ライフサイエンスコーパス: Krebs cycle

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

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

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

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

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

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

7 ottlenecks of carbon substrate flux into the Krebs cycle.

8 rganic acids, including intermediates of the Krebs cycle.

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

10 carbon metabolism linking glycolysis to the Krebs cycle.

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

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

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

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

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

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

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

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

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

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

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

22 female mouse kidneys towards glycolysis and Krebs cycle activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Krebs cycle enzyme activity in Bacillus subtilis was exa

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

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

53 Eight Krebs cycle enzyme components were isolated upon chemica

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Krebs cycle flux was also stimulated by CGP37157 when gl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Krebs cycle intermediates such as succinate, citrate, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 [2-(13)C]pyruvate was also used to evaluate Krebs cycle metabolism and demonstrated a unique marker

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

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

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

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

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

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

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

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

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

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

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

128 extensive catabolism via the glycolytic and Krebs cycle pathways.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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