ライフサイエンスコーパス: oxaloacetate

1 fixation and increased ATP yield (1 ATP per oxaloacetate).

2 he enzyme (converting phosphoenolpyruvate to oxaloacetate).

3 tamate abrogated inhibition of Complex II by oxaloacetate.

4 ion of malate supplied from the cytoplasm to oxaloacetate.

5 e capacity to accommodate the TCA metabolite oxaloacetate.

6 ysed reversible interconversion of malate to oxaloacetate.

7 l-CoA to pyruvate to yield propionyl-CoA and oxaloacetate.

8 -CoA to pyruvate, yielding propionyl-CoA and oxaloacetate.

9 ear high enough to abolish any channeling of oxaloacetate.

10 ehydrogenase specifically oxidizes malate to oxaloacetate.

11 izing 2-methylcitrate from propionyl-CoA and oxaloacetate.

12 ghly specific for the oxidation of malate to oxaloacetate.

13 itself or its temperature-labile substrate, oxaloacetate.

14 drogenase does not exhibit any channeling of oxaloacetate.

15 activity and was blocked by the CS substrate oxaloacetate.

16 citrate, succinate, alpha-ketoglutarate, and oxaloacetate.

17 etyl-coenzyme A, in its ternary complex with oxaloacetate.

18 ent the negatively charged carboxyl group in oxaloacetate.

19 yl transfer to pyruvate substrate to produce oxaloacetate.

20 but only AOX1A is additionally activated by oxaloacetate.

21 ibution from either plasma glucose or muscle oxaloacetate.

22 m and an active site variant in complex with oxaloacetate.

23 pyruvate with CO(2) (as HCO(3) (-)), forming oxaloacetate.

24 action mechanism promotes decarboxylation of oxaloacetate.

25 miting step in the biosynthesis of AcCoA and oxaloacetate.

26 K) kinetic isotope effect observed on C-4 of oxaloacetate [(13)(V/K) = 1.0117 +/- 0.0005] indicates t

27 ic enzyme (275%); elevated concentrations of oxaloacetate (150%), malate (250%), citrate (140%), and

28 ial extracts was made to oscillate by adding oxaloacetate (5 micromol/l) to inhibit the enzyme.

29 ne with (k(cat)/K(m)(pyruvate))/(k(cat)/K(m)(oxaloacetate)) = 6.1 x 10(-9) to one with that ratio = 2

30 ized by succinate + glutamate generated more oxaloacetate (a potent inhibitor of succinate dehydrogen

31 cosubstrates, 2-oxoglutarate, pyruvate, and oxaloacetate, Ab-ArAT4 possesses strong substrate prefer

32 e mitochondria energized by succinate alone, oxaloacetate accumulates and inhibits succinate dehydrog

33 mino acid sequence identity to the confirmed oxaloacetate acetyl hydrolase (OAH), an enzyme that belo

34 ough several different biochemical pathways, oxaloacetate acetylhydrolase (OAH)-catalyzed hydrolytic

35 Finally, deletion of the oxaloacetate acetylhydrolase gene in H915-1 eliminated o

36 exhibited a 52 +/- 7% reduction in cytosolic oxaloacetate, an 83 +/- 4% reduction in malonyl-CoA leve

37 MgATP-dependent carboxylation of pyruvate to oxaloacetate, an important anaplerotic reaction in mamma

38 tate with pyruvate, alpha-ketoglutarate, and oxaloacetate and (ii) mercaptopicolinate and pyruvate.

39 ed should cleave protein bound citryl-CoA to oxaloacetate and a protein-bound CoA derivative.

40 bisubstrate adduct indicate that each of the oxaloacetate and acetyl-CoA substrates is bound to an in

41 onversion of citrate and coenzyme A (CoA) to oxaloacetate and acetyl-CoA(1-5).

42 routes glutamine metabolism to generate both oxaloacetate and acetyl-CoA, enabling persistent tricarb

43 and MgATP-dependent cleavage of citrate into oxaloacetate and acetyl-CoA, representing a key step in

44 lving a reductive glyoxylate pathway without oxaloacetate and alpha-ketoglutarate-implying that the e

45 Simple dehydration of tartrates to oxaloacetate and an ensuing decarboxylation to form pyru

46 nd the TCA cycle, such as pyruvate, acetate, oxaloacetate and cholesterol.

47 enolpyruvate then reacts with CO(2) to form oxaloacetate and complete the reaction.

48 le, heart, and brown adipose mitochondria by oxaloacetate and complex I electron flow.

49 peroxide dismutase 1 (SOD1) (G93A) mice with oxaloacetate and evaluated their neuromuscular function

50 ates determined at varying concentrations of oxaloacetate and fixed concentrations of oxamate reveale

51 inase (GOT2), catalyzes the reaction between oxaloacetate and glutamate generating aspartate and alph

52 al transport fluxes of pyruvate, acetyl-CoA, oxaloacetate and glycine.

53 into acetyl-CoA and toward the formation of oxaloacetate and into the gluconeogenic pathway.

54 es the cell with only one pathway, involving oxaloacetate and l-glutamate, for de novo synthesis of h

55 ve determined the ternary complex bound with oxaloacetate and magnesium, revealing some of the conser

56 tion of 2SNAC, resulting in its breakdown to oxaloacetate and N-acetylcysteine, which is deacetylated

57 ed production of the TCA cycle intermediates oxaloacetate and NADPH, and impaired oxygen consumption.

58 complex ferricyanide, and 3) the keto-acids oxaloacetate and pyruvate (and phosphoenolpyruvate, a me

59 malate or that cannot convert malate to both oxaloacetate and pyruvate are also avirulent and protect

60 mitochondria enables the generation of both oxaloacetate and pyruvate for tricarboxylic acid (TCA) c

61 s and identified a high futile cycle between oxaloacetate and pyruvate, indicating a highly active in

62 virulence, malate must be converted to both oxaloacetate and pyruvate.

63 nitor the PC-catalyzed formation of [4-(13)C]oxaloacetate and subsequent transfer of (13)CO(2) from o

64 oor or moderate KDM5B inhibitors, except for oxaloacetate and succinate, which were shown to compete

65 0 forms a hydrogen bond with the carbonyl of oxaloacetate and the alcohols of the citryl-coenzyme A a

66 led pyruvate leads to formation of [1,2-13C2]oxaloacetate and to multiply labeled glutamate and succi

67 Structural analyses of the complexes with oxaloacetate and with a bisubstrate adduct indicate that

68 A Glu198Gln variant are incubated with DHAP, oxaloacetate, and ammonium chloride, conditions under wh

69 d vesicles catalyzed the exchange of malate, oxaloacetate, and aspartate for phosphate plus a proton

70 y the TCA intermediates alpha-ketoglutarate, oxaloacetate, and pyruvate, confirming that in infected

71 ate to pyruvate, via pyruvate carboxylase to oxaloacetate, and via PCK2 to phosphoenolpyruvate.

72 olase (OAH)-catalyzed hydrolytic cleavage of oxaloacetate appears to be an especially important route

73 In the aerobic regime, 75% of mitochondrial oxaloacetate arises from anaplerotic carboxylation of py

74 oxidative decarboxylation was stepwise, with oxaloacetate as an intermediate, or concerted.

75 is essential for the conversion of malate to oxaloacetate as part of the proper functioning of the Kr

76 that only d-tartrate is dehydrated, yielding oxaloacetate as product.

77 d [U-(13)C]aspartate is formed from [U-(13)C]oxaloacetate, as is [U-(13)C]lactate.

78 iet, HFD-fed mice displayed higher levels of oxaloacetate, aspartate, and malate, along with increase

79 ubsite, and uncouples the decarboxylation of oxaloacetate at subsite 2 from the formation of ATP at s

80 Treatment with oxaloacetate beginning in the presymptomatic stage signi

81 dehydrogenase (MDH) to assess the chances of oxaloacetate being channeled between the MDH and CS acti

82 d with the specific example of channeling of oxaloacetate between Escherichia coli aspartate aminotra

83 mitochondrial malate dehydrogenase channels oxaloacetate between the active sites.

84 Pyruvate and oxaloacetate bind to the 2-oxoglutarate site of HIF-1alp

85 through carbonyl bond polarization, not just oxaloacetate binding in the active site, is required for

86 enzyme A but also forms the back wall of the oxaloacetate-binding site.

87 evealed that alpha-ketoglutarate, malate and oxaloacetate bound to the RsbU periplasmic domain.

88 the cytoplasm where it can be converted into oxaloacetate by aspartate transaminase (GOT1).

89 the enzyme fumarase and further oxidized to oxaloacetate by malate dehydrogenase with the accompanyi

90 Furthermore, the exclusive formation of oxaloacetate by phosphoenolpyruvate (PEP) carboxylation

91 f these mutants can activate the carbonyl of oxaloacetate by polarization.

92 is of 2-methylcitrate from propionyl-CoA and oxaloacetate by the PrpC protein.

93 The D375 mutants polarize the oxaloacetate carbonyl as well as wild-type.

94 olpyruvate carboxylase [PEPC; orthophosphate:oxaloacetate carboxy-lyase (phosphorylating), EC 4.1.1.3

95 olpyruvate carboxylase [PEPC; orthophosphate:oxaloacetate carboxy-lyase (phosphorylating), EC 4.1.1.3

96 lely dependent on the hydrolytic cleavage of oxaloacetate catalyzed by OAH.

97 athway for the interconversion of malate and oxaloacetate catalyzed by the enzyme malate dehydrogenas

98 Oxidation of malate to oxaloacetate, catalyzed by either malate dehydrogenase (

99 ated by a carbamylated lysine, except in the oxaloacetate complex in which the product's carboxylate

100 The dicarboxylate ligand in oxaloacetate-containing crystals appears to be the same

101 While efficient oxaloacetate conversion in Arabidopsis thaliana still ma

102 on the enzymatic conversion of glyoxylate to oxaloacetate coupled to the reduction of oxidized nicoti

103 Stimulation of this oxaloacetate decarboxylase activity in the presence of s

104 ervation with carboxyltransferase domains in oxaloacetate decarboxylase and transcarboxylase, the str

105 ceptor domain from the Klebsiella pneumoniae oxaloacetate decarboxylase are extracted with 5 M urea o

106 ichment analyses identify an operon encoding oxaloacetate decarboxylase as diagnostic for the tongue-

107 Aspartate aminotransferase and oxaloacetate decarboxylase were less effective competito

108 ge amounts of aspartate aminotransferase and oxaloacetate decarboxylase, as competing enzymes for the

109 inotransferase and then decarboxylation with oxaloacetate decarboxylase.

110 pyruvate, indicating a highly active in vivo oxaloacetate decarboxylase.

111 bject to enzymatic decarboxylation; however, oxaloacetate decarboxylases (ODx) were so far not identi

112 sults presented here indicate that dedicated oxaloacetate decarboxylases exist in eukaryotes.

113 n of the two enzymes required are described; oxaloacetate decarboxylating malic dehydrogenase is also

114 atase to convert fumarate to malate and uses oxaloacetate decarboxylating malic dehydrogenase to conv

115 phogluconate aldolase exhibiting alternative oxaloacetate decarboxylation activity that modulates day

116 pe and V-type ATPases and SMF generation via oxaloacetate decarboxylation are among the most highly e

117 no effect on the rate of biotin-independent oxaloacetate decarboxylation.

118 Administration of the metabolite oxaloacetate decreased the oxygen consumption rate of th

119 indicative of a glyoxylate-induced state of oxaloacetate deficiency, acetate overload, and ketoacido

120 ansfer preceding hydride transfer (malate to oxaloacetate direction), (2) the existence of two transi

121 xpressed to access the one-step synthesis of oxaloacetate directly from phosphoenolpyruvate without p

122 (alpha)-H cleavage, ketimine hydrolysis, and oxaloacetate dissociation to the rate limitation with th

123 cetyl cysteine or the TCA cycle intermediate oxaloacetate efficiently rescues Gln starvation-induced

124 ial-derived malate levels, reduced cytosolic oxaloacetate, elevated MDH1 levels, and a high cytoplasm

125 Oxaloacetate enhanced the interaction only when it was p

126 tterns of Asp and Thr suggested formation of oxaloacetate exclusively via the phosphoenolpyruvate car

127 as a complete, albeit bifurcated, TCA cycle; oxaloacetate flows to succinate both through citrate/alp

128 erate reductive power (NADPH) and to restore oxaloacetate for continued TCA cycle function (anapleros

129 ter, respectively, whereas those for GTP and oxaloacetate (for the phosphoenolpyruvate formation acti

130 bound PEP, brought subtle effects, lowering oxaloacetate formation rate but enhancing PEP formation

131 eaction which produces acetyl-coenzyme A and oxaloacetate from citrate and coenzyme A (CoA).

132 lactate, alanine from pyruvate, malate, and oxaloacetate from fumarate.

133 phorylation), substrate channeling (e.g., of oxaloacetate from malate dehydrogenase to citrate syntha

134 The diffusion of oxaloacetate from one of the active sites of malate dehy

135 ial pyruvate metabolism; (e) the transfer of oxaloacetate from the cytosol to the mitochondria is lar

136 the substrate, fumarate, and the inhibitors oxaloacetate, glutarate, and 3-nitropropionate.

137 on the activities of MDH is unidirectional (oxaloacetate --> malate).

138 ed, and that for the physiological substrate oxaloacetate has been diminished, through the replacemen

139 a metabolite of plant photorespiration, into oxaloacetate in a highly efficient carbon-, nitrogen-, a

140 ces the rate of enzymatic decarboxylation of oxaloacetate in the carboxyl transferase domain of pyruv

141 etyl-CoA (3 micromol/l), which combines with oxaloacetate in the citrate synthase reaction and lowers

142 bound in the ASH domain, with an additional oxaloacetate in the CSH domain, which could function in

143 ith glutamine, and favor the accumulation of oxaloacetate in the cytoplasm.

144 Channeling of oxaloacetate in the malate dehydrogenase and citrate syn

145 orm, CA5b, which is critical in replenishing oxaloacetate in the mitochondrial tricarboxylic acid (TC

146 talysis of the interconversion of malate and oxaloacetate in the tricarboxylic acid cycle.

147 ow that the glucose metabolites pyruvate and oxaloacetate inactivate HIF-1alpha decay in a manner sel

148 K(m) values for oxaloacetate increased 2-2.8-fold.

149 The high reactivity of PFR1 toward oxaloacetate indicates that in vivo, fermentation might

150 AP as well as glyceraldehyde 3-phosphate and oxaloacetate inhibited activity of both yeast and human

151 zed O(2) flux likely due at least in part to oxaloacetate inhibition of succinate dehydrogenase.

152 Oxaloacetate inhibits E1o activity at physiological conc

153 The channeling of the oxaloacetate intermediate was the same for the porcine f

154 ools through the conversion of mitochondrial oxaloacetate into phosphoenolpyruvate.

155 Oxaloacetate is also a substrate for HCS, but with lower

156 Synthesis of phosphoenolpyruvate (PEP) from oxaloacetate is an absolute requirement for gluconeogene

157 d (ii) intrinsic inhibition of Complex II by oxaloacetate is an inherent mechanism that protects agai

158 e presence of oxamate, the apparent K(m) for oxaloacetate is artificially suppressed (from 15 to 4-5

159 Subsequently, this oxaloacetate is converted into malate and then pyruvate,

160 ation rate, which suggests that an excess of oxaloacetate is converted to aspartate and reintroduced

161 The oxaloacetate is converted to malate, leading to malic ac

162 The results show that oxaloacetate is not transferred directly from AATase to

163 H) catalyzed oxidation/reduction of L-malate/oxaloacetate is pH-dependent due to the proton generated

164 In bacteria, oxaloacetate is subject to enzymatic decarboxylation; ho

165 lycolysis; (c) the majority of the cytosolic oxaloacetate is synthesized via anaplerotic carboxylatio

166 random, suggesting that the enol tautomer of oxaloacetate is the product; this expectation was confir

167 to the discovery that PA4872 decarboxylates oxaloacetate (kcat = 7500 s(-1) and Km = 2.2 mM) and 3-m

168 the enzyme first, followed by the binding of oxaloacetate/L-malate.

169 dentified (2R)-ethyl, (3S)-methylmalate, and oxaloacetate [likely to bind as the hydrate, C(2)(OH)(2)

170 tabolic end products of lignin (pyruvate and oxaloacetate) must enter the tricarboxylic acid (TCA) cy

171 c enzyme in the phosphoenolpyruvate-pyruvate-oxaloacetate node that is a central switch point for car

172 The decline resulted from oxaloacetate (OAA) accumulation and inhibition of succin

173 To test how one intermediate, oxaloacetate (OAA) affects brain bioenergetics, insulin

174 he crystal structure of AaCS, complexed with oxaloacetate (OAA) and the inhibitor carboxymethyldethia

175 recognition of phosphoenolpyruvate (PEP) and oxaloacetate (OAA) by cytosolic phosphoenolpyruvate carb

176 Metabolomic analysis revealed high levels of oxaloacetate (OAA) in RABV-infected mouse brains.

177 Oxaloacetate (OAA) is a central liver metabolite fundame

178 Oxaloacetate (OAA) is converted to aspartate by mitochon

179 -oxidation (redox) homeostasis is the malate-oxaloacetate (OAA) shuttle.

180 y intriguing condensation of acetyl-CoA with oxaloacetate (OAA) to form citryl-CoA and the subsequent

181 uconeogenesis by conversion of mitochondrial oxaloacetate (OAA) to phosphoenolpyruvate, regulates glu

182 cinate dehydrogenase oxidizes malate to enol-oxaloacetate (OAA), a metabolically inactive form of OAA

183 Oxaloacetate (OAA), pyruvate, and glutarate behave as de

184 mation of the binary complex with substrate, oxaloacetate (OAA).

185 ner, and recuperates photorespiratory CO2 as oxaloacetate (OAA).

186 H274G cannot properly activate either oxaloacetate or acetyl-coenzyme A, and the condensation

187 gative charge of the substrate side-chain of oxaloacetate or alpha-ketomalonate, charge repulsion wou

188 he ketimine of pyridoxamine 5'-phosphate and oxaloacetate or pyruvate.

189 talysis, such as the conversion of malate to oxaloacetate or the activation of the toxin 3-nitropropi

190 and bound to its substrate pyruvate, product oxaloacetate, or inhibitor 2-ketobutyrate.

191 r via measurement of D(V/K), T(V/K), and the oxaloacetate partition ratio.

192 zes of amino acids derived from pyruvate and oxaloacetate, polyamine precursors, and compatible solut

193 pathways, including pyruvate, glutamate and oxaloacetate pools, and urea production from arginine, w

194 PpcA was the only recognizable oxaloacetate-producing enzyme in Methanopyrus kandleri,

195 ACLY with acetyl-CoA and oxaloacetate products shows the products bound in the AS

196 ASH-CSH interface to produce acetyl-CoA and oxaloacetate products.

197 ganic substrate provided (glucose, pyruvate, oxaloacetate, protein, urea, and amino acids).

198 analyses with succinate, fumarate, L-malate, oxaloacetate, pyruvate and D- and L-2HG support the kine

199 ate, succinate, 2-hydroxyglutarate, citrate, oxaloacetate, pyruvate, isocitrate, and lactate using a

200 sparagine), yielding alpha-ketoglutarate and oxaloacetate, respectively.

201 catalyzes the readily reversible reaction of oxaloacetate reversible malate using either NADH or NADP

202 In catalysis, oxaloacetate serves as a nucleophile by forming an enola

203 that in glucose grown cells, both the malate/oxaloacetate shuttle and a glycerol-3-phosphate dehydrog

204 are transferred to the cytosol by the malate/oxaloacetate shuttle.

205 The results with the series of oxaloacetate site mutants, H320X, strongly suggest that

206 vely, and (3) reactant (malate) and product (oxaloacetate) states that are nearly isoenergetic.

207 es identified in PCS, destabilization of the oxaloacetate substrate carbonyl and stabilization of the

208 ained decarboxylase activity for the smaller oxaloacetate substrate, which is not inhibited by excess

209 Burkholderia species utilize acetyl-CoA and oxaloacetate, substrates for citrate synthase in the TCA

210 ble alpha-ketoglutarate, but not pyruvate or oxaloacetate, suggesting an important role for reductive

211 decrease in malic acid, and lower amounts of oxaloacetate, suggesting that malate metabolism plays an

212 ing lysine feedback inhibition, and boosting oxaloacetate supply.

213 In Methanothermobacter thermautotrophicus, oxaloacetate synthesis is a major and essential CO(2)-fi

214 is presented that, in Methanosarcina barkeri oxaloacetate synthesis, an essential and major CO(2) fix

215 1) For oxaloacetate synthesis, V(max) decreased 1.4-4-fold.

216 aplerosis through reduction of mitochondrial oxaloacetate synthesis.

217 provision for pyruvate carboxylase-mediated oxaloacetate synthesis.

218 results and the existence of an alternative oxaloacetate synthesizing enzyme phosphoenolpyruvate car

219 This methanogenic archaeon possesses two oxaloacetate-synthesizing enzymes, pyruvate carboxylase

220 ctivity, but with K(m) values for malate and oxaloacetate that are surprisingly unaffected.

221 tenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, d

222 For producing oxaloacetate, the enzyme utilized both GDP and IDP; ADP

223 gATP, the oxamate-induced decarboxylation of oxaloacetate, the phosphorylation of MgADP by carbamoyl

224 determined for the forward reaction to form oxaloacetate, the reverse reaction to form MgATP, the ox

225 sion reduced TCA cycle activity and diverted oxaloacetate, the substrate of CS, into production of th

226 gest that activation of the first substrate, oxaloacetate, through carbonyl bond polarization, not ju

227 ase reaction and lowers the concentration of oxaloacetate, thus beginning another oscillation.

228 th the portion of the citric acid cycle from oxaloacetate to alpha-ketoglutarate via cis-aconitate.

229 An efficient prebiotic transformation of oxaloacetate to aspartate via N-carbamoyl aspartate enab

230 glutarate with the concomitant conversion of oxaloacetate to aspartate.

231 lyase, ultimately regenerating mitochondrial oxaloacetate to complete this non-canonical TCA cycle.

232 e base, its failure to further condense with oxaloacetate to form a sulfur-less analog of citryl-coen

233 sible decarboxylation and phosphorylation of oxaloacetate to form phosphoenolpyruvate.

234 (PEPCK), forward TCA cycle flux of [4-(13)C]oxaloacetate to generate (13)CO(2) at isocitrate dehydro

235 eir decarboxylation enables the reduction of oxaloacetate to malate and of fumarate to succinate, whe

236 rease the rate of the coupled L-aspartate to oxaloacetate to malate sequence only if the direct metab

237 f the enzymatic conversion of hyperpolarized oxaloacetate to malate, the two signal components are se

238 atalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase

239 te and subsequent transfer of (13)CO(2) from oxaloacetate to oxamate.

240 provides the acetyl-CoA that condenses with oxaloacetate to support citrate production.

241 The diet may limit the availability of oxaloacetate to the aspartate aminotransferase reaction,

242 , the malate dehydrogenase 1 (MDH1)-mediated oxaloacetate-to-malate flux is reversed and elevated in

243 To this end, we evaluated glutamate-oxaloacetate transaminase (GOT) activity in hemolysates

244 can be productively metabolized by glutamate oxaloacetate transaminase (GOT) to maintain cellular ene

245 s work demonstrated the ability of glutamate oxaloacetate transaminase (GOT) to metabolize neurotoxic

246 e, and associated enzymes, such as glutamate-oxaloacetate transaminase (GOT1), glutamate-pyruvate tra

247 uced significant increase in serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruva

248 role for glutamate metabolism and glutamate oxaloacetate transaminase 1 (GOT1)-dependent redox balan

249 Mitochondrial glutamate-oxaloacetate transaminase 2 (GOT2) is part of the malate

250 Knockdown of glutamate-oxaloacetate transaminase activity significantly reduced

251 gage the neuroprotective effect of glutamate oxaloacetate transaminase against stroke.

252 C-transformed cells depend on both glutamate-oxaloacetate transaminase and glutamate dehydrogenase to

253 Glutamate oxaloacetate transaminase enables anaplerotic refilling

254 e, DR, which is closely related to glutamate-oxaloacetate transaminase, EC 2.6.1.1.

255 GOT2 encodes the mitochondrial glutamate oxaloacetate transaminase.

256 to the mitochondria and cytoplasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogena

257 ansported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD t

258 t understanding would not have predicted the oxaloacetate transforming activity of Ser101Leu102 or th

259 For lifespan analysis, oxaloacetate treatment did not show a statistically sign

260 Oxaloacetate treatment has a neuroprotective effect in r

261 sults suggest that the beneficial effects of oxaloacetate treatment in SOD1(G93A) mice may reflect th

262 However, oxaloacetate treatment reverted these abnormal levels to

263 Oxaloacetate treatment starting in the symptomatic stage

264 tein returned to that of wild-type mice with oxaloacetate treatment.

265 ing cataplerotic decarboxylation of [4-(13)C]oxaloacetate via phosphoenolpyruvate carboxykinase (PEPC

266 se (DET0724-0727) and pyruvate conversion to oxaloacetate via pyruvate carboxylase (DET0119-0120).

267 lex or the biotin-dependent carboxylation to oxaloacetate via pyruvate carboxylase (Pcx).

268 arboxylation was suppressed, and anaplerotic oxaloacetate was derived from glutamine.

269 Interestingly, the glucose-6-phosphate and oxaloacetate was higher in T2DMs compared to T1DMs.

270 ffer between GOT2KO and WT mitochondria, and oxaloacetate was not detectable.

271 An unexpected binding mode for oxaloacetate was observed in which it coordinates the ac

272 bstrate analog: the gem-diol of 3,3-difluoro-oxaloacetate) was determined for the purpose of identify

273 e, as competing enzymes for the intermediate oxaloacetate, was examined.

274 protein could account for the channeling of oxaloacetate we observed with the yeast fusion protein.

275 late through protocatechuate to pyruvate and oxaloacetate were demonstrated in cells or cell extracts

276 -hydroxyoctadecadienoic acid, glutamine, and oxaloacetate were higher after the WG diet than after th

277 oglutarate, succinate, fumarate, malate, and oxaloacetate) were tested for their influence on AOX1A,

278 boxylase were less effective competitors for oxaloacetate when precipitated citrate synthase and mito

279 rate of decarboxylation of the intermediate oxaloacetate which occurs at 11 s-1.

280 liberated enzymatically by transamination to oxaloacetate with aspartate aminotransferase and then de

281 Substrate channeling of oxaloacetate with citrate synthase-mitochondrial malate

282 IL23A expression by yielding acetyl-CoA and oxaloacetate, with the latter one supporting glycolysis