ライフサイエンスコーパス: TCA cycle

1 (PDH) complex (PDC) links glycolysis and the TCA cycle.

2 nucleotide synthesis but low activity of the TCA cycle.

3 decreases the flux of carbohydrates into the TCA cycle.

4 oxidation of excess quinols generated by the TCA cycle.

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

6 diates shuttling into and cycling within the TCA cycle.

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

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

9 decreased, which confirmed disruption of the TCA cycle.

10 MTHFD2, and MTHFD2 knockdown suppresses the TCA cycle.

11 sed glutamine uptake serves to replenish the TCA cycle.

12 cells could be rescued by supplementing the TCA cycle.

13 diverting glucose-derived pyruvate into the TCA cycle.

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

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

16 d fatty acids all contributed carbons to the TCA cycle.

17 in flux through the individual steps of the TCA cycle.

18 to the contribution of glutaminolysis to the TCA cycle.

19 ioenergetic dysfunction lies upstream of the TCA cycle.

20 es encode members of the tricarboxylic acid (TCA) cycle.

21 f glucose to support the tricarboxylic acid (TCA) cycle.

22 r glucose in feeding the tricarboxylic acid (TCA) cycle.

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

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

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

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

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

28 ch enzymatic step of the tricarboxylic acid (TCA) cycle.

29 on of metabolites by the tricarboxylic acid (TCA) cycle.

30 tial intermediate in the tricarboxylic acid (TCA) cycle.

31 of substrates within the tricarboxylic acid (TCA) cycle.

32 encoding enzymes of the tricarboxylic acid (TCA) cycle.

33 away from lipogenesis toward ketogenesis and TCA cycle, a milieu which can hasten oxidative stress an

34 damaging reactive oxygen species (ROS) when TCA cycle activity exceeds the ability of oxidative phos

35 , we found that high dietary sugar increases TCA cycle activity, alters neurochemicals, and depletes

36 genic flux and sustained tricarboxylic acid (TCA) cycle activity, which are concurrent to onset of ox

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

38 ced by murine macrophages is responsible for TCA cycle alterations and citrate accumulation associate

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

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

41 s of intermediate metabolites of glycolysis, TCA cycle, amino acids, pentose phosphate pathway, and u

42 tly, both STAT5 inhibition and disruption of TCA cycle anaplerosis are associated with reduced IL-2 p

43 AT5 activity for amino acid biosynthesis and TCA cycle anaplerosis.

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

47 triggers uptake and nitrogen metabolism, the TCA cycle and carbon oxidation are decreased, while carb

48 itions, unphosphorylated ManX stimulates the TCA cycle and carbon oxidation, while unphosphorylated P

49 l, which is essential to drive the oxidative TCA cycle and DHODH activity.

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

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

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

53 More importantly, the induction of TCA cycle and lipogenesis occurred together with the dow

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 o the perturbation of amino acid metabolism, TCA cycle and oxidative stress.

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

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

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

60 ghlighted the differential regulation of the TCA cycle and the GABA shunt between Ain1 and Osl1.

61 ism further promotes favorable fluxes in the TCA cycle and the gluconeogenesis-anaplerosis nodes, des

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

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

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

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

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

67 metabolic enzymes in the tricarboxylic acid (TCA) cycle and electron transport chain (ETC).

68 of hepatic mitochondrial tricarboxylic acid (TCA) cycle and lipogenesis are central features of embry

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

70 producing processes, the tricarboxylic acid (TCA) cycle and oxidative phosphorylation.

71 ic pathways, such as the tricarboxylic acid (TCA) cycle and the pentose phosphate pathway.

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

73 ation of genes related to glycolysis and the TCA cycle, and a lower rate of cell cycle.

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

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

78 is, gluconeogenesis, the tricarboxylic acid (TCA) cycle, and amino acid synthesis/catabolism.

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

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

81 such as glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation (Oxphos), and

82 ing Pyruvate Metabolism, Tricarboxylic acid (TCA) cycle, and Oxidative Phosphorylation (OXPHOS), whic

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

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

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

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

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

88 ways like amino acid and tricarboxylic acid (TCA) cycle are also profoundly perturbed.

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

90 elationship between photorespiration and the TCA cycle, as TPP riboswitch mutants accumulate less pho

91 However, due to the block in the TCA cycle at SDH, the high glutamine oxidation activity

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 ng the connection between glycolysis and the TCA cycle by inactivation of PDC has only minor effects

96 is for ATP production, operates a bifurcated TCA cycle by increasing flux through the glyoxylate shun

97 on and lactate production, whereas inhibited TCA cycle by reducing the amounts of Acetyl-CoA.

98 y from glycolysis to the tricarboxylic acid (TCA) cycle by producing acetyl coenzyme A from pyruvate.

99 uding those of the tricarboxylic acid cycle (TCA cycle), by mixed-mode reversed-phase chromatography,

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

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

102 f fumarate hydratase, a tumor suppressor and TCA cycle component, confers resistance to cysteine-depr

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

104 The tricarboxylic acid (TCA) cycle converts the end products of glycolysis and f

105 ant changes in the anaplerotic flux into the TCA cycle could be the critical defect underlying CAN pr

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

107 2 by revealing an unprecedented link between TCA cycle defects and positive modulation of mTOR functi

108 ere mapped to pathways of glycolysis and the TCA cycle demonstrating tumor metabolic behavior.

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

110 ecreased flux toward the tricarboxylic acid (TCA) cycle during the metabolism of glycolytic substrate

111 arkedly enhanced respiration and deregulated TCA cycle dynamics suggesting decreased resource efficie

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

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

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

115 2 showed reduced activity of a rate-limiting TCA cycle enzyme, alpha-ketoglutarate dehydrogenase.

116 utations of the FH gene that encodes for the TCA cycle enzyme, fumarate hydratase.

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

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

119 e and key glycolytic and tricarboxylic acid (TCA) cycle enzyme levels, and triggers synapse maturatio

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

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

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

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

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

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

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

127 complex II, and certain tricarboxylic acid (TCA) cycle enzymes, which led to mitochondrial membrane

128 ulfur cluster-containing proteins, including TCA-cycle enzymes, result in decreased respiration, lowe

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

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

131 xylic acid-mediated ripening, including AOX, TCA cycle, fatty acid metabolism, amino acid metabolism,

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

133 sis (four genes) and the tricarboxylic acid (TCA) cycle (five genes), and four genes (GmFATB1a, GmPDA

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

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

136 bon metabolism, abnormal tricarboxylic acid (TCA) cycle flux and glutamate metabolism, dysfunctional

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

138 that link the key mitochondrial lipid CL to TCA cycle function and energy metabolism.

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

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

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

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

143 DH activation, generation of acetyl-CoA, and TCA cycle function, findings that link the key mitochond

144 associated with impaired tricarboxylic acid (TCA) cycle function and metabolite induction.

145 htly coupled to the transcription signals of TCA cycle genes but escapes all known posttranscriptiona

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

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

148 carbon flux between the tricarboxylic acid (TCA) cycle, glyoxylate shunt and methylcitrate cycle at

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

150 ates, combined with expression of a complete TCA cycle, heterotrophic pathways for carbon assimilatio

151 metabolic routes to import pyruvate into the TCA cycle in an energy substrate specific way.

152 g as a starting point the involvement of the TCA cycle in PPGL development, we aimed to identify unre

153 and further strengthens the relevance of the TCA cycle in PPGL development.

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

155 s of infused [(13)C(5)]-glutamine enters the TCA cycle in the tumors and tumors utilize anaplerotic g

156 s of infused [(13)C(5)]-glutamine enters the TCA cycle in the tumors.

157 nce CRCs utilizes glutamine to replenish the TCA cycle in vivo, suggesting that targeting glutamine m

158 r TCA metabolites in the tricarboxylic acid (TCA) cycle in mediating lipid accumulation and oxidative

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

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

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

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

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

164 cifically reduced intracellular succinate, a TCA cycle intermediate that serves as a direct electron

165 specifically bind to the tricarboxylic acid (TCA) cycle intermediate succinate.

166 d by the addition of the tricarboxylic acid (TCA) cycle intermediate, alpha-ketoglutarate, suggesting

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

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

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

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

171 lic changes, typified by accumulation of the TCA cycle intermediates citrate, itaconate, and succinat

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

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

174 dipocytes increased labeling of pyruvate and TCA cycle intermediates from U(13)C-glucose.

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

176 carnitines and increased pyruvate along with TCA cycle intermediates in females (HFD > CD).

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

178 asma metabolomic analysis of amino acids and TCA cycle intermediates in subjects with type 1 diabetes

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

180 trate, alpha-ketoglutarate and succinate are TCA cycle intermediates that also play essential roles i

181 the Rsb system responding differentially to TCA cycle intermediates to regulate metabolism and key d

182 type PIK3CA, labeling from glutamine to most TCA cycle intermediates was higher in PIK3CA-mutant subc

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

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

185 y elevated glycolytic intermediates, reduced TCA cycle intermediates, and reduced levels of long chai

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

187 Recent evidence confers a new role for TCA cycle intermediates, generally thought to be importa

188 cells can metabolize glutamine to replenish TCA cycle intermediates, leading to a dependence on glut

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

190 ich was counteracted by supplying downstream TCA cycle intermediates.

191 , including lactate metabolism and increased TCA cycle intermediates.

192 e metabolic process involved in replenishing TCA cycle intermediates.

193 hat loss of MPC1 led to impaired labeling of TCA cycle intermediates.

194 o several metabolic reactions, which produce TCA cycle intermediates.

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

196 increased quantities of tricarboxylic acid (TCA) cycle intermediates and increased oxygen consumptio

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

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

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

200 c substrate to replenish tricarboxylic acid (TCA) cycle intermediates that have been consumed.

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

202 ses such as amino acids, tricarboxylic acid (TCA) cycle intermediates, fatty acids, secondary metabol

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

204 metabolize glucose into tricarboxylic acid (TCA) cycle intermediates.

205 M2 and M4 isotopomers of tricarboxylic acid (TCA) cycle intermediates.

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

207 Furthermore, the TCA cycle is dispensable for survival during osteomyelit

208 flux analysis, we show that the respiratory TCA cycle is upregulated in association with increased n

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

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

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

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

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

214 Thus, the flow from glycolysis to the TCA cycle mediated by PDH plays a pivotal role in the di

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

216 athways involved in amino acid, glucose, and TCA cycle metabolism.

217 identify alterations in Tricarboxylic Acid (TCA) cycle metabolism following even low-level Abeta exp

218 Our observations suggest that TCA cycle metabolite alterations are germane to the path

219 We found consistent TCA cycle metabolite alterations in cases with various g

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

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

222 ctly by enhancing a Tet2 suppressor, the key TCA cycle metabolite, succinate.

223 chanisms by which the abundance of different TCA cycle metabolites controls cellular function and fat

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

225 itate or acetate, and measured production of TCA cycle metabolites or fatty acids.

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

227 -y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with insulin resistance and T2D in

228 -y changes in glycolysis/gluconeogenesis and TCA cycle metabolites with subsequent T2D risk using wei

229 nction as seen by similar alterations in (1) TCA cycle metabolites, (2) tryptophan and kynurenic acid

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

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

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

233 ly, we demonstrated that tricarboxylic acid (TCA) cycle metabolites are more abundant in CSCs compare

234 For example, tricarboxylic acid (TCA) cycle metabolites generated and metabolized in the

235 ysis/gluconeogenesis and tricarboxylic acid (TCA) cycle metabolites have been associated with type 2

236 d oxidation activity and tricarboxylic acid (TCA) cycle metabolites were measured in cells collected

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

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

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

240 c metabolism, including those related to the TCA cycle, mitochondria respiration, and glycolysis, wer

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

242 glutamate metabolism and tricarboxylic acid (TCA) cycle node in prostate cancer-derived cells.

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

244 Inhibition of mitochondrial TCA cycle or electron transfer chain (ETC) mitigated mit

245 mmunostaining exclusively in tumors carrying TCA-cycle or EPAS1 mutations.

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

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

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

249 pathway proteins and 18 tricarboxylic acid (TCA) cycle proteins compared to CsP alone, accompanied b

250 correlates with transcriptional input to the TCA cycle, providing an effective mechanism for the cell

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

252 triction-mediated effect could be rescued by TCA cycle re-stimulation, which yielded increased mitoch

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

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

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

256 this, we applied a targeted sequencing of 37 TCA-cycle-related genes to DNA from 104 PPGL-affected in

257 Only the combination of TCA cycle replenishment plus asparagine supplementation

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

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

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

261 ed Ca(2+) flux machinery and that depends on TCA cycle substrate availability.

262 TCA cycle substrate-dependent MICU1 expression was media

263 but not to malate, and were depleted in all TCA cycle substrates between alpha-ketoglutarate and mal

264 We investigated the effect of TCA cycle substrates on MCU-mediated mitochondrial matri

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

266 encode the components of glycolysis and the TCA cycle, suggesting that they can re-program fundament

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

268 try of glucose and glutamine carbon into the TCA cycle, TGFbeta induced the biosynthesis of proline f

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

270 at encode enzymes of the tricarboxylic acid (TCA) cycle that contain iron-sulfur clusters.

271 A phosphorylation drives PDHc activation and TCA cycle to empower cancer cells adaptation to metastat

272 tamine is an essential carbon source for the TCA cycle to generate energy and macromolecules required

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

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

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

276 genase complex (PDHc) activation to maintain TCA cycle (tricarboxylic acid cycle) and promotes cancer

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

278 tron transport chain and tricarboxylic acid (TCA) cycle, two central bioenergetic pathways.

279 Significant differences in TCA cycle utilization were found for growth on the diffe

280 bstrates but, due to carbon recycling to the TCA cycle via enhanced anaplerosis, the metabolism of gl

281 RT3 depletion impaired glutamine flux to the TCA cycle via glutamate dehydrogenase and reduction in a

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

283 increased glycolysis and tricarboxylic acid (TCA) cycle volume.

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

285 o arginine and proline metabolism as well as TCA cycle was most prominently detected.

286 ution of labeled palmitate or acetate to the TCA cycle was reduced in organoids derived from Hnf4alph

287 t enzyme for anaplerotic replenishing of the TCA cycle, was elevated in TAZ-KO cells, which also exhi

288 oduction pathways, metal transportation, and TCA cycle were active under Cd(II) stress.

289 FAO genes, FAO activity, and metabolites of TCA cycle were all significantly decreased, but fatty ac

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

291 zymes in glycogen metabolism, glycolysis and TCA cycle were hypomethylated in active relative to inac

292 Metabolites related to the TCA cycle were increased in GCTs.

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

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

295 ndent flux through the bottom portion of the TCA cycle while accumulating pyruvate and aspartate that

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

297 arbon metabolism via the tricarboxylic acid (TCA) cycle, while PtsN controls nitrogen uptake, exopoly

298 effective mechanism for the cell to link the TCA cycle with acetate metabolism pathways.

299 shift that combines reduced flux through the TCA cycle with increased synthesis of serine, glycine, a

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