ライフサイエンスコーパス: TCA

1 TCA cycle substrate-dependent MICU1 expression was media

2 TCA was induced by laparoscopic liver lobe resection com

3 TCA, LA, and CVI deserve further study in subjects on th

4 TCA, LA, and CVI may differ between patients with AD, MC

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

6 rmore, catalytic reductions of aqueous 1,1,1-TCA alone or concomitant with TCE catalytic co-reduction

7 removal fluxes were 1.5 g/m(2)/day for 1,1,1-TCA and 1.7 g/m(2)/day for TCE.

8 operation, removals were up to 95% for 1,1,1-TCA and 99% for TCE.

9 Here, we investigated 1,1,1-TCA and TCE co-reduction using palladium nanoparticle (P

10 The catalytic activities for 1,1,1-TCA and TCE reductions reached 9.9 and 11 L/g-Pd/min, va

11 1,1,1-Trichloroethane (1,1,1-TCA) and trichloroethene (TCE) are common recalcitrant c

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

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

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

15 Here, we conducted a TCA targeted metabolomics study on 511 individuals with

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

17 that, although this correlates with abnormal TCA fasciculation, it does not induce topographical erro

18 Conclusions about TCA, however, are based on a limited number of cases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 sed on extraction with trichloroacetic acid (TCA), reaction with 2-thiobarbituric acid (TBA) and quan

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

79 adjustment for age, sex, and visual acuity, TCA was significantly greater in patients with AD (B = 2

80 n into barrels and thalamocortical afferent (TCA) segregation.

81 he mode of action of targeted cancer agents (TCAs) differs from classic chemotherapy, which leads to

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

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

84 We also performed omics-based analyses, TCA-related metabolite determination, and (13)C(5)-gluta

85 fer to as tripartite constellation analysis (TCA), we focused on large-diameter dorsal-root ganglion

86 SNRI (OR: 11.07; 95% CI: 3.265 to 33.82) and TCA (OR: 12.16; 95% CI: 1.503 to 71.58) and implant fail

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

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

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

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

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

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

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

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

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

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

97 ns revealed that the encapsulation of OR and TCA within micelles crucially improved their antibacteri

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

99 Patients taking SNRI and TCA were at the highest risk of implant loss, when compa

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

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

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

103 nhibitors [SNRI], tricyclic antidepressants [TCA], atypical antidepressants [AA], and monoamine oxida

104 RIs], tricyclic and related antidepressants [TCAs], serotonin and norepinephrine reuptake inhibitors

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

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

107 ing ImageJ software, and total choroid area (TCA), luminal area (LA), and stromal area (SA) were segm

108 Total choroidal area (TCA), luminal area (LA), and the choroidal vascularity i

109 idal thickness (SFCT), total choroidal area (TCA), luminal choroidal area (LCA), and stromal choroida

110 hemorrhage-induced traumatic cardiac arrest (TCA).

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

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

113 Thalamocortical axons (TCAs) cross several tissues on their journey to the cort

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

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

116 ermined that this problem is often caused by TCA contamination of the cork stopper, which releases TC

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

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

119 prescribed first antidepressant, followed by TCAs (35.7%).

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

121 essential oil (OR) and trans-cinnamaldehyde (TCA) was studied.

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

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

124 d mitochondrial respiration, and compromised TCA flux compared with DLBCL cells expressing wild type

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

126 semblies of T80, swollen micelles containing TCA were successfully produced.

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

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

129 e mutations in the tricarboxylic acid cycle (TCA) gene succinyl-CoA ligase subunit-beta (SUCLA2), cau

130 o replenishment of tricarboxylic acid cycle (TCA) intermediates and synthesis of adenosine triphospha

131 ine stimulation generates citric acid cycle (TCA) intermediates from both glucose and glutamine revea

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

133 es involved in the tricarboxylic acid cycle (TCA), and have abnormal mitochondrial membrane potential

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

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

136 RORbeta, and Thsd7a knock-out alone disrupts TCA organization in adult barrels.

137 ich was counteracted by supplying downstream TCA cycle intermediates.

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

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

140 the thalamic environment is instructive for TCA navigation and that the molecular cues netrin 1 and

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

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

143 ossibility of prescreening cork stoppers for TCA contamination would be an enormous advantage.

144 The human threshold for TCA is extremely low.

145 the thalamus contains navigational cues for TCAs, we used slice culture transplants and gene express

146 with increasing number of TLs, similarly for TCAs (with/without chemotherapy) and chemotherapy only.

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

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

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

150 This affected metabolic homeostasis: TCA, purine and pyrimidine intermediates, and oxidized N

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

152 he frequency of implant failure was 33.3% in TCA users, 31.3% in SNRI users, 6.3% in SSRI users, 5.2%

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

154 e, but the importance of the diencephalon in TCA mapping is unknown.

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

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

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

158 splay hallmark APOBEC signature mutations in TCA/T motifs.

159 uctions in CMT and SFCT, while reductions in TCA and LCA were only noted at the 1-month follow-up int

160 study than non-oxygen carrying solutions in TCA.

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

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

163 Indeed, TCA treatment of HSCs promoted accumulation of ceramide

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

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

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

167 Contaminations with <0.5 ng/L TCA are commonly considered negligible and are not perce

168 A wine contaminated by 1-2 ng/L TCA can be perceived as tainted.

169 2 showed reduced activity of a rate-limiting TCA cycle enzyme, alpha-ketoglutarate dehydrogenase.

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

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

172 Baseline mean TCA and LCA were 2.30 +/- 1.41 mm(2) and 1.23 +/- 0.73 m

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

174 serine biosynthesis, one carbon metabolism, TCA lipid oxidation and amino acid availability, while i

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

176 unclear whether deprivation of mitochondrial TCA substrates alters mitochondrial Ca(2+) flux.

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

178 ntrinsically preferred trinucleotide motifs (TCA/TCG/TCT).

179 utions were easily accommodated in the Na(+)/TCA cotransporting polypeptide structure model.

180 Only the combination of TCA cycle replenishment plus asparagine supplementation

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

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

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

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

185 nce and differential scanning fluorimetry of TCA intermediates and potential metabolites from a virtu

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

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

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

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

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

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

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

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

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

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

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

197 sented, representing the largest data set of TCA analysis on cork stoppers within the literature and

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

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

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

201 1.1 perform well for response assessment of TCAs.

202 r major tumor types and different classes of TCAs.

203 cate that the correct topographic mapping of TCAs onto the cortex requires the order to be establishe

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

205 and usage of DEF have the largest impacts on TCA reduction.

206 se from 50 clinical trials with at least one TCA.

207 Moreover, the OR or TCA loaded-micelles had only a slight droplet size varia

208 ted an essential role of succinate and other TCA metabolites in the tricarboxylic acid (TCA) cycle in

209 as a single agent (37%), combined with other TCAs (7%), or as chemotherapy (56%); 28% received chemot

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

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

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

213 GLS2 expression rescued cell proliferation, TCA anaplerosis, redox balance, and mitochondrial functi

214 oved capable of nondestructively quantifying TCA contamination in a single cork stopper in 3 s, with

215 al test on the industrial scale, quantifying TCA contamination in more than 10000 cork stoppers in a

216 11% breast, and 25% other); 15,620 received TCAs, predominantly transduction or angiogenesis inhibit

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

218 elation with standard methods for releasable TCA quantification is also discussed.

219 mination of the cork stopper, which releases TCA into the wine.

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

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

222 that, under aerobic conditions, respiratory TCA metabolism is responsible for the supply of addition

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

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

225 address the protein present in quinoa seeds, TCA/Acetone protein extraction was performed using four

226 substitutions (S267X) with three substrates (TCA, estrone-3-sulfate, and rosuvastatin).

227 : the total costs of aftertreatment systems (TCA) of the three cases are reduced to $11,400(1.63 c/km

228 tegral membrane protein, Na(+)/taurocholate (TCA) cotransporting polypeptide, at the site of a pharma

229 The tested TCA intermediates were poor or moderate KDM5B inhibitors

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

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

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

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

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

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

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

237 oxidation of excess quinols generated by the TCA cycle.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 decreases the flux of carbohydrates into the TCA cycle.

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

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

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

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

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

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

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

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

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

262 ioenergetic dysfunction lies upstream of the TCA cycle.

263 nucleotide synthesis but low activity of the TCA cycle.

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

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

266 estructive method capable of quantifying the TCA contamination in cork stoppers is impelling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 to the contribution of glutaminolysis to the TCA cycle.

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

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

285 diates shuttling into and cycling within the TCA cycle.

286 the sphingolipid pathway as a target of the TCAs.

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

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

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

290 asure was CVI, defined as the ratio of LA to TCA.

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

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

293 2,4,6-Trichloroanisole (TCA) contamination of wine determines huge economic loss

294 antly (p < 0,05) the 2,4,6-trichloroanisole (TCA) content of initial wine.

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

296 seline at months 1 and 3 (P < .001), whereas TCA and LCA showed a significant decrease only at the 1-

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

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

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

300 in evaluating tumor response in trials with TCAs.