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1 I fatty acid synthesis and elongation (FAE), tricarboxylic acid, amino sugar, heme, lipoate, and shik
3 as identified as benzene dicarboxylic acids, tricarboxylic acids, and tetracarboxylic acid isomers, c
5 and upregulation of molecules linked to the tricarboxylic acid cycle (eg, aspartate aminotransferase
6 ssumed to be burned fully by tissues via the tricarboxylic acid cycle (TCA cycle) to carbon dioxide.
7 sis of organic acids, including those of the tricarboxylic acid cycle (TCA cycle), by mixed-mode reve
8 rom patients with recessive mutations in the tricarboxylic acid cycle (TCA) gene succinyl-CoA ligase
9 sumption has been linked to replenishment of tricarboxylic acid cycle (TCA) intermediates and synthes
10 IRT3 deacetylase activates the rate-limiting tricarboxylic acid cycle (TCA) isocitrate dehydrogenase
12 -accumulation of metabolites involved in the tricarboxylic acid cycle (TCA), and have abnormal mitoch
13 AGI-6780 combination significantly decreased tricarboxylic acid cycle activity and adenosine triphosp
14 hese compounds involving deregulation of the tricarboxylic acid cycle activity and suppression of mit
16 P/O2 kidneys inferring relative increases in tricarboxylic acid cycle activity versus HMP/Air kidneys
17 abolism, photosynthesis, remobilization, and tricarboxylic acid cycle activity) allow to refix 79% of
19 flux of glutamine-derived carbon through the tricarboxylic acid cycle and by concurrently activating
21 MmOGOR from its native role in the reductive tricarboxylic acid cycle and drive it directly with ligh
22 chondrial functional pathways, including the tricarboxylic acid cycle and electron transport chain.
23 at impaired the routing of pyruvate into the tricarboxylic acid cycle and established a metabolic sta
24 flux to glutamate both from glucose via the tricarboxylic acid cycle and from glutamine were increas
26 ling of glucose-derived metabolites into the tricarboxylic acid cycle and glutathione biosynthesis, r
27 that genes encoding proteins involved in the tricarboxylic acid cycle and glycolysis pathways were hi
28 examination of significant compounds in the tricarboxylic acid cycle and glycolysis reveals that tre
29 d effects, promoting pyruvate entry into the tricarboxylic acid cycle and inhibiting terminal effecto
30 BACH1 decreases glucose utilization in the tricarboxylic acid cycle and negatively regulates transc
32 , this limits glutamate availability for the tricarboxylic acid cycle and other biosynthetic reaction
33 atively more prominent at the expense of the tricarboxylic acid cycle and oxidative metabolism in gen
34 y mitochondria to fuel ATP production by the tricarboxylic acid cycle and oxidative phosphorylation (
35 wnregulation of enzymes participating in the tricarboxylic acid cycle and oxidative phosphorylation.
36 ycolysis, whereas M2 macrophages rely on the tricarboxylic acid cycle and oxidative phosphorylation;
37 o mitochondria is also known to activate the tricarboxylic acid cycle and seems to be crucial for mat
38 enzyme complex that is involved in both the tricarboxylic acid cycle and the electron transport chai
39 tion of fatty acids to supply carbon for the tricarboxylic acid cycle as well as production of sucros
40 ic flux of benzoate-derived carbons from the tricarboxylic acid cycle did not reach the upper Embden-
41 is made by diverting aconitate away from the tricarboxylic acid cycle during inflammatory macrophage
43 ubunit I relative to actin; in cortex, lower tricarboxylic acid cycle enzyme aconitase and higher pro
45 ctivating mutations of the gene encoding the tricarboxylic acid cycle enzyme fumarate hydratase (FH)
46 (HLRCC), a disease in which mutation of the tricarboxylic acid cycle enzyme fumarate hydratase (FH)
48 chondrial isocitrate dehydrogenase (IDH)2, a tricarboxylic acid cycle enzyme mutated in subsets of ac
50 labeling data suggest the inhibition of the tricarboxylic acid cycle enzyme succinate dehydrogenase,
52 ctokinase, glucokinase, pyruvate kinase, and tricarboxylic acid cycle enzymes, indicating ATP product
53 anced mitochondrial function and accelerated tricarboxylic acid cycle flux coupled with reduced fat c
54 lutamine uptake was approximately 50% of the tricarboxylic acid cycle flux, the rate of ATP productio
56 to glucose as the carbon source to fuel the tricarboxylic acid cycle for vaccinia virus replication.
58 s of TRIM24 iHMECs revealed a glycolytic and tricarboxylic acid cycle gene signature, alongside incre
59 in cohesive operation of glycolysis and the tricarboxylic acid cycle in a normal glucose-replete mil
62 arbon metabolism, sucrose synthesis, and the tricarboxylic acid cycle in leaves and oil synthesis in
63 decreased flux from glycolysis entering the tricarboxylic acid cycle in Muller cells accompanied by
64 ssion and covalent regulation, and hence the tricarboxylic acid cycle influx of pyruvate-derived acet
67 showed that substantial accumulation of the tricarboxylic acid cycle intermediate alpha-ketoglutaric
68 ize heme from the amino acid glycine and the tricarboxylic acid cycle intermediate succinyl CoA for i
69 show that alpha-ketoglutarate (alpha-KG), a tricarboxylic acid cycle intermediate, extends the lifes
70 esting that glutamine's ability to replenish tricarboxylic acid cycle intermediates (anaplerosis) is
72 (N2,N2-dimethylguanosine, N1-methylinosine), tricarboxylic acid cycle intermediates (malate, fumarate
73 tal nitrogen added as N2O and large pools of tricarboxylic acid cycle intermediates and amino acids.
74 ts of perfusion and (11)C incorporation into tricarboxylic acid cycle intermediates and bicarbonate a
75 The kinetics of acetate incorporation into tricarboxylic acid cycle intermediates and into lipids s
76 response is concurrent with rapid changes in tricarboxylic acid cycle intermediates and large changes
78 d for the conversion of 4-hydroxybenzoate to tricarboxylic acid cycle intermediates as well as the ma
79 equires fatty acid oxidation and shunting of tricarboxylic acid cycle intermediates for de novo lipid
80 xpression increased anaplerotic refilling of tricarboxylic acid cycle intermediates in mouse brain du
82 re metabolism, leading to elevated levels of tricarboxylic acid cycle intermediates, amino acids, sug
83 respiration rates, changes in the levels of tricarboxylic acid cycle intermediates, and accumulation
84 oenergetics as measured by altered levels of tricarboxylic acid cycle intermediates, NAD(+)/NADH, and
86 considered incapable of de novo synthesis of tricarboxylic acid cycle intermediates; therefore they r
88 wed enhanced glycolysis, glutaminolysis, and tricarboxylic acid cycle metabolism with high alpha-keto
91 succinate, fumarate and total 2HG) and other tricarboxylic acid cycle metabolites (alpha-ketoglutarat
92 idopsis are differentially fine-regulated by tricarboxylic acid cycle metabolites (most likely depend
93 lipophilic methyl-conjugates of pyruvate and tricarboxylic acid cycle metabolites bypassed the gateke
94 nd the global declines in the glycolytic and tricarboxylic acid cycle metabolites characteristic of n
97 dance of dipeptide metabolites, depleted key tricarboxylic acid cycle metabolites, and slowed progres
98 decreased cellular ATP and depleted critical tricarboxylic acid cycle metabolites, leading to suppres
100 biopsies revealed a glutamate metabolism and tricarboxylic acid cycle node that was specific to prost
102 and metabolism of [U-(13)C3]glycerol in the tricarboxylic acid cycle prior to gluconeogenesis or gly
105 bundance plots of selected analytes from the tricarboxylic acid cycle revealed differences between he
106 HFD-fed SIRT3 knockout (KO) mice showed that tricarboxylic acid cycle substrate-based respiration is
107 eviously suggested that, during hypoxia, the tricarboxylic acid cycle switches to a noncyclic operati
108 r- and redox-driven variant of the reductive tricarboxylic acid cycle that is capable of producing li
110 ng cells shifted their metabolism to use the tricarboxylic acid cycle to metabolize acetate in contra
111 otoxic extracellular Glu through a truncated tricarboxylic acid cycle under hypoglycemic conditions.
114 in ndufv1, fluxes through glycolysis and the tricarboxylic acid cycle were dramatically increased com
115 iling suggested that both glycolysis and the tricarboxylic acid cycle were suppressed in a similar ma
116 lex (PDHc) activation to maintain TCA cycle (tricarboxylic acid cycle) and promotes cancer metastasis
118 ive pentose phosphate pathway, Calvin cycle, tricarboxylic acid cycle, and amino acid biosynthetic pa
119 ehydrogenase glutathionylation, impaired the tricarboxylic acid cycle, and depleted ATP in leukemia s
120 energy metabolism, including glycolysis, the tricarboxylic acid cycle, and electron transport chain,
121 esis, ascorbate and aldarate metabolism, the tricarboxylic acid cycle, and glycolysis-diverting pathw
122 rmediates of glycolysis/gluconeogenesis, the tricarboxylic acid cycle, and monosaccharide and disacch
123 metabolic processes, such as glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation.
124 , and proline), sugars, intermediates of the tricarboxylic acid cycle, and polyamines and lower level
125 components of the electron transport chain, tricarboxylic acid cycle, and protein import apparatus.
126 ut also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclea
127 f the leg; and released intermediates of the tricarboxylic acid cycle, balancing anaplerosis from ami
128 unt generates catabolites that may enter the tricarboxylic acid cycle, but it is unknown whether cata
129 abolites including amino acids, fatty acids, tricarboxylic acid cycle, carbohydrates and associated i
130 ght-modulated metabolites participate in the tricarboxylic acid cycle, carbon balance, phytohormone b
131 rate that is associated with reversal of the tricarboxylic acid cycle, coupled with increased ketogen
132 nses a blockage at the aconitase step of the tricarboxylic acid cycle, either through elevated citrat
133 the expression of genes encoding enzymes of tricarboxylic acid cycle, electron transport chain, oxid
134 performed to compare metabolism through the tricarboxylic acid cycle, fermentation, alanine metaboli
135 arbon and nitrogen metabolism, including the tricarboxylic acid cycle, glycolysis, respiration, and t
136 ate dehydrogenase (MDH), a key enzyme in the tricarboxylic acid cycle, has been identified to be acet
137 lytic pathway and decreased flux through the tricarboxylic acid cycle, in order to decrease mitochond
138 ral key mitochondrial functions, such as the tricarboxylic acid cycle, mitochondrial electron transfe
139 ed in fermentation, hydrogen production, the tricarboxylic acid cycle, NAD biosynthesis, nitrate and
140 genes and pathways of immunity, glycolysis, tricarboxylic acid cycle, OX-PHOS, nicotinamide dinucleo
141 , there is a metabolic remodelling involving tricarboxylic acid cycle, polyol and pentose phosphate p
142 photosynthetic light and dark reactions, the tricarboxylic acid cycle, protein metabolism, and redox
143 ong been known to act as an inhibitor of the tricarboxylic acid cycle, the fate of the amino acid flu
144 erse reaction, supporting anaplerosis of the tricarboxylic acid cycle, under conditions leading to sl
145 ites decreases citrate oxidation through the tricarboxylic acid cycle, whereas increased glutamine up
146 etone body production and breakdown, and the tricarboxylic acid cycle, which inversely correlated wit
147 Ketoglutarate (AKG) is a key intermediate of tricarboxylic acid cycle, which is generated during endu
148 reased expression of genes that regulate the tricarboxylic acid cycle, which resulted from microbe pr
149 ase fatty acid uptake and oxidation into the tricarboxylic acid cycle, while reducing glucose and lac
150 oxoglutarate dehydrogenase-an enzyme of the tricarboxylic acid cycle-specifically results in increas
177 d by a decreased glycolysis and an increased tricarboxylic acid cycle/oxidative pathway, preceded the
179 R-beta-selective ligand increased markers of tricarboxylic acid-dependent and -independent energy bio
180 rioxo-2, 5,11,13-tetraazahexadecane-10,14,16-tricarboxylic acid)), have demonstrated promising result
181 2 (also known as HKUST-1; BTC, benzene-1,3,5-tricarboxylic acid) infiltrated with the molecule 7,7,8,
182 was associated with decreased levels of some tricarboxylic acid intermediates and amino acids, wherea
183 IDO)-dependent tryptophan metabolites (TMs), tricarboxylic acid intermediates, and purine metabolites
185 1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reduc
186 expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase
187 In the presence of slow reacting di- and tricarboxylic acids (oxalic, malonic, succinic, and citr
189 sm of amino acids, nucleotides, fatty acids, tricarboxylic acids, photosynthesis and photorespiration
190 quantify the melanin biomarker pyrrole-2,3,5-tricarboxylic acid (PTCA) was evaluated as a means of no
191 rdial metabolic networks such as the reverse tricarboxylic acid (rTCA) cycle and clay mineral catalys
192 imordial nature of the non-enzymatic reverse tricarboxylic acid (rTCA) cycle and describe a modeling
194 ne, associated to accumulation of glutamate, tricarboxylic acid (TCA) anaplerotic intermediates and G
195 ), amino acid synthesis (four genes) and the tricarboxylic acid (TCA) cycle (five genes), and four ge
196 n and iron limitation dramatically decreased tricarboxylic acid (TCA) cycle activity, creating a meta
197 e remodeling of ketogenic flux and sustained tricarboxylic acid (TCA) cycle activity, which are concu
199 did not cause energy distress, but impaired tricarboxylic acid (TCA) cycle anaplerosis, macromolecul
200 ncover a previously unknown link between the tricarboxylic acid (TCA) cycle and cell cycle progressio
201 stimulates glutamine catabolism through the tricarboxylic acid (TCA) cycle and consequently lowers i
202 (Fh1), a key component of the mitochondrial tricarboxylic acid (TCA) cycle and cytosolic fumarate me
203 e cells and by reducing carbon flux into the tricarboxylic acid (TCA) cycle and de novo lipid biosynt
204 cose deprivation stimulated re-wiring of the tricarboxylic acid (TCA) cycle and early steps of glucon
205 tbeats to stimulate metabolic enzymes in the tricarboxylic acid (TCA) cycle and electron transport ch
206 at steady induction of hepatic mitochondrial tricarboxylic acid (TCA) cycle and lipogenesis are centr
207 include mitochondrial genes involved in the tricarboxylic acid (TCA) cycle and other nuclear-encoded
208 expression of genes encoding enzymes of the tricarboxylic acid (TCA) cycle and oxidative phosphoryla
209 wo essential energy-producing processes, the tricarboxylic acid (TCA) cycle and oxidative phosphoryla
210 hird, the relative flux through the complete tricarboxylic acid (TCA) cycle and succinate dehydrogena
211 zymes in key metabolic pathways, such as the tricarboxylic acid (TCA) cycle and the pentose phosphate
212 rient metabolic pathways like amino acid and tricarboxylic acid (TCA) cycle are also profoundly pertu
213 y regulated in BMSCs from T2D mice, with the tricarboxylic acid (TCA) cycle being one of the primary
214 pening of the gateway from glycolysis to the tricarboxylic acid (TCA) cycle by producing acetyl coenz
216 tation, we capture decreased flux toward the tricarboxylic acid (TCA) cycle during the metabolism of
217 glycolysis enzyme abundance and decreases in tricarboxylic acid (TCA) cycle enzyme abundance with inc
218 Germ line mutations of the gene encoding the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase
220 te, decreases lactate and key glycolytic and tricarboxylic acid (TCA) cycle enzyme levels, and trigge
221 ars, inherited and acquired mutations in the tricarboxylic acid (TCA) cycle enzymes have been reporte
222 cation of cancer-associated mutations in the tricarboxylic acid (TCA) cycle enzymes isocitrate dehydr
223 e mutations in nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle enzymes that produce onco
224 elevated activity of complex II, and certain tricarboxylic acid (TCA) cycle enzymes, which led to mit
225 n (pyruvate and oxaloacetate) must enter the tricarboxylic acid (TCA) cycle first and then use phosph
226 accelerated one carbon metabolism, abnormal tricarboxylic acid (TCA) cycle flux and glutamate metabo
227 (leuZ) prevents sRNA-dependent remodeling of tricarboxylic acid (TCA) cycle fluxes and decreases anti
228 cells attempt to direct acetyl-CoA into the tricarboxylic acid (TCA) cycle for ATP production rather
229 tabolic quiescence, associated with impaired tricarboxylic acid (TCA) cycle function and metabolite i
230 f succinate and other TCA metabolites in the tricarboxylic acid (TCA) cycle in mediating lipid accumu
232 nd functionally, to specifically bind to the tricarboxylic acid (TCA) cycle intermediate succinate.
233 was partially rescued by the addition of the tricarboxylic acid (TCA) cycle intermediate, alpha-ketog
234 abolyzed to alpha-ketoglutarate (alphaKG), a tricarboxylic acid (TCA) cycle intermediate, through two
235 significant alterations in the levels of key tricarboxylic acid (TCA) cycle intermediates and amino a
236 r treatment revealed increased quantities of tricarboxylic acid (TCA) cycle intermediates and increas
238 ding to less glucose carbons contributing to tricarboxylic acid (TCA) cycle intermediates and the pen
239 sed anabolic demands, wherein glycolytic and tricarboxylic acid (TCA) cycle intermediates are shunted
240 ine as an anaplerotic substrate to replenish tricarboxylic acid (TCA) cycle intermediates that have b
241 ve oxygen species with oxidative stress, and tricarboxylic acid (TCA) cycle intermediates were quanti
242 emical compound classes such as amino acids, tricarboxylic acid (TCA) cycle intermediates, fatty acid
251 ational modeling, we identify alterations in Tricarboxylic Acid (TCA) cycle metabolism following even
257 nveiled an aberrant glutamate metabolism and tricarboxylic acid (TCA) cycle node in prostate cancer-d
258 d to changes in the levels of glycolysis and tricarboxylic acid (TCA) cycle pathway intermediates.
259 tive phosphorylation pathway proteins and 18 tricarboxylic acid (TCA) cycle proteins compared to CsP
260 s for respiratory chain flavoproteins or for tricarboxylic acid (TCA) cycle resulted in increased res
261 sed longevity suggesting that anaplerosis of tricarboxylic acid (TCA) cycle substrates likely plays a
262 V. cholerae genes that encode enzymes of the tricarboxylic acid (TCA) cycle that contain iron-sulfur
263 Plant mitochondria have a fully operational tricarboxylic acid (TCA) cycle that plays a central role
265 multiple anaplerotic routes into a canonical tricarboxylic acid (TCA) cycle to satisfy their energy r
267 s, including important intermediaries of the tricarboxylic acid (TCA) cycle, amino acids including pr
268 , including glycolysis, gluconeogenesis, the tricarboxylic acid (TCA) cycle, and amino acid synthesis
269 s, including conspicuous cristae, mtDNA, the tricarboxylic acid (TCA) cycle, and ATP synthesis powere
270 L-malic acid in mitochondria as part of the tricarboxylic acid (TCA) cycle, and in the cytosol/nucle
271 and pathways, including Pyruvate Metabolism, Tricarboxylic acid (TCA) cycle, and Oxidative Phosphoryl
272 te available energy, such as glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphoryl
273 e components of mitochondrialbeta-oxidation, tricarboxylic acid (TCA) cycle, and respiratory chain.
274 at the level of pyruvate metabolism and the tricarboxylic acid (TCA) cycle, and these perturbations
275 ent assimilation of these compounds into the tricarboxylic acid (TCA) cycle, and, correspondingly, th
276 scription of HAP4 and genes required for the tricarboxylic acid (TCA) cycle, electron transport chain
277 rboxykinase (PCK2), the hub molecule linking tricarboxylic acid (TCA) cycle, glycolysis and gluconeog
278 otal role regulating carbon flux between the tricarboxylic acid (TCA) cycle, glyoxylate shunt and met
279 marate hydratase, an essential enzyme in the tricarboxylic acid (TCA) cycle, has been identified as o
280 ine-derived metabolic intermediates into the Tricarboxylic Acid (TCA) cycle, leading to reduced citra
281 several multienzyme systems involved in the tricarboxylic acid (TCA) cycle, photorespiration, and th
282 rossroad of the electron transport chain and tricarboxylic acid (TCA) cycle, two central bioenergetic
283 in kinase in coordinating glycolysis and the tricarboxylic acid (TCA) cycle, which is instrumental in
284 X controls central carbon metabolism via the tricarboxylic acid (TCA) cycle, while PtsN controls nitr
286 lyses from these mouse studies revealed that tricarboxylic acid (TCA) cycle-related urinary metabolit
300 the reaction of the dianion of pyrrole-1,2,5-tricarboxylic acid tert-butyl ester dimethyl ester with