ライフサイエンスコーパス: TCA

1 TCA was induced by laparoscopic liver lobe resection com

2 -specific chlorine isotope analysis of 1,1,1-TCA was performed for the first time, and transformation

3 The sample was extracted with 5% TCA and cleaned up with Florisil providing 83.7% recover

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

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

6 technology, we present the development of a TCA reader, a platform technology that significantly imp

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

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

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

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

11 increased by 2.6-fold and taurocholic acid (TCA) level reduced by 71%.

12 Taurocholic acid (TCA), taurochenodeoxycholic acid (TCDCA) as well as taur

13 the absorption pathway of taurocholic acid (TCA)-linked heparin and docetaxel (DTX) conjugate, which

14 cumulation of glutamate, tricarboxylic acid (TCA) anaplerotic intermediates and GSH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 out by the addition of trichloroacetic acid (TCA) and subsequent centrifugation.

73 ncomplete oxidation of trichloroacetic acid (TCA) and trifluoroacetic acid (TFA) resulted in lower re

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

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

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

77 Thus, although TCAs are not required to guide the tangential migration

78 limitations, thermal contrast amplification (TCA) is a new method that is based on the laser excitati

79 m (PEPCK-C) potentiating gluconeogenesis and TCA flux.

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

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

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

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

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

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

86 s was observed in toxicokinetics of PERC and TCA in every tissue examined.

87 ighly variable relationship between PERC and TCA toxicokinetics and toxicodynamics at the population

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

89 All measurements (GM, WM, and TCA) were inversely correlated with Expanded Disability

90 progenitors (IPCs), whereas interneurons and TCAs are of extrinsic origin.

91 nd 1.37 mm2 [13.2%]; P < .001 at T9/T10) and TCAs (mean differences [COV]: 3.66 mm2 [9.0%]; P < .001

92 CXCR4 expression in the forming thalamus and TCAs, we identified a CXCR4-dependent growth-promoting e

93 ) and the tricyclic class of antidepressant (TCA) agents.

94 RIs compared with tricyclic antidepressants (TCAs) among new users of antidepressants and according t

95 Four hits were tricyclic antidepressants (TCAs), and they repressed expression of pro-fibrotic fac

96 es the actions of tricyclic antidepressants (TCAs).

97 Total cord areas (TCAs), GM areas, and WM areas at the disc levels C2/C3,

98 hemorrhage-induced traumatic cardiac arrest (TCA).

99 rneuron migration and thalamo-cortical axon (TCA) pathfinding follow similar trajectories and timing,

100 neurons and individual thalamocortical axon (TCA) arbors that synapse with them.

101 arrel rings encircling thalamocortical axon (TCA) clusters while mGluR5 knock-out (KO) neurons were p

102 Some thalamocortical axons (TCAs) also fail to leave the diencephalon or abnormally

103 rgic interneurons and thalamocortical axons (TCAs) are essential elements of the cerebrocortical netw

104 nsory information via thalamocortical axons (TCAs).

105 r levels of PERC, TCA, and triglycerides; b) TCA levels in liver and kidney; and c) TCA levels in ser

106 2 by revealing an unprecedented link between TCA cycle defects and positive modulation of mTOR functi

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

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

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

110 s; b) TCA levels in liver and kidney; and c) TCA levels in serum, brain, fat, and lung.

111 l of lactate, which is a primary circulating TCA substrate in most tissues and tumours.

112 A3H-I also associates with clonal TCA/T-biased mutations in lung adenocarcinoma suggesting

113 encoded using unique combinations of codons (TCA-[X]4-GGAGGAGGA, AGT-[X]4-GGTGGTGGT, etc., where [X]4

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

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

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

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

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

119 the rate-limiting tricarboxylic acid cycle (TCA) isocitrate dehydrogenase 2 and superoxide dismutase

120 key enzyme in its tricarboxylic acid cycle (TCA) pathway.

121 that S. elongatus does not require a cyclic TCA process.

122 and PLS algorithms can be used to determine TCA and TPC in intact wax jambu fruit.

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

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

125 c shift compared to values obtained with EA (TCA Deltadelta(13)C(EA/LC-IRMS) = 8.8 per thousand, TFA

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

127 The first TCA rewiring occurs in mice in 2-day hypoxia and is medi

128 arate, providing mechanistic explanation for TCA cycle fragmentation.

129 stone deacetylase 5, which are important for TCA responsiveness.

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

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

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

133 omparative studies were conducted using free TCA as a pre-administration and exhibited the maximum ab

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

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

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

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

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

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

140 r-Cyc/VMito by 20-30-fold, increased hepatic TCA metabolite concentrations 2-3-fold, and increased en

141 ed fruity, coconut/wood/vanilla and humidity/TCA notes, but not the leather/animal/ink note.

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

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

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

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

146 lyamines and nucleotides, but an increase in TCA and urea cycle intermediates.

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

148 study than non-oxygen carrying solutions in TCA.

149 , including lactate metabolism and increased TCA cycle intermediates.

150 Indeed, TCA treatment of HSCs promoted accumulation of ceramide

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

152 geal Cxcl12 intact, attenuates intracortical TCA growth and disrupts tangential interneuron migration

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

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

155 uch as the importance of a truncated, linear TCA pathway, low flux toward amino acid synthesis from p

156 ea under the curve (AUC), the range of liver TCA levels spanned nearly an order of magnitude ( 8-fold

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

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

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

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

161 dicts that stored red blood cells metabolize TCA intermediates to regenerate important cofactors, suc

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

163 erexpression of Cyp7a1 and Cyp8b1 normalizes TCA level, bile acid composition, and intestinal cholest

164 lated with rates for 1,1-DCE and TCE but not TCA.

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

166 Only the combination of TCA cycle replenishment plus asparagine supplementation

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

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

169 Here we report that disruption of TCA innervation, or TCA-derived glutamate, affected the

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

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

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

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

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

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

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

177 e catabolism, there is near complete loss of TCA intermediates, with no compensation from glucose-der

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

179 he role of glutaminolysis and metabolites of TCA in supporting myofibroblast differentiation.

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

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

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

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

184 hyde assay was used to follow the release of TCA-soluble peptides over a 24h period.

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

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

187 ors control proper navigation of a subset of TCA and CTA projections through the VTel.

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

189 Tests indicated that the use of TCA was most effective when added in the final step of t

190 mal interneuron lamination in the absence of TCAs.

191 lular mechanisms that mediate the actions of TCAs in neuropathic pain states.

192 allowing coordinated neocortical invasion of TCAs and interneurons.

193 cortical neurogenesis to the progression of TCAs and interneurons spatially and temporally.

194 Finally, the abnormal projection of TCAs toward the amygdala is also present in mice carryin

195 ected the influence of IPC-derived CXCL12 on TCAs and interneurons by showing that Cxcl12 ablation in

196 pendent growth-promoting effect of CXCL12 on TCAs in thalamus explants.

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

198 ificant differences in either the WM area or TCA.

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

200 eport that disruption of TCA innervation, or TCA-derived glutamate, affected the laminar distribution

201 itochondrial metabolites (e.g. AMP and other TCA).

202 Oxidative TCA flux was achieved through enhanced reliance on gluta

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

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

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

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

207 was observed among a) liver levels of PERC, TCA, and triglycerides; b) TCA levels in liver and kidne

208 a cell-autonomous role of CXCR4 in promoting TCA growth.

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

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

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

212 tly in the numbers of trinucleotide repeats (TCA, TCG, or TCT) in the serine repeat region, with only

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

214 of exogenous alpha-ketoglutarate replenishes TCA intermediates and rescues cellular growth, but simul

215 e metabolic process involved in replenishing TCA cycle intermediates.

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

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

218 Surprisingly, absence of the Salmonella TCA enzyme aconitase induced rapid NLRP3 inflammasome ac

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

220 The tested TCA intermediates were poor or moderate KDM5B inhibitors

221 At the morphological level, we find that TCA arbors fail to develop into discrete, concentrated p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 diverting glucose-derived pyruvate into the TCA cycle.

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

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

242 on glutamine to anaplerotically maintain the TCA cycle.

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

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

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

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

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

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

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

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

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

252 decreased, which confirmed disruption of the TCA cycle.

253 ion in the NAc increases the efficacy of the TCA desipramine and dramatically accelerates its onset o

254 The development of the TCA reader enables simple, highly sensitive quantificati

255 o facilitate the clinical translation of the TCA technology, we present the development of a TCA read

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

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

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

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

260 sed glutamine uptake serves to replenish the TCA cycle.

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

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

263 More specifically, the TCA reader demonstrated up to an 8-fold enhanced analyti

264 cells could be rescued by supplementing the TCA cycle.

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

266 MTHFD2, and MTHFD2 knockdown suppresses the TCA cycle.

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

268 ed in human subjects, demonstrating that the TCA double rewiring represents an essential factor for t

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

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

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

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

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

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

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

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

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

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

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

280 diates shuttling into and cycling within the TCA cycle.

281 the sphingolipid pathway as a target of the TCAs.

282 This TCA reader provides enhanced sensitivity over visual det

283 state, the contribution of glucose to tissue TCA metabolism is primarily indirect (via circulating la

284 t of cortical glutamatergic neurons close to TCA clusters; (2) the regulation of dendritic complexity

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

286 CH (RR, 1.17; 95% CI, 1.02-1.35) relative to TCAs, highest during the first 30 days of use (RR, 1.44;

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

288 of dendritic complexity and outgrowth toward TCA clusters; (3) spinogenesis; and (4) tuning of excita

289 dendritogenesis: orienting dendrites toward TCAs, adding de novo dendritic segments, and elongating

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

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

292 imary oxidative metabolite trichloroacetate (TCA) in multiple tissues.

293 = 34) was lower than 1,1,1-trichloroethane (TCA) but similar to 1,1-dichloroethene (1,1-DCE) and tri

294 ichloroethene (TCE) > 1,1,1-trichloroethane (TCA).

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

296 er cytochrome P4502E1 did not correlate with TCA levels.

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

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

299 Current use of SSRIs compared with TCAs and strong compared with weak serotonin reuptake in

300 Cytosine mutations within TCA/T motifs are common in cancer.