ライフサイエンスコーパス: ketoglutarate

1 b's cycle intermediates (succinate and alpha-ketoglutarate).

2 ementation with TCA cycle intermediate alpha-ketoglutarate.

3 tion of 2-hydroxyglutarate and reduced alpha-ketoglutarate.

4 genases, efficiently oxidized D-2HG to alpha-ketoglutarate.

5 ive carboxylation of glutamine-derived alpha-ketoglutarate.

6 mate to pyruvate, yielding alanine and alpha-ketoglutarate.

7 cy compared with that of KDM5B at 1 mm alpha-ketoglutarate.

8 B-04 is not a competitive inhibitor of alpha-ketoglutarate.

9 the concentration of its co-substrate alpha-ketoglutarate.

10 roducing 2-hydroxyglutarate (2HG) from alpha-ketoglutarate.

11 of O(2)-regulated metabolites such as alpha-ketoglutarate.

12 nverted to 3-deoxy-2-keto-hexarate and alpha-ketoglutarate.

13 hlorite oxidation afforded the 1-monooctyl 2-ketoglutarate.

14 4PE and a noncompetitive inhibitor vs alpha-ketoglutarate.

15 er than that towards the natural substrate 2-ketoglutarate.

16 ase in GDH affinity for its substrate, alpha-ketoglutarate.

17 n of saccharopine to give l-lysine and alpha-ketoglutarate.

18 of succinate to glutamate, fumarate to alpha-ketoglutarate, 2HG to glutamate, and D-2HG to L-2HG were

19 ioxygenases using the essential metabolite 2-ketoglutarate (2KG) as a cofactor.

20 ate export and that supplementation of alpha-ketoglutarate, a key downstream metabolite of glutamate,

21 transcription and, thus, production of alpha-ketoglutarate, a key metabolite in the regulation of ESC

22 f Nrd1 or Ogdh leads to an increase in alpha-ketoglutarate, a substrate for OGDH, which in turn leads

23 d NADPH production, an accumulation of alpha-ketoglutarate, aconitate, and citrate that is associated

24 irs to demonstrate that treatment with alpha-ketoglutarate (aKG) esters elicits rapid death of OXPHOS

25 alpha-Ketoglutarate (AKG) is a key intermediate of tricarboxyl

26 cells leads to increased production of alpha-ketoglutarate (aKG) within mesenchymal stem cells (MSCs)

27 However, HPV was not increased by 1 mm alpha-ketoglutarate alone, and HPV in the absence of alpha-ket

28 and IDH2, decarboxylate isocitrate to alpha-ketoglutarate (alpha-KG) and reduce NADP to NADPH.

29 mechanism is steady state ordered with alpha-ketoglutarate (alpha-Kg) binding prior to acetyl-CoA (Ac

30 G) is an oncometabolite generated from alpha-ketoglutarate (alpha-KG) by mutant isocitrate dehydrogen

31 nthase (HOAS), the E1 component of the alpha-ketoglutarate (alpha-KG) dehydrogenase complex (KDHC), d

32 Mononuclear nonheme Fe(II) (MNH) and alpha-ketoglutarate (alpha-KG) dependent halogenases activate

33 genes necessary for the utilization of alpha-ketoglutarate (alpha-KG) in Pseudomonas aeruginosa PAO1.

34 was also activated by induction of an alpha-ketoglutarate (alpha-KG) paracrine signaling system.

35 oxylic acid cycle metabolism with high alpha-ketoglutarate (alpha-KG) production.

36 oup from branched-chain amino acids to alpha-ketoglutarate (alpha-KG) thereby regenerating glutamate,

37 osphate (NADPH)-dependent reduction of alpha-ketoglutarate (alpha-KG) to 2-HG.

38 hed-chain amino acids while converting alpha-ketoglutarate (alpha-KG) to glutamate.

39 Glutaminolysis converts Gln into alpha-ketoglutarate (alpha-KG), a critical intermediate in the

40 Here we show that alpha-ketoglutarate (alpha-KG), a tricarboxylic acid cycle int

41 Fe(II)- and alpha-ketoglutarate (alpha-KG)-dependent dioxygenases are a la

42 leven-translocation (TET) proteins are alpha-ketoglutarate (alpha-KG)-dependent dioxygenases that oxi

43 tion is catalyzed by the non-heme iron alpha-ketoglutarate (alpha-KG)-dependent SnoK in the biosynthe

44 levels of the Krebs cycle intermediate alpha-ketoglutarate (alpha-KG).

45 drogenases (IDH) convert isocitrate to alpha-ketoglutarate (alpha-KG).

46 of D-2-hydroxyglutarate (D-2-HG) from alpha-ketoglutarate (alpha-KG).

47 roduces 2-hydroxyglutarate (2-HG) from alpha-ketoglutarate (alpha-KG).

48 cation (TET) family enzymes, which are alpha-ketoglutarate (alpha-KG)/Fe(II)-dependent dioxygenases.

49 mitochondrial Ca(2+) uptake increased alpha-ketoglutarate (alphaKG) abundance and the NAD(+)/NADH ra

50 decarboxylation of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) and the NADPH/CO(2)-dependent re

51 and glutaminolysis yielding increased alpha-ketoglutarate (alphaKG) bioavailability.

52 tricarboxylic acid cycle intermediate alpha-ketoglutarate (alphaKG) can both sustain naive mouse emb

53 dent conversion of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) in the cytosol and peroxisomes.

54 To investigate the role of alpha-ketoglutarate (alphaKG) in the epimetabolic control of D

55 a physiologic plasma concentration of alpha-ketoglutarate (alphaKG) influences the kinetic interacti

56 Alpha-ketoglutarate (alphaKG) is an essential intermediate in

57 ephalopathy and a urinary excretion of alpha-ketoglutarate (alphaKG) that was markedly increased and

58 atic activity allowing them to convert alpha-ketoglutarate (alphaKG) to 2-hydroxyglutarate (2HG), whi

59 y of enzymes that use Fe(2+), O(2) and alpha-ketoglutarate (alphaKG) to perform a variety of halogena

60 ivity that catalyzes the conversion of alpha-ketoglutarate (alphaKG) to the oncometabolite D-(2)-hydr

61 ad can reverse the direction of apical alpha-ketoglutarate (alphaKG) transport in the proximal tubule

62 Glutamine is catabolyzed to alpha-ketoglutarate (alphaKG), a tricarboxylic acid (TCA) cycl

63 talyze the conversion of isocitrate to alpha-ketoglutarate (alphaKG), whereas conferring a gain of a

64 tes anaplerotic flux from glutamine to alpha-ketoglutarate (alphaKG), which subsequently enters the c

65 he citric acid(TCA) cycle intermediate alpha-ketoglutarate (alphaKG), which via its OXGR1 receptor pl

66 use models to ask if inhibition of the alpha-ketoglutarate (alphaKG)-dependent dioxygenase Egln1, whi

67 FIH is a non-heme Fe(II), alpha-ketoglutarate (alphaKG)-dependent dioxygenase that inhib

68 His-1-carboxylate) facial triad in the alpha-ketoglutarate (alphaKG)-dependent dioxygenases clavamina

69 s (P4Hs) are mononuclear non-heme iron alpha-ketoglutarate (alphaKG)-dependent dioxygenases that cata

70 r (HIF) prolyl hydroxylases (PHDs) are alpha-ketoglutarate (alphaKG)-dependent dioxygenases that func

71 In particular, the family of alpha-ketoglutarate (alphaKG)-dependent dioxygenases, which in

72 g hypoxia-inducible factor (FIH) is an alpha-ketoglutarate (alphaKG)-dependent enzyme which catalyzes

73 For the alpha-ketoglutarate (alphaKG)-dependent nonheme iron enzymes,

74 (Th1) were regulated by glutamine and alpha-ketoglutarate (alphaKG)-induced events, in part through

75 ive decarboxylation of isocitrate into alpha-ketoglutarate (alphaKG).

76 maintain a high level of intracellular alpha-ketoglutarate (alphaKG).

77 DH1) reversibly converts isocitrate to alpha-ketoglutarate (alphaKG).

78 hrough reductive carboxylation (RC) of alpha-ketoglutarate (alphaKG).

79 s of PDAC leads to the accumulation of alpha-ketoglutarate (alphaKG, also known as 2-oxoglutarate), a

80 The use of alpha-ketoglutarate (alternatively termed 2-oxoglutarate) as a

81 is is a cell-permeable prodrug form of alpha-ketoglutarate, an important intermediate in the tricarbo

82 H2 and reduces levels of intracellular alpha-ketoglutarate, an obligatory cofactor for various histon

83 (CD) studies using a non-decarboxylatable 2-ketoglutarate analog and determined the distribution of

84 tes to mtDNA loss by acting as a toxic alpha-ketoglutarate analog.

85 arate alone, and HPV in the absence of alpha-ketoglutarate and cysteine was not attenuated by asparta

86 ents would ensure the replenishment of alpha-ketoglutarate and glutamate, which provide the carbon ba

87 yme, produces 2-hydroxy-3-oxoadipate using 2-ketoglutarate and glyoxylate.

88 ed in all TCA cycle substrates between alpha-ketoglutarate and malate despite high rates of glutamino

89 e in cell proliferation was rescued by alpha-ketoglutarate and overexpression of IDH2, whereas prolif

90 a-keto analog of asparagine), yielding alpha-ketoglutarate and oxaloacetate, respectively.

91 rnary complex of HygX with cosubstrate alpha-ketoglutarate and putative product hygromycin B identifi

92 he intracellular levels of its product alpha-ketoglutarate and subsequent metabolite fumarate.

93 re flushed in situ with histidine-tryptophan-ketoglutarate and subsequently preserved either by simpl

94 Citrate, alpha-ketoglutarate and succinate are TCA cycle intermediates

95 itric acid cycle intermediates such as alpha-ketoglutarate and succinate, NaDC3 transports other comp

96 ctivity to IDH2-mediated production of alpha-ketoglutarate and through it, the activity of key epigen

97 H1 R132H competitively with respect to alpha-ketoglutarate and uncompetitively with respect to NADPH.

98 lows to succinate both through citrate/alpha-ketoglutarate and via malate/fumarate.

99 substrate required addition of Fe(2+), alpha-ketoglutarate, and ascorbic acid, confirming that KdoO i

100 mitochondrial enzymes, mainly lactate, alpha-ketoglutarate, and branched chain keto-acids.

101 (E3) is associated with the pyruvate, alpha-ketoglutarate, and glycine dehydrogenase complexes.

102 EI(Ntr) activity was not affected by alpha-ketoglutarate, and no binding between the EIGAF and alph

103 he enzyme in a complex with NAD(H) and alpha-ketoglutarate, and the enzyme in a complex with NAD(H) a

104 x enzymes are involved, including four alpha-ketoglutarate- and iron(II)-dependent dioxygenases that

105 ls, but causes a drop in the levels of alpha-ketoglutarate, another output of the pathway and a trica

106 BMDACs) with dimethyloxalylglycine, an alpha-ketoglutarate antagonist that induces hypoxia-inducible

107 els of TCA-cycle metabolites including alpha-ketoglutarate are high, and levels of the key regulatory

108 e phenazine reduction with pyruvate or alpha-ketoglutarate as electron donors.

109 ate production from either pyruvate or alpha-ketoglutarate as potential translatable metabolic biomar

110 rolyl 4-hydroxylases that use O(2) and alpha-ketoglutarate as substrates to hydroxylate conserved pro

111 ific activity of DapL using ll-DAP and alpha-ketoglutarate as substrates was 24.3 + or - 2.0 nmol min

112 used for GC-MS/MS analysis of alanine, alpha-ketoglutarate, asparagine, aspartic acid, cystathionine,

113 JmjC domain with conserved Fe(II) and alpha-ketoglutarate binding sites, and displays H3K9me1/2 deme

114 onstitutes the cofactor (metal ion and alpha-ketoglutarate) binding characteristics of other structur

115 cued with exogenous membrane-permeable alpha-ketoglutarate, but not pyruvate or oxaloacetate, suggest

116 product, l-lyxonate, is catabolized to alpha-ketoglutarate by a previously characterized pathway.

117 n addition, reductive carboxylation of alpha-ketoglutarate by isocitrate dehydrogenase 1 (IDH1) and 2

118 pe IDH1, only hyperpolarized [1-(13)C] alpha-ketoglutarate can be detected.

119 proof-of-concept study, that [1-(13)C] alpha-ketoglutarate can serve as a metabolic imaging agent for

120 ive carboxylation of glutamine-derived alpha-ketoglutarate (catalyzed by reverse flux through isocitr

121 several cellular conditions where the alpha-ketoglutarate/citrate ratio is changed due to an altered

122 ions that result in an increase in the alpha-ketoglutarate/citrate ratio.

123 ne (DMOG, 200 mug/g), an antagonist of alpha-ketoglutarate cofactor and inhibitor for HIF PHD, on pos

124 /glutamine (10/2 mM) did not influence alpha-ketoglutarate concentrations but caused 120 and 33% incr

125 , and no binding between the EIGAF and alpha-ketoglutarate could be detected.

126 the gamma-aminobutyric acid pathway or alpha-ketoglutarate decarboxylase/succinic semialdehyde dehydr

127 Here we show that the alpha-ketoglutarate dehydrogenase (alpha-KGDH) complex is loca

128 rganization of the multienzyme complex alpha-ketoglutarate dehydrogenase (alpha-KGDH).

129 ound an increase in phosphorylation of alpha-ketoglutarate dehydrogenase (alphaKGDH) in female hearts

130 in amino acid dehydrogenase (BCDH) and alpha-ketoglutarate dehydrogenase (KDH).

131 such as pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase (KGDH), and the glycine clea

132 aperones and assists in the folding of alpha-ketoglutarate dehydrogenase (OGDH), a rate-limiting enzy

133 cofactor of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase and other mitochondrial targ

134 ons of regulation of the activities of alpha-ketoglutarate dehydrogenase and the aspartate-glutamate

135 proteins, including the E2 subunit of alpha-ketoglutarate dehydrogenase and the glutathione S-transf

136 xes, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and the glycine cleavage com

137 The activity of the alpha-ketoglutarate dehydrogenase complex (KGDHC), an arguably

138 hyl transferase, and components of the alpha-ketoglutarate dehydrogenase complex in conjunction with

139 target DLST-the E2 subcomponent of the alpha-ketoglutarate dehydrogenase complex, a rate-controlling

140 A to the reduction of NAD(+) using the alpha-ketoglutarate dehydrogenase complex.

141 , we demonstrate that the pyruvate and alpha-ketoglutarate dehydrogenase complexes directly catalyze

142 nslational lipoylation of pyruvate and alpha-ketoglutarate dehydrogenase complexes, resulting in dimi

143 nent of the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes.

144 xes, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and branched-chain ketoacid

145 y of a rate-limiting TCA cycle enzyme, alpha-ketoglutarate dehydrogenase.

146 le enzymes, pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase.

147 ation was changed in 1797 genes [e.g., alpha-ketoglutarate dependent dioxygenase (FTO), interleukin 6

148 treatment promoted GBM survival in an alpha-ketoglutarate-dependent (alphaKG-dependent) manner.

149 functional subtypes of nonheme Fe(II)/alpha-ketoglutarate-dependent aspartyl beta-hydroxylases are i

150 172K mutant IDH2 resulted in increased alpha-ketoglutarate-dependent consumption of NADPH compared to

151 The KDM5/JARID1 family of Fe(II)- and alpha-ketoglutarate-dependent demethylases remove methyl group

152 NA for alkylation damage repair by the alpha-ketoglutarate-dependent dioxygenase AlkBH3.

153 s lipid-A by hydroxylation by the Fe2+/alpha-ketoglutarate-dependent dioxygenase enzyme (LpxO).

154 oreover, we applied a key biosynthetic alpha-ketoglutarate-dependent dioxygenase enzyme in a biotrans

155 emethylation are members of the Fe(II)/alpha-ketoglutarate-dependent dioxygenase family.

156 Inactivation of Fe(II)/alpha-ketoglutarate-dependent dioxygenase gene fr9P led to los

157 didomain protein, DdaD, and an Fe(II)/alpha-ketoglutarate-dependent dioxygenase homologue, DdaC.

158 demethylation of thebaine by an Fe(II)/alpha-ketoglutarate-dependent dioxygenase.

159 Iron-(II)/alpha-ketoglutarate-dependent dioxygenases can oxidize 5mC to

160 The AlkB family of Fe(II)- and alpha-ketoglutarate-dependent dioxygenases is a class of ubiqu

161 Fumarate has been shown to inhibit alpha-ketoglutarate-dependent dioxygenases that are involved i

162 d PtmO6 are two functionally redundant alpha-ketoglutarate-dependent dioxygenases that generate a cry

163 The PHDs are alpha-ketoglutarate-dependent dioxygenases that have low K(m)

164 ranslocation) proteins are Fe(ii)- and alpha-ketoglutarate-dependent dioxygenases that modify the met

165 ne synthesis, which in turn stimulates alpha-ketoglutarate-dependent dioxygenases that remove the rep

166 igenetic effects through inhibition of alpha-ketoglutarate-dependent dioxygenases that require iron a

167 lutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases' by Xu and colleagu

168 ctive-site plasticity of these Fe(II) /alpha-ketoglutarate-dependent dioxygenases, and suggest activi

169 endent methyltransferases, Fe(II)- and alpha-ketoglutarate-dependent dioxygenases, base excision glyc

170 proteins, a family of AlkB-like Fe(II)/alpha-ketoglutarate-dependent dioxygenases, can oxidize 5mC to

171 ibit a superfamily of enzymes known as alpha-ketoglutarate-dependent dioxygenases, leading to epigene

172 and establish the role of an iron- and alpha-ketoglutarate-dependent enzyme (Fe/alphaKG) in the pathw

173 ly distinct bifunctional non-heme iron alpha-ketoglutarate-dependent enzyme responsible for the termi

174 A third subtype of nonheme Fe(II)/alpha-ketoglutarate-dependent enzymes (IbetaH(His)) hydroxylat

175 tion and genomic localization of these alpha-ketoglutarate-dependent enzymes in the maintenance of pl

176 natively activated macrophages require alpha-ketoglutarate-dependent epigenetic reprogramming to elic

177 DdaC catalyzes Fe(II)- and alpha-ketoglutarate-dependent epoxidation of the covalently bo

178 We show that Fe(II)- and alpha-ketoglutarate-dependent fat mass and obesity-associated

179 d in vivo by hyperammonemia through an alpha-ketoglutarate-dependent inhibition of the mammalian targ

180 gillus fumigatus is the first reported alpha-ketoglutarate-dependent mononuclear non-haem iron enzyme

181 Notably, we characterized an alpha-ketoglutarate-dependent non-heme Fe(II) dioxygenase that

182 Specifically, alpha-ketoglutarate-dependent non-heme iron enzymes, CitB and

183 caC) in three consecutive, Fe(II)- and alpha-ketoglutarate-dependent oxidation reactions.

184 5caC in three consecutive, Fe(II)- and alpha-ketoglutarate-dependent oxidation reactions.

185 om nucleic acids by a unique iron- and alpha-ketoglutarate-dependent oxidation strategy.

186 due, the inclusion of a non-heme iron, alpha-ketoglutarate-dependent oxygenase for hydroxylation of t

187 ied a conserved group of nonheme iron, alpha-ketoglutarate-dependent oxygenases likely responsible fo

188 of histone demethylases are Fe2+- and alpha-ketoglutarate-dependent oxygenases that are essential co

189 he enzymatic function of many of these alpha-ketoglutarate-dependent proteins is required for pluripo

190 Residue F159 in taurine alpha-ketoglutarate dioxygenase (TauD) is demonstrated to play

191 homolog 7 (ALKBH7) is a mitochondrial alpha-ketoglutarate dioxygenase required for DNA alkylation-in

192 dufs4-KO mice, a cell-permeable KG, dimethyl ketoglutarate (DMKG) was administered.

193 locking serine synthesis or repressing alpha-ketoglutarate-driven demethylation facilitates malignant

194 uctive metabolism of glutamine-derived alpha-ketoglutarate even in normoxic conditions.

195 The Jumonji C domain Fe(II) alpha-ketoglutarate family of proteins performs the majority o

196 a pathway initiated by the Fe(II) and alpha-ketoglutarate (Fe/alphaKG)-dependent aryloxyalkanoate di

197 PHF2 belongs to a class of alpha-ketoglutarate-Fe(2)(+)-dependent dioxygenases.

198 The sequential activities of PhnY, an alpha-ketoglutarate/Fe(II)-dependent dioxygenase, and PhnZ, a

199 y 'ancient' CoA-dependent pyruvate and alpha-ketoglutarate ferredoxin oxidoreductases.

200 ive carboxylation of glutamine-derived alpha-ketoglutarate for de novo lipogenesis.

201 that steric constraints could prevent alpha-ketoglutarate from undergoing an "off-line"-to-"in-line"

202 AMPKalpha2 regulates alpha-ketoglutarate generation, hypoxia-inducible factor-1alph

203 Uniquely, after alpha-ketoglutarate has bound to the mononuclear iron centre i

204 Reducing O-GlcNAcylation increases alpha-ketoglutarate, HIF-1 hydroxylation, and interaction with

205 ylation covalent intermediate derived from 2-ketoglutarate; however, it decreases the abundance of th

206 to static storage with histidine-tryptophan-ketoglutarate (HTK) at 4 degrees C (HTK group, n=5) or S

207 olled trials (RCTs) and histidine-tryptophan-ketoglutarate (HTK) in two RCTs.

208 erfused with oxygenated histidine-tryptophan-ketoglutarate (HTK) solution at 10-15 degrees C for 6 ho

209 osomolar citrate (HOC), histidine-tryptophan-ketoglutarate (HTK), or University of Wisconsin (UW) sol

210 n solutions such as new histidine-tryptophan-ketoglutarate (HTK-N) and TiProtec on the individual tis

211 ent carboxylation of glutamine-derived alpha-ketoglutarate in hypoxia is associated with a concomitan

212 nvert glutamine-derived glutamate into alpha-ketoglutarate in the mitochondria to fuel the tricarboxy

213 tricarboxylic acid cycle intermediate alpha-ketoglutarate, in turn, serves as the cofactor for the e

214 increase in reductive carboxylation of alpha-ketoglutarate (increased concentrations of 2-hydroxyglut

215 the tricarboxyclic acid cycle product alpha-ketoglutarate, indicating the critical function of GLS1

216 e deficiency, through the reduction of alpha-ketoglutarate, inhibits the AlkB homolog (ALKBH) enzymes

217 r minireviews deal with aspects of the alpha-ketoglutarate/iron-dependent dioxygenases in this eighth

218 alpha-Ketoglutarate is an important metabolic intermediate tha

219 Glutamine-derived alpha-ketoglutarate is reductively carboxylated by the NADPH-l

220 bolic fate of hyperpolarized [1-(13)C] alpha-ketoglutarate is studied in isogenic glioblastoma cells

221 s with the alpha-carboxylate moiety of alpha-ketoglutarate, is also uniquely positioned to bestow spe

222 NMN up-regulated alpha-ketoglutarate (KG) levels in Ndufs4-KO muscle, a metabol

223 (suc(2-)) through glutarate (glu(2-)), alpha-ketoglutarate (kglu(2-)), adipate (adi(2-)), pimelate (p

224 tion factor RTG1 Furthermore, elevated alpha-ketoglutarate levels also suppress 2HG-mediated respirat

225 of the IDH3 heterotetramer, decreased alpha-ketoglutarate levels and increased the stability and tra

226 Genetic modulation of alpha-ketoglutarate levels demonstrates a key regulatory role

227 In contrast, alpha-ketoglutarate levels increase at midlevel heteroplasmy a

228 ver, enhanced glutamine flux increases alpha-ketoglutarate levels, which in turn increases proline an

229 DHs, which correlated with the reduced alpha-ketoglutarate levels.

230 a virtual screen of RsbU revealed that alpha-ketoglutarate, malate and oxaloacetate bound to the RsbU

231 iates with good sensitivity, including alpha-ketoglutarate, malate, fumarate, succinate, 2-hydroxyglu

232 tricarboxylic acid cycle metabolites (alpha-ketoglutarate, malic acid, and glutamate) in frozen and

233 novel pathogenicity island involved in alpha-ketoglutarate metabolism under anaerobic conditions.

234 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH l

235 , carried by Dld3, to convert D-2HG to alpha-ketoglutarate, namely an FAD-dependent transhydrogenase

236 acid, confirming that KdoO is a Fe(2+)/alpha-ketoglutarate/O(2)-dependent dioxygenase.

237 hough two enzymes that catalyze Fe(2+)/alpha-ketoglutarate/O(2)-dependent hydroxylation of deoxyuridi

238 three coordination sites, a bidentate alpha-ketoglutarate occupying two sites, and an aquo ligand in

239 phosphoenolpyruvate and the inhibitor alpha-ketoglutarate, on the structure and dynamics of EI using

240 h an NAD(+) precursor or its substrate alpha-ketoglutarate or treatment with a poly(ADP ribose) polym

241 or 30 hr CI in saline, histidine-tryptophan-ketoglutarate or University of Wisconsin preservation so

242 it forms with either the co-substrate (alpha-ketoglutarate) or the substrate (fumitremorgin B).

243 te (SerC and PdxA), we have found that alpha-ketoglutarate, oxaloacetic acid, and pyruvate are equall

244 cluded an unexpected pathway bypassing alpha-ketoglutarate-oxidizing steps in the tricarboxylic acid

245 One such enzyme is the 2-oxoglutarate (alpha-ketoglutarate) oxidoreductase (OOR), which catalyzes the

246 k could be relieved by addition of the alpha-ketoglutarate precursor glutamate.

247 Histidine-tryptophan-ketoglutarate preservation solution slightly decreased i

248 ours of cold storage in histidine-tryptophan-ketoglutarate preservation solution.

249 rdingly, serine starvation or enforced alpha-ketoglutarate production antagonizes squamous cell carci

250 by fueling serine biosynthesis-derived alpha-ketoglutarate production in breast-cancer-derived lung m

251 atoms of N-oxalylglycine (an analog of alpha-ketoglutarate) provide four coordinations in the equator

252 the enzyme that converts isocitrate to alpha-ketoglutarate, providing mechanistic explanation for TCA

253 Glucose, galacturonic acid, alpha-ketoglutarate, pyruvate, acetoin and acetaldehyde were d

254 pe I IFN controls the cellular citrate/alpha-ketoglutarate ratio and inhibits expression and activity

255 e characterized the stereochemistry of alpha-ketoglutarate reduction by showing that d-2-HGA, but not

256 2-oxoglutarate (2-OG or alpha-ketoglutarate) relates mitochondrial metabolism to cell

257 Mechanistically, addition of exogenous alpha-ketoglutarate replenishes TCA intermediates and rescues

258 ochondria via glutamate synthesis from alpha-ketoglutarate resulting in cataplerosis.

259 A cell-permeable ester of alpha-ketoglutarate reversed the low TCA cycle intermediates a

260 inhibitor Meloxicam via histidine-tryptophan-ketoglutarate showed the best graft-protective attribute

261 NEVKP or in 4 degrees C histidine-tryptophan-ketoglutarate solution (SCS), followed by kidney autotra

262 rgans were flushed with histidine tryptophan ketoglutarate solution and subjected to static cold stor

263 Histidine-Tryptophan-Ketoglutarate solution could have an economically superi

264 ither preserved in cold histidine-tryptophan-ketoglutarate solution for 8 hours (n = 5), or subjected

265 of Wisconsin solution, histidine-tryptophan-ketoglutarate solution, and Belzer-machine perfusion sol

266 3 hr of cold storage in histidine-tryptophan-ketoglutarate solution.

267 ersity of Wisconsin and Histidine-Tryptophan-Ketoglutarate solutions are clinically equivalent.

268 was dependent on the concentration of alpha-ketoglutarate substrate in glioma cell lines and could b

269 boxylic acid (TCA) cycle intermediate, alpha-ketoglutarate, suggesting that exogenous glutamine is an

270 , which is suppressed by glutamate and alpha-ketoglutarate supplementation.

271 tricarboxylic acid cycle intermediate alpha-ketoglutarate through glutaminase and alanine aminotrans

272 neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate" by Ward and colleag

273 neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate".

274 c enzymatic activity: the reduction of alpha-ketoglutarate to d-2-hydroxyglutaric acid, which is prop

275 osynthesis pathway, in addition reduce alpha-ketoglutarate to D-2HG using NADH and represent major in

276 ion of E78A, which exhibits binding of alpha-ketoglutarate to E and E.NADH.

277 stimulated reductive carboxylation of alpha-ketoglutarate to generate citrate via retrograde TCA cyc

278 ucine catabolism and transamination of alpha-ketoglutarate to glutamate, with impaired TCA anaplerosi

279 versible transamination of leucine and alpha-ketoglutarate to KIC and glutamate, the first step of le

280 olysis, the conversion of glutamine to alpha-ketoglutarate to maintain the TCA cycle (anaplerosis) an

281 combination of 1 mm cysteine and 1 mm alpha-ketoglutarate to promote sulphide synthesis via the cyst

282 onvert substantially more glutamine to alpha-ketoglutarate to replenish the tricarboxylic acid cycle

283 OR), which catalyzes the conversion of alpha-ketoglutarate to succinyl coenzyme A (succinyl-CoA) and

284 uman cells use reductive metabolism of alpha-ketoglutarate to synthesize AcCoA for lipid synthesis.

285 alteration that leads to catalysis of alpha-ketoglutarate to the oncometabolite D-2-hydroxyglutarate

286 ain-of-function activity by converting alpha-ketoglutarate to the oncometabolite R-2-hydroxyglutarate

287 addition of the TCA cycle intermediate alpha-ketoglutarate to the Rb TKO MEFs reversed the inhibitory

288 iron and 2-oxoglutarate (also known as alpha-ketoglutarate) to function, although their affinities fo

289 ears to be increased by Histidine-Tryptophan-Ketoglutarate-use (p = 0.018), this effect could not be

290 Only Meloxicam in histidine-tryptophan-ketoglutarate was demonstrated to be a safe drug without

291 Apparently, alpha-ketoglutarate was generated from unlabeled glutamate via

292 ation, net synthesis of glutamate from alpha-ketoglutarate was impaired in GDH-deficient islets.

293 (13)C]glutamate produced from [1-(13)C]alpha-ketoglutarate were significantly higher in temozolomide-

294 lutaminolysis catabolites particularly alpha-ketoglutarate, which are generated in an mTORC2-dependen

295 increasing production of glutamate and alpha-ketoglutarate, which in turn results in enhanced mitocho

296 enase expression and the production of alpha-ketoglutarate, which negatively regulate hypoxia-inducib

297 he enzyme (conversion of isocitrate to alpha-ketoglutarate) while conferring a new enzymatic function

298 tion with the mitochondrial metabolite alpha-ketoglutarate, whose synthesis is regulated by RIP1/RIP3

299 outcomes when comparing histidine-tryptophan-ketoglutarate with either of the University of Wisconsin

300 by Q-derived glutamate is converted to alpha-ketoglutarate with the concomitant conversion of oxaloac