.

296 cted cells do not metabolize glucose via the TCA cycle when GLN is depleted, as revealed by (13)C-glu

297 ating glycolysis and the tricarboxylic acid (TCA) cycle, which is instrumental in cancer metabolism a

298 e in the intermediates of glycolysis and the TCA cycle while increasing ketones.

299 naplerotic activity is high to replenish the TCA cycle with the intermediaries withdrawn for ectoines

300 There are few known variations of a complete TCA cycle, with the common notion being that the enzymes