ライフサイエンスコーパス: Krebs cycle

1 mplex for enhanced flux of pyruvate into the Krebs cycle.

2 nitate, which is further catabolized via the Krebs cycle.

3 a rate-limiting enzyme in the mitochondrial Krebs cycle.

4 ymes of the tricarboxylic acid branch of the Krebs cycle.

5 formation of acetyl CoA from glucose and the Krebs cycle.

6 -rehydration of citrate to isocitrate in the Krebs cycle.

7 ow labeling of late glycolytic steps and the Krebs cycle.

8 ds but only when malate is used to prime the Krebs cycle.

9 cesses: the electron transport chain and the Krebs cycle.

10 uite of biorelevant molecules central to the Krebs cycle.

11 mming, enhancing glycolysis and altering the Krebs cycle.

12 cleotides, and metabolites of purine and the Krebs cycle.

13 lectron transport chain and aconitase of the Krebs cycle.

14 ate as part of the proper functioning of the Krebs cycle.

15 genase (OGDH), a rate-limiting enzyme in the Krebs cycle.

16 n uptake for cellular function, e.g. for the Krebs cycle.

17 ottlenecks of carbon substrate flux into the Krebs cycle.

18 rganic acids, including intermediates of the Krebs cycle.

19 carbon metabolism linking glycolysis to the Krebs cycle.

20 ve decarboxylation of alpha-ketoacids in the Krebs' cycle.

21 s a key component of the tricarboxylic acid (Krebs) cycle.

22 itive [4Fe-4S] (de)hydratases, including the Krebs cycle aconitase and the Entner-Doudoroff pathway 6

23 mitochondrial metabolism, including partial Krebs' cycle activation and significant accumulation of

24 ore phagocytotic and chemotactic with higher Krebs cycle activity and less glycolysis than M(IFNgamma

25 The in vivo decrease in Krebs cycle activity in the 6-week post-MI heart may rep

26 alterations after MI in which reductions in Krebs cycle activity precede a reduction in pyruvate deh

27 At 6 weeks after MI, in vivo mitochondrial Krebs cycle activity was impaired, with decreased (13)C-

28 ally improves glucose homeostasis, increases Krebs cycle activity, and reduces the levels of acylcarn

29 owth inhibition was accompanied by perturbed Krebs cycle activity, inhibition of lipid and nucleotide

30 female mouse kidneys towards glycolysis and Krebs cycle activity.

31 mulation is dependent on calcium release and Krebs cycle activity.

32 findings, thiazides significantly attenuated Krebs cycle anaplerosis through reduction of mitochondri

33 e findings indicate a connection between the Krebs cycle and aerobic respiration that directs electro

34 es are aberrantly accumulated from disrupted Krebs cycle and affect the catalytic activity of a-ketog

35 le in cellular energetics as a member of the Krebs cycle and as complex II of the aerobic respiratory

36 ized energy production components, including Krebs cycle and electron transport genes, decreased by 4

37 ydratase-1 resulted in the inhibition of the Krebs cycle and enhanced pyruvate shunting toward the gl

38 Variable reprogrammed Krebs cycle and glutamine-fueled synthesis of UTP in WGP

39 is the only membrane-bound component of the Krebs cycle and in addition functions as a member of the

40 drogenase (PDH) is the main regulator of the Krebs cycle and is located upstream of the electron tran

41 Labeling of Krebs cycle and late steps of glycolysis was primarily f

42 ndria, the expression of key elements of the Krebs cycle and oxidative phosphorylation (OXPHOS).

43 nes modifying protein ubiquitination and the Krebs cycle and oxidative phosphorylation pathways.

44 ocytes results in a global downregulation of Krebs cycle and OXPHOS gene expression, defective mitoch

45 xidizes succinate to fumarate as part of the Krebs cycle and reduces ubiquinone in the electron trans

46 s from supplied glutamine flow via oxidative Krebs cycle and reductive carboxylation routes to positi

47 ve stress, antioxidant enzyme, activities of Krebs cycle and respiratory chain enzymes, mitochondrial

48 for monosaccharides and amino acids into the Krebs cycle and thus integral for mitochondrial bioenerg

49 ct of H(2)S required a basal activity of the Krebs cycle and was most pronounced at intermediate conc

50 intermediate in the tricarboxylic acid (TCA, Krebs) cycle and a promising therapeutic agent in its ow

51 peak in cyclical pathways (particularly the Krebs Cycle) and a progressive decrease in molecular sim

52 molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase.

53 onitor effects of Firsocostat on glycolytic, Krebs cycle, and fatty acid metabolism.

54 ative phosphorylation, glutamine metabolism, Krebs cycle, and fatty acid oxidation.

55 as glucose, amino acid and lipid metabolism, Krebs cycle, and immune responses and those hitherto unk

56 Mqo catalyzes an essential reaction in the Krebs cycle, and in vivo survival of mycobacterial patho

57 erent as fuel procurement, catabolism in the Krebs cycle, and stepwise oxidation of reducing equivale

58 ion of genes involved in beta-oxidation, the Krebs cycle, and the electron transport chain concomitan

59 d dysregulation of electron transport chain, Krebs cycle, and the fatty acid oxidation pathway protei

60 y acid carbons substantially replenished the Krebs cycle, and were incorporated into aspartate (a nuc

61 omprise contemporary metabolism, such as the Krebs cycle, are of particular prebiotic relevance and a

62 e carbon into glucose via glutamine entering Krebs cycle at alpha-ketoglutarate or 2) through simple

63 of molecules, including citrate, leaving the Krebs cycle at every turn.

64 ation against a benchmarked dataset from the Krebs cycle, based on the known chemical transformations

65 tance not only for flux of fuel entering the Krebs cycle but for overall energy homeostasis.

66 in glycogen metabolism, glycolysis, and the Krebs cycle, but the levels of pentose phosphate pathway

67 ntal occurrence of P3N, which shuts down the Krebs cycle by inactivating succinate dehydrogenase and

68 Supranormal stimulation of the Krebs cycle by methyl pyruvate can, however, overwhelm i

69 t PM(2.5) exposure led to a reduction in the Krebs cycle capacity.

70 eased substrate supply for the mitochondrial Krebs cycle compared with APAP alone.

71 nd showed reduced substrate flux through the Krebs cycle compared with GSH.

72 neoplasms, displays genetic modifications of Krebs cycle components as well as electron transport cha

73 ciated with mdx disease progression and that Krebs cycle deficiencies are a downstream consequence of

74 the selective mitochondrial vulnerability in Krebs cycle-deficient cancers for future therapeutic int

75 Accordingly, Ca(2+)-induced stimulation of Krebs cycle dehydrogenases during beta-adrenergic stimul

76 horylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases, illustrating how the model c

77 ements and balances the bioenergetic role of Krebs cycle-derived electron donors.

78 ctyl itaconate (4-OI) is a derivative of the Krebs cycle-derived metabolite itaconate and displays an

79 aconate (4-OI), a chemical derivative of the Krebs cycle-derived metabolite itaconate, enhances oncol

80 -Octyl itaconate (4-OI), a derivative of the Krebs cycle-derived metabolite itaconate, has recently g

81 intermediates succinate and citrate, and the Krebs cycle-derived metabolite itaconate.

82 Several Krebs cycles, or Krebs-cycle-derived metabolites, including succinate, a-

83 Several Krebs cycles, or Krebs-cycle-derived metabolites, including succinate, al

84 mulation and (ii) energy deprivation through Krebs cycle disruption associated with branched-chain ke

85 t prevented Ca(2+)-induced activation of the Krebs cycle during B-adrenergic stimulation, oxidizing p

86 se (PNPase), a DEAD-box RNA helicase and the Krebs cycle enzyme aconitase.

87 The Krebs cycle enzyme aconitate decarboxylase 1 (ACOD1) med

88 Krebs cycle enzyme activity in Bacillus subtilis was exa

89 ible glutathionylation and inhibition of the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase.

90 Our forward genetic selection unearthed the Krebs cycle enzyme citrate synthase (CitA) as a checkpoi

91 production of 2-methylcitrate (2-MC) by the Krebs cycle enzyme citrate synthase (GltA).

92 Eight Krebs cycle enzyme components were isolated upon chemica

93 al carcinoma, is caused by inactivation of a Krebs cycle enzyme due to mutation.

94 Mutations in the gene encoding the Krebs cycle enzyme fumarate hydratase (FH) predispose to

95 llelic inactivation of the gene encoding the Krebs cycle enzyme fumarate hydratase, an early shift to

96 In Escherichia coli, the homodimeric Krebs cycle enzyme isocitrate dehydrogenase (EcIDH) is r

97 helate magnesium and to inhibit aconitase, a Krebs cycle enzyme.

98 We show that this Krebs-cycle enzyme is essential for mtDNA maintenance in

99 tilization and in the activities of specific Krebs cycle enzymes alpha-ketoglutarate dehydrogenase (K

100 These data suggest a common origin for these Krebs cycle enzymes in mitochondria and CFB group bacter

101 nt of electron transport chain complexes and Krebs cycle enzymes revealed that alpha-ketoglutarate de

102 secretion, blockers of pyruvate transport or Krebs cycle enzymes were without effect.

103 of central carbon metabolic pathways (e.g., Krebs cycle enzymes), as well as transporters and enzyme

104 The nuclear-encoded Krebs cycle enzymes, fumarate hydratase (FH) and succina

105 cterial growth; depressed activities of many Krebs cycle enzymes, including pyruvate:ferredoxin oxido

106 zyme of the tricarboxylic acid branch of the Krebs cycle, exhibited reduced growth yield in broth med

107 evidence of profoundly dampened glycolysis, Krebs cycle, fatty acid beta oxidation and amino acid me

108 odelling indicates altered metabolic fluxes (Krebs cycle, fatty acid, carbohydrate, amino acid metabo

109 h that of other metabolites, indicating that Krebs cycle flux can be measured directly.

110 In this study, we measured Krebs cycle flux in real time in perfused rat hearts usi

111 Krebs cycle flux was also stimulated by CGP37157 when gl

112 to supply sufficient pyruvate for increased Krebs cycle flux when glucose is limiting.

113 n may reflect an inability to upregulate the Krebs cycle following exercise.

114 m via three different pathways: (1) the mini-Krebs-cycle, fuelled by glutamine and branched chain ami

115 howed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysregulated fatty acid oxidati

116 ethylation, we delineated the effects on the Krebs cycle, gamma-aminobutyrate metabolism, gluconeogen

117 found to be primarily the result of reduced Krebs cycle gene transcription.

118 Therefore, CcpA controls expression of Krebs cycle genes directly by regulating transcription o

119 zyme of the tricarboxylic acid branch of the Krebs cycle, had a greatly reduced ability to sporulate.

120 Perhaps surprisingly for immunologists, the Krebs cycle has emerged as the central immunometabolic h

121 DH and alpha-ketoglutarate (alpha-KG) to the Krebs cycle, hence increasing the beta-cell ATP-to-ADP r

122 wo components of the oxidative branch of the Krebs cycle, IDH and citrate synthase.

123 involved in basic metabolic processes (e.g. Krebs cycle), (iii) genes required to survive oxidative

124 Finally, we show that supplementing the Krebs cycle in an ex vivo fatigue/recovery assay signifi

125 Lysine metabolism in plasma and the Krebs cycle in CSF were significantly affected in MCI vs

126 ts showed that the control and fluxes of the Krebs cycle in heart disease can be studied using hyperp

127 tanoin, which provides key substrates to the Krebs cycle in the brain, we wished to assess its therap

128 and fumarate, its immediate precursor in the Krebs cycle, in affected subjects' fibroblasts.

129 tion of glycolysis, cataplerotic/anaplerotic Krebs cycle including reductive carboxylation, the pento

130 d isocitrate dehydrogenase activities of the Krebs cycle increased at 2, 3, 12, and/or 14 h, and thes

131 hortage and a reduction in the levels of the Krebs cycle intermediate alpha-ketoglutarate (alpha-KG).

132 )cysteine (2SC) is formed by reaction of the Krebs cycle intermediate fumarate with cysteine residues

133 R1 is a sensor of extracellular succinate, a Krebs cycle intermediate generated in excess during oxid

134 of chemical modification of proteins by the Krebs cycle intermediate, fumarate, is significantly inc

135 formed by a Michael addition reaction of the Krebs cycle intermediate, fumarate, with cysteine residu

136 Succinate, a Krebs cycle intermediate, increases after dysregulated e

137 o an increased concentration of succinate, a Krebs cycle intermediate.

138 trogenic, sodium-dependent transport of most Krebs cycle intermediates (Km = 20-60 microM), including

139 everal previous studies, our method included Krebs cycle intermediates (m/z <200), which we found to

140 pyruvate concentrations coupled with reduced Krebs cycle intermediates and short-chain acylcarnitines

141 yze the Na(+)-driven concentrative uptake of Krebs cycle intermediates and sulfate into cells; disrup

142 tanedioic acid, which is likely converted to Krebs cycle intermediates by BbdG.

143 betaHB oxidation increased the Krebs cycle intermediates citrate, 2-oxoglutarate and su

144 oic acid (2,6-DCBA) that ultimately leads to Krebs cycle intermediates for growth and energy conserva

145 Kidney proximal tubule cells take up Krebs cycle intermediates for metabolic purposes and for

146 orporation of [14C] bicarbonate into several Krebs cycle intermediates in 3T3-F442A adipocytes.

147 of mitochondrial stress and accumulation of Krebs cycle intermediates in adipose tissue in diabetes

148 t), involved in the transport and storage of Krebs cycle intermediates in tissues important in fly me

149 idative metabolism with decreases in several Krebs cycle intermediates including citric acid, cis-aco

150 The metabolism of Krebs cycle intermediates is of fundamental importance f

151 and tandem mass spectrometry measurement of Krebs cycle intermediates revealed a negative impact of

152 activation, there is an accumulation of the Krebs cycle intermediates succinate and citrate, and the

153 Krebs cycle intermediates such as succinate, citrate, an

154 Decreased (13)C-Krebs cycle intermediates suggested that PM(2.5) exposur

155 radioactivity into and the concentrations of Krebs cycle intermediates was not of sufficient magnitud

156 ite concentrations (glycolytic, anaplerotic, Krebs cycle intermediates).

157 rmined to be significantly altered including Krebs cycle intermediates, amino acids that have not bee

158 onsequently, the mitochondrial products ATP, Krebs cycle intermediates, glutamate, and acetoacetate w

159 th increased cellular ATP (1.7-3.0-fold) and Krebs cycle intermediates, including citrate, isocitrate

160 r effects on HIF-1 are not mimicked by other Krebs cycle intermediates, including succinate and fumar

161 orrelated well with GSIS, in particular some Krebs cycle intermediates, malonyl-CoA, and lower ADP le

162 ion, extracellular matrix structure, sugars, Krebs cycle intermediates, microbe-derived metabolites a

163 Interestingly, among Krebs cycle intermediates, only succinic acid monomethyl

164 betaHB oxidation alone increased Krebs cycle intermediates, reduced mitochondrial Q and i

165 We first demonstrate that Krebs cycle intermediates, such as fumaric acid esters,

166 NaDC-1, couples the transport of sodium and Krebs cycle intermediates, such as succinate and citrate

167 s apoptosis was preceded by depletion of the Krebs cycle intermediates, was prevented by two Krebs cy

168 ger than those elicited by other (equimolar) Krebs cycle intermediates.

169 ansporter-a membrane protein that transports Krebs cycle intermediates.

170 ral sCache domain that responds primarily to Krebs cycle intermediates.

171 they are cataplerotic, causing depletion of Krebs cycle intermediates; therefore their utilisation r

172 c switch to aerobic glycolysis, accumulating Krebs' cycle intermediates that alter transcription of i

173 of mitochondrial reactive oxygen species and Krebs' cycle intermediates, and increased resistance to

174 The Krebs cycle is a central metabolic pathway within all ma

175 Disruption of the Krebs cycle is a hallmark of cancer, and MDH2 has been r

176 Aconitase activity associated with the Krebs cycle is also reduced in the striatum of PINK1(-/-

177 in LNCaP about 21% of pyruvate entering the Krebs cycle is converted via pyruvate carboxylase as an

178 acrophages because of the disturbance in the Krebs cycle is itaconate, which is derived from cis-acon

179 lic acid (TCA) cycle, otherwise known as the Krebs cycle, is a central metabolic pathway that perform

180 genase (IDH), a key regulatory enzyme in the Krebs cycle, is a multi-tetrameric enzyme.

181 is generated internally in humans during the Krebs cycle, is an attractive alternative to these thera

182 the substrate flux through the mitochondrial Krebs cycle, it was observed that the reduced liver inju

183 articularly at the amino acid metabolism and Krebs cycle level.

184 [2-(13)C]pyruvate was also used to evaluate Krebs cycle metabolism and demonstrated a unique marker

185 We report that glycolytic but not Krebs cycle metabolism of glucose is critically involved

186 evelopmental lethality as well as defects in Krebs cycle metabolism, which was fully rescued by expre

187 eceptors appeared to uncouple glycolytic and Krebs-cycle metabolism via three different pathways: (1)

188 previously been shown to be modulated by the Krebs cycle metabolite citrate in Escherichia coli.

189 rations were inversely correlated with urine Krebs cycle metabolite concentrations.

190 A critical distinguishing pathway was Krebs cycle metabolite depletion in mdx urine.

191 edge on the anti-inflammatory effects of the Krebs cycle metabolite derivatives 4-OI and DMF.

192 methyl fumarate (DMF), a derivate of another Krebs cycle metabolite fumarate, which is already in use

193 rs, fatty acid oxidation, phospholipids, and Krebs cycle metabolites traceable to mitochondrial funct

194 Five of seven detected Krebs cycle metabolites were depleted in mdx urine, with

195 ncentrations and decreased levels of urinary Krebs cycle metabolites when compared to controls, sugge

196 This work outlines the use of a Krebs cycle metabolon catalyst obtained through the in s

197 estigation of enzyme organization within the Krebs cycle metabolon was accomplished by in vivo cross-

198 ural evidence of substrate channeling in the Krebs cycle metabolon.

199 and AD patients included energy metabolism, Krebs cycle, mitochondrial function, neurotransmitter an

200 The article presents a Krebs cycle model based on queueing theory.

201 ling to the glycolysis, gluconeogenesis, and Krebs cycle (n = 48) and an exploration by the next-gene

202 The Krebs cycle, neoribogenesis, gamma-aminobutyrate metabol

203 d for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells.

204 detections of carboxylic acids linked to the Krebs cycle on the Ryugu asteroid and Murchison meteorit

205 Several Krebs cycles, or Krebs-cycle-derived metabolites, includ

206 Several Krebs cycles, or Krebs-cycle-derived metabolites, includ

207 LECA later acquired the fully aerobic Krebs cycle-oxidative phosphorylation-mitochondrial meta

208 dinated set of enzymes of the glycolytic and Krebs cycle pathways, which we propose may antagonize Tr

209 extensive catabolism via the glycolytic and Krebs cycle pathways.

210 ltered activities of specific enzymes in the Krebs cycle, pentose phosphate pathway, gluconeogenesis,

211 The Krebs cycle plays a fundamental role in cardiac energy p

212 Besides being oxidized through the Krebs cycle, proline is used to make citrate via reducti

213 al. (2016) identify a mechanism that uses a Krebs cycle protein to control local activation of a ubi

214 such as the molecular chaperone Hsp60p and a Krebs cycle protein, Kgd2p.

215 fumA genes, encoding key constituents of the Krebs cycle, proved to be repressed by the loss of both

216 ocarboxylate transporters (MCT-1 and MCT-4), Krebs cycle redox metabolism, or glutaminolysis will syn

217 ctivated macrophages, distinct breaks in the Krebs cycle regulate macrophage effector function throug

218 at pyruvate, the precursor substrate for the Krebs cycle, regulates I(crac) to prolong Ca(2+) influx

219 We did not detect glycolysis or Krebs-cycle-related defects in the iar4 mutant, and a T-

220 proceed in the same sequence as the reverse Krebs cycle, resembling a protometabolic pathway, with g

221 esults in the inhibition of aconitase in the Krebs cycle, resulting in the accumulation of citrate an

222 d diminished production of the mitochondrial Krebs cycle substrate citrate, a precursor to cellular l

223 required to allow the use of glutamine as a Krebs cycle substrate in T cells.

224 Krebs cycle substrates (KCS) can stabilise the colour of

225 ting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities bu

226 bs cycle intermediates, was prevented by two Krebs cycle substrates, but was unrelated to ATP synthes

227 demonstrated protometabolic analogues of the Krebs cycle, suggest that there can be a natural emergen

228 HL) protein is a rate-limiting enzyme in the Krebs cycle that plays a pivotal role in mitochondrial m

229 A key bioenergetic target for the Krebs cycle, the electron transport chain, also becomes

230 ires gluconeogenesis, valine metabolism, the Krebs cycle, the GABA shunt, the glyoxylate shunt and th

231 )C enrichment in products of glycolysis, the Krebs cycle, the pentose phosphate pathway, nucleobases,

232 s transported to mitochondria for use in the Krebs cycle to generate ATP.

233 and PSNO adduct formation also reprogram the Krebs cycle to generate metabolites vital for interorgan

234 e oxidation of respiratory substrates in the Krebs cycle to generate NADH and flavin adenine dinucleo

235 This process links the Krebs cycle to oxidative phosphorylation and ATP synthes

236 rial membrane protein complex that links the Krebs cycle to the electron transport system.

237 ly consumes O2, rendering standard assays of Krebs cycle turnover unusable.

238 amino acids, fumarate and malate, suggesting Krebs cycle up-regulation.

239 In addition, the mitochondrial Krebs cycle was modulated to increase synthesis of malic

240 on affecting activity of enzymes involved in Krebs cycle was simulated and compared with available ex

241 zyme of the tricarboxylic acid branch of the Krebs cycle, was shown to be required for de novo synthe

242 s by phosphoenolpyruvate carboxylase and the Krebs cycle were measured by 13C incorporation from [1-1

243 n of organic molecules in a process known as Krebs' Cycle, where the enzyme isocitrate dehydrogenase

244 enzyme A (CoA) species incorporated into the Krebs cycle, whereas the myocardial concentration of ace

245 s, ATP machinery, fatty acid metabolism, and Krebs cycle, which further decreased in expression durin

246 ynthesis requires precursors supplied by the Krebs cycle, which in turn requires anaplerosis to reple

247 also use mitochondrial respiration, feed the Krebs cycle with glutamine, and favor the accumulation o

248 and decrease the entry of pyruvate into the Krebs cycle-without compromising the consumption of oxyg