ライフサイエンスコーパス: citrate synthase

1 l-CoA dehydrogenase activity or its ratio to citrate synthase.

2 e target proteins, alcohol dehydrogenase and citrate synthase.

3 ses the aggregation of thermally inactivated citrate synthase.

4 etic patients, although it modestly elevated citrate synthase.

5 oxidative branch of the Krebs cycle, IDH and citrate synthase.

6 otide binding domain 1, insulin B chain, and citrate synthase.

7 the ability of PA700 to promote refolding of citrate synthase.

8 ed in the screen, pyruvate dehydrogenase and citrate synthase.

9 Similar results were also obtained with citrate synthase.

10 application of this method to porcine heart citrate synthase.

11 dues to individual steps in the mechanism of citrate synthase.

12 but not cytosolic malate dehydrogenase with citrate synthase.

13 T2, a gene encoding a peroxisomal isoform of citrate synthase.

14 dihydrofolate reductase, but not with bound citrate synthase.

15 mechanistic features distinct from those of citrate synthase.

16 ndrial reactive oxygen species and bacterial citrate synthase.

17 to evaluate thermally induced aggregation of citrate synthase.

18 n also suppresses the thermal aggregation of citrate synthase.

19 , MP1 does not process the precursor form of citrate synthase.

20 tipode of the citrate synthesized by the (S)-citrate synthase].

21 Hindlimb muscle oxidative (citrate synthase, 21%; beta-HAD, 32%) and glycolytic (PF

22 eobacter species, expression and function of citrate synthase, a key enzyme in the TCA cycle that is

23 red the activities of the following enzymes: citrate synthase, a marker of oxidative metabolism; beta

24 event the aggregation of thermally denatured citrate synthase, a measure of passive chaperoning activ

25 A. aceti citrate synthase (AaCS), a hexameric type II citrate syn

26 the previously unexplained role of A. aceti citrate synthase (AarA) in acetic acid resistance at a l

27 Here we showed that citrate synthase, aconitase, isocitrate dehydrogenase, f

28 chondrial density and cytochrome oxidase and citrate synthase activities relative to M-ERRalphaWT.

29 Creatine kinase and citrate synthase activities were measured as markers of

30 ransporter, citrate transporter protein, and citrate synthase activities.

31 Additionally, citrate synthase activity (normal, 0.33 +/- 0.14; heart

32 ter normalization for a moderate decrease in citrate synthase activity (P<0.05).

33 ion was normalized to muscle wet weight, and citrate synthase activity (standard measure of mitochond

34 Myocilin protected citrate synthase activity against thermal inactivation f

35 layed reduced mitochondrial content (reduced citrate synthase activity and cytochrome c protein) and

36 the eoPE group and an increase of P/O ratio, citrate synthase activity and decrease of Ca(2+)-induced

37 Mitochondrial content was normalized to citrate synthase activity and mitochondrial function was

38 al dysfunction, which is revealed by reduced citrate synthase activity and mtDNA copy number.

39 dative function was impaired, with decreased citrate synthase activity and spare respiratory capacity

40 mice showed a approximately 25% increase in citrate synthase activity but no further increase with t

41 Citrate synthase activity decreased in autotrophic and a

42 Citrate lyase activity was higher than ATP citrate synthase activity in autotrophic cultures.

43 This was associated with a 17% decrease in citrate synthase activity in both the soleus and plantar

44 d muscle PGC-1a expression and mitochondrial citrate synthase activity in chronically exercised mice.

45 a, together with the significant increase in citrate synthase activity in heart, but not in soleus an

46 d glucose tolerance, liver NAD(+) levels and citrate synthase activity in offspring.

47 muscle HK-II activity correlated with muscle citrate synthase activity in the normal subjects (r = 0.

48 Similarly, skeletal muscle citrate synthase activity increased by 13% in the exerci

49 aintained levels of cytochrome C oxidase and citrate synthase activity levels.

50 as induced in the absence of any increase in citrate synthase activity or in subunit IV of the cytoch

51 an uncoupler and expressed as a function of citrate synthase activity per total amount of protein.

52 eart weight (mg/g body weight) and planteris citrate synthase activity than their sedentary controls.

53 Citrate synthase activity was decreased significantly on

54 Citrate synthase activity was lower (P < 0.0001) and cyt

55 Also, citrate synthase activity was reduced in type 2 diabetic

56 These results suggested that citrate synthase activity was the source of the increase

57 hat, in the wild-type strain, high levels of citrate synthase activity were the source of a toxic met

58 lowest for patients in the middle tertile of citrate synthase activity when normalized to either musc

59 otide (NADH) oxidase activity (normalized to citrate synthase activity) in lymphocytic mitochondria f

60 content (cytochrome c, COXIV-subunit I, and citrate synthase activity) significantly increased (P <

61 ss, mitochondrial DNA depletion, and reduced citrate synthase activity, an index of mitochondrial mas

62 Total mtDNA content, citrate synthase activity, and cytochrome c oxidase acti

63 nstrated by increases in oxygen consumption, citrate synthase activity, and induction of key metaboli

64 opy number (mtDNA), OXPHOS gene transcripts, citrate synthase activity, and maximal mitochondrial ATP

65 me c content, cytochrome c oxidase activity, citrate synthase activity, and oxygen consumption, param

66 s exercise training improved cardiac output, citrate synthase activity, and peak tissue diffusing cap

67 Disruption of citrate synthase activity, however, suppressed the effec

68 Citrate synthase activity, mitochondrial DNA (mtDNA) abu

69 Measurements of renal cardiolipin levels, citrate synthase activity, rotenone-sensitive NADH oxida

70 drial superoxide dismutase (SOD2), and lower citrate synthase activity, the first step in the tricarb

71 s, and mitochondrial densities, assessed via citrate synthase activity, were consistent between group

72 ining, mitochondrial DNA quantification, and citrate synthase activity.

73 ing, DNA quantification, and measurements of citrate synthase activity.

74 rmalized to creatine kinase activity, as was citrate synthase activity.

75 nate-resistant strain contained 12-fold less citrate synthase activity.

76 acid cycle deficiency without affecting the citrate synthase activity.

77 e dismutase 2, concomitant with increases in citrate synthase activity.

78 l muscle this was paralleled by a decline in citrate synthase activity.

79 n rat heart extracts, after normalization to citrate synthase activity.

80 (per million fibroblasts), of protein, or of citrate synthase activity.

81 There was also no increase in citrate synthase activity.

82 to alphaB-crystallin, MTB HSP16.3 suppressed citrate synthase aggregation and in the presence of 3.5

83 xtended apo conformation in the context of a citrate synthase aggregation assay.

84 Insulin and citrate synthase aggregation assays showed 38 and 30% im

85 e highly conserved Glu-240, fails to prevent citrate synthase aggregation at 43 degrees C.

86 y luciferase as well as in the prevention of citrate synthase aggregation.

87 lasses of secondary structure such as alpha (citrate synthase), alpha + beta (lysozyme), beta (concav

88 hrome c, delta-aminolevulinate synthase, and citrate synthase also occurred before an increase in PGC

89 Citrate synthase and aconitase activities in cells grown

90 n artificial chaperone-assisted refolding of citrate synthase and artificial chaperone-assisted refol

91 n levels of complexes I, II, and IV, whereas citrate synthase and ATP synthase were unaffected.

92 taneous and glucose-induced second wind; and citrate synthase and beta-hydroxyacyl coenzyme A dehydro

93 ygen uptake (14%), cardiac output (15%), and citrate synthase and beta-hydroxyacyl coenzyme A dehydro

94 Functional assays of mitochondrial citrate synthase and complex IV, key rate-limiting steps

95 microm PQQ for 24-48 h resulted in increased citrate synthase and cytochrome c oxidase activity, Mito

96 lary density were analyzed by stereology and citrate synthase and cytochrome c oxidase by biochemical

97 illary density were three times greater, and citrate synthase and cytochrome c oxidase were only appr

98 ), activity of muscle mitochondrial enzymes (citrate synthase and cytochrome c oxidase, 45-76%) and m

99 Mitochondrial citrate synthase and cytochrome oxidase activity decreas

100 and mitochondrial malate dehydrogenase, and citrate synthase and cytosolic malate dehydrogenase.

101 yethylene glycol or with a co-precipitate of citrate synthase and cytosolic malate dehydrogenase.

102 rogenase occurred but no interaction between citrate synthase and cytosolic malate dehydrogenase.

103 We report the utilization of an alternative citrate synthase and describe a dynamic branching of the

104 ompanied by a three- to fourfold increase in citrate synthase and fatty acid synthase activity.

105 ors, in the CIT1 gene encoding the TCA cycle citrate synthase and in other genes of oxidative metabol

106 o fibrillization or aggregation of alphaSyn, citrate synthase and insulin.

107 : FKBP65 inhibits the thermal aggregation of citrate synthase and is active in the denatured rhodanes

108 he citZ gene, which encodes the cell's major citrate synthase and is subject to carbon catabolite rep

109 ase (citH) was found downstream of genes for citrate synthase and isocitrate dehydrogenase.

110 two classical chaperone substrate proteins, citrate synthase and luciferase.

111 It protected citrate synthase and malate dehydrogenase from thermal a

112 on model of porcine mitochondrial enzymes of citrate synthase and malate dehydrogenase was used, show

113 nd inactivation of the heat-labile proteins, citrate synthase and malate dehydrogenase.

114 The interactions between pig heart citrate synthase and mitochondrial malate dehydrogenase

115 mpetitors for oxaloacetate when precipitated citrate synthase and mitochondrial malate dehydrogenase

116 is method showed that an interaction between citrate synthase and mitochondrial malate dehydrogenase

117 ed using polyethylene glycol precipitates of citrate synthase and mitochondrial malate dehydrogenase,

118 was able to protect the heat-labile enzymes citrate synthase and Nde1 from thermal aggregation and i

119 ough it could prevent thermal aggregation of citrate synthase and Nde1, was unable to refold and rest

120 A fusion protein of porcine citrate synthase and porcine cytosolic malate dehydrogen

121 olding intermediates of chemically denatured citrate synthase and prevents their aggregation in vitro

122 bundance of the mitochondrial matrix-located citrate synthase and pyruvate dehydrogenase complex E1al

123 aining, we measured markers of mitochondria (citrate synthase and succinate dehydrogenase) and glucos

124 ncrease (p < 0.05) in the activities of both citrate synthase and superoxide dismutase in the digastr

125 that citrate is produced by a putative (Re)-citrate synthase and then enters the oxidative (forward)

126 complex inhibited the thermal aggregation of citrate synthase and was active in the denatured rhodane

127 that a fusion protein of yeast mitochondrial citrate synthase and yeast mitochondrial malate dehydrog

128 osition of the SbnG active site to TCA cycle citrate synthases and site-directed mutagenesis suggests

129 muscle homogenates (cytochrome c oxidase and citrate synthase) and in isolated mitochondria (citrate

130 to CO(2), enzymatic activities (beta-HAD and citrate synthase), and the expression levels of cytochro

131 of oxaloacetate from malate dehydrogenase to citrate synthase), and use of alternative cofactors (e.g

132 between mitochondrial malate dehydrogenase, citrate synthase, and aconitase were identified.

133 olism, such as pyruvate dehydrogenase (PDH), citrate synthase, and acyl-CoA dehydrogenases.

134 gregation of reduced insulin, heat-denatured citrate synthase, and alcohol dehydrogenase.

135 sc66 suppressed aggregation of rhodanese and citrate synthase, and ATP caused effects consistent with

136 tured model substrate proteins rhodanese and citrate synthase, and calorimetric and surface plasmon r

137 activated receptor-gamma coactivator 1alpha, citrate synthase, and cytochrome c oxidase I.

138 lated conditions for assay of hexokinase and citrate synthase, and for immunohistochemical labeling o

139 cular chaperone activity by protecting DrdI, citrate synthase, and GAPDH from thermal inactivation.

140 , TRAP1 (TNF receptor-associated protein 1), citrate synthase, and GDH (glutamate dehydrogenase 1), a

141 nstrate our method on lactate dehydrogenase, citrate synthase, and lactoferrin.

142 model substrate proteins, such as rhodanese, citrate synthase, and luciferase.

143 ferent model substrates, firefly luciferase, citrate synthase, and malate dehydrogenase (MDH) provide

144 < 0.02), OXPHOS gene transcripts (P < 0.01), citrate synthase, and MAPR (P < 0.03) were higher in Ind

145 escue of mitochondrial malate dehydrogenase, citrate synthase, and Rubisco, are related to the large

146 ase-1, mitochondrial transcription factor 1, citrate synthase, and uncoupling protein-3, although KPF

147 ies formation and energy metabolism, such as citrate synthase ( approximately 19 and approximately 5%

148 roximately 25%) and the mitochondrial enzyme citrate synthase ( approximately 20%).

149 Mitochondrial malate dehydrogenase and citrate synthase are sequential enzymes in the Krebs tri

150 The energetics of citrate synthase are surprisingly tightly coupled.

151 dehydrogenase complex, NAD-malic enzyme, and citrate synthase, are similarly low in mitochondria from

152 erone activity of HuAtp12p was studied using citrate synthase as a model substrate.

153 ity with alcohol dehydrogenase, insulin, and citrate synthase as substrates compared to the other alp

154 ) to cytological position 5F3 and identified citrate synthase as the affected gene.

155 ngle-chain monellin (SCM) at 80 degreesC and citrate synthase at 40 degreesC.

156 the activity of L-lactate dehydrogenase and citrate synthase at least in part by disruption of prote

157 Inactivation of citrate synthase, but not down-stream enzymes suppressed

158 mplex between the antigen and heat-denatured citrate synthase can be detected and isolated using high

159 se reaction and anaplerotic pathways) and Re-citrate synthase (Ccar_06155) was a key enzyme in its tr

160 encoding the tricarboxylic acid cycle enzyme citrate synthase Cit1p, an "assembly mutation," i.e. a m

161 A deletion in the peroxisomal citrate synthase CIT2 in Deltayfh1 cells decreased the r

162 tabolite repression of the Bacillus subtilis citrate synthase (citZ) and aconitase (citB) genes, prev

163 or, represses the transcription of genes for citrate synthase (citZ) and aconitase (citB) in response

164 The citrate synthase (citZ) gene was found to be part of a c

165 yme activity in cell extracts, and the major citrate synthase (citZ) transcript was present at higher

166 cle, aconitase (citB) and to a lesser extent citrate synthase (citZ).

167 ow spinning speed 13C NMR spectra of the CMX-citrate synthase complex were obtained under a variety o

168 biochemical analysis revealed a reduction in citrate synthase-corrected complex I and complex II/III

169 Citrate synthase-corrected complex II-III activity was m

170 oxaloacetate in the malate dehydrogenase and citrate synthase-coupled systems was tested using polyet

171 reen in Drosophila cells using mitochondrial Citrate synthase (CS) activity as the primary readout.

172 levels of mitochondrial proteins as well as citrate synthase (CS) activity.

173 as much as 39% and 28% when measured by the citrate synthase (CS) aggregation assay.

174 Citrate synthase (CS) and beta-HAD mRNA were rapidly inc

175 conducted on an artificial fusion protein of citrate synthase (CS) and malate dehydrogenase (MDH) to

176 A citrate synthase (CS) deletion mutant of Agrobacterium t

177 wt alphaB crystallin in protecting unfolded citrate synthase (CS) from aggregation.

178 y, actively participates in the refolding of citrate synthase (CS) in vitro.

179 Citrate synthase (CS) performs two half-reactions: the m

180 st mitochondrial malate dehydrogenase (MDH), citrate synthase (CS), and aconitase (ACO).

181 raldehyde 3-phosphate dehydrogenase (GAPDH), citrate synthase (CS), and total p38 content.

182 ey mutations in the gltA gene, which encodes citrate synthase (CS), occurred both before and after Es

183 RNAi screening revealed that suppression of citrate synthase (CS), the first TCA cycle enzyme, preve

184 ein in mitochondrial extracts, identified as citrate synthase (CS).

185 Mitochondrial content (estimated by citrate synthase [CS] activity, cardiolipin content, and

186 Protein and citrate synthase data were grouped into tertiles and 5-y

187 ntrast, PGC-1a expression did not change and citrate synthase decreased by approximately 30% in SKM-D

188 eticulin) as well as a mitochondrial enzyme (citrate synthase) did not interact with COX genes.

189 nteresting situations in aspartyl proteases, citrate synthase, EF hands, haemoglobins, lipocalins, gl

190 However, concomitant loss of IDH and of citrate synthase eliminates these effects, suggesting th

191 mitochondrial protein synthesis, and COX and citrate synthase enzyme activities were increased by ins

192 le (vastus lateralis) mitochondrial content (citrate synthase enzyme activity).

193 vitro experiments performed with homogeneous citrate synthase enzyme indicated that this enzyme was c

194 in assessing rates of hepatic mitochondrial citrate synthase flux (V CS) and pyruvate carboxylase fl

195 ruvate dehydrogenase (VPDH) flux relative to citrate synthase flux (VCS) in healthy lean, elderly sub

196 rs yielded a noninvasive estimate of hepatic citrate synthase flux of 74 +/- 12 micromol/kg/min for 2

197 culate the anaplerotic flux (0.90 +/- 0.07 x citrate synthase flux) and [2-13C]acetyl-CoA fractional

198 Geobacter sulfurreducens did not require citrate synthase for growth with hydrogen as the electro

199 hilum (TpCS), are compared with those of the citrate synthase from a mesophile, pig heart (PCS).

200 The kinetics and mechanism of the citrate synthase from a moderate thermophile, Thermoplas

201 The gene encoding citrate synthase from a novel bacterial isolate (DS2-3R)

202 xtending the number of crystal structures of citrate synthase from different organisms to a total of

203 The crystal structure of citrate synthase from the thermophilic Archaeon Sulfolob

204 termediates in the reaction catalyzed by the citrate synthase from Thermoplasma acidophilum is accomp

205 A comparison of their atomic structures with citrate synthases from mesophilic and psychrophilic orga

206 Citrate synthases from Thermoplasma acidophilum (optimal

207 nction and oxygen consumption but increasing citrate synthase function.

208 partially bypassed by deletion of the major citrate synthase gene (citZ), by raising the pH of the m

209 al DNA intergenic spacer regions (ISR) and a citrate synthase gene (gltA) fragment and by amplified f

210 ition, there were striking increases in both citrate synthase gene expression and enzymatic activity

211 gene, 16S-23S intergenic spacer region, and citrate synthase gene identified the isolates as B. clar

212 fragment length polymorphism analysis of the citrate synthase gene, and 16S rRNA gene sequencing.

213 Expression of the citrate synthase gene, gltA, was repressed by a transcri

214 equence data obtained from a fragment of the citrate synthase gene, we compared ELB, Rickettsia austr

215 designated citZ, encoding a homolog of known citrate synthase genes from other bacteria.

216 hylogenetic analysis of the 16S rRNA and the citrate synthase genes showed that the novel Bartonella

217 comparison of DNA sequences of three genes (citrate synthase gltA, 60-kDa heat shock protein gene gr

218 isolate, including partial sequencing of the citrate synthase (gltA) and 16S rRNA genes indicated tha

219 A 337-bp fragment of the citrate synthase (gltA) gene amplified by polymerase cha

220 PCR and DNA sequence analyses of the citrate synthase (gltA) gene and the 16S-23S intergenic

221 d resistance to propionate was mapped to the citrate synthase (gltA) gene.

222 plasmid pJG400 was also able to complement a citrate synthase (gltA) mutation of E. coli W620.

223 isolate, including partial sequencing of the citrate synthase (gltA), groEL, and 16S rRNA genes, indi

224 thylcitrate (2-MC) by the Krebs cycle enzyme citrate synthase (GltA).

225 icity is likely due to the fact that as a si-citrate synthase, GltA may produce multiple isomers of 2

226 Its ability to protect citrate synthase, glyceraldehyde-3-phosphate dehydrogena

227 that strain 195 may contain an undocumented citrate synthase (>95% Re-type stereospecific), i.e., a

228 rboxymethyldethia coenzyme A (CMX), bound to citrate synthase have been investigated using solid stat

229 6 A crystal structure of one such complex, a citrate synthase homodimer.

230 nner, with nearly full protection of 1.5 muM citrate synthase in the presence of 650 nM myocilin.

231 acetyl-CoA and oxaloacetate, substrates for citrate synthase in the TCA cycle, to produce oxalic aci

232 ta(H) crystallin, alcohol dehydrogenase, and citrate synthase in vitro.

233 ctures generated on the basis of that of pig citrate synthase indicate very high structural and elect

234 evisiae encode mitochondrial and peroxisomal citrate synthases involved in the Krebs tricarboxylic ac

235 The activity of citrate synthase is determined in every experiment as a

236 f amino acid sequences indicates that DS2-3R citrate synthase is most closely related to the enzyme f

237 citrate synthase (AaCS), a hexameric type II citrate synthase, is required for acetic acid resistance

238 which encodes a glyoxylate cycle isoform of citrate synthase, is responsive to the functional state

239 ic acid cycle enzymes: malate dehydrogenase, citrate synthase, isocitrate dehydrogenase, and succinyl

240 erent unfolded protein substrates, including citrate synthase, lactate dehydrogenase, malate dehydrog

241 denylate kinase, aspartate aminotransferase, citrate synthase, liver alcohol dehydrogenase, and the c

242 egulation of TCA cycle components, including citrate synthase, malate dehydrogenase, and aconitase, r

243 In the second case, that of a citrate synthase-malate dehydrogenase fusion protein, a

244 Substrate channeling of oxaloacetate with citrate synthase-mitochondrial malate dehydrogenase prec

245 The symbiotic defect of a citrate synthase mutant could thus be due to disruption

246 ic network is disrupted; and (c) P. furiosus citrate synthase mutants in which the C-terminal arms th

247 urating concentrations of the analog for six citrate synthase mutants with single changes in active s

248 diminished again in malate dehydrogenase and citrate synthase mutants.

249 vs middle tertile; HR = 2.93; P = 0.008) and citrate synthase normalized to protein concentration (lo

250 The major citrate synthase of Bacillus subtilis (CS-II) was purifi

251 ges of GroEL alone and with bound rhodanese, citrate synthase, or dihydrofolate reductase were studie

252 With denatured citrate synthase, PDI does not facilitate aggregation, b

253 , in contrast to (Si)-citrate synthase, (Re)-citrate synthase produces a different isomer of 2-fluoro

254 ll mutant also exhibited increased levels of citrate synthase protein and enzyme activity in cell ext

255 sed mitochondrial transcription factor-A and citrate synthase protein levels; and augmented mtDNA cop

256 as homologous to both archaeal and bacterial citrate synthases; PrpD showed homology to yeast and Bac

257 Moreover, in contrast to (Si)-citrate synthase, (Re)-citrate synthase produces a diffe

258 /l), which combines with oxaloacetate in the citrate synthase reaction and lowers the concentration o

259 nsition/intermediate states in the multistep citrate synthase reaction.

260 Citrate synthase reactivation experiments in the presenc

261 Citrate synthase readily catalyzes solvent proton exchan

262 directed mutations in the gene that encodes citrate synthase reversed the bright luminescence of aco

263 This bacterium also possesses a second citrate synthase, SbnG, that is necessary for supplying

264 he conservation of that residue in all known citrate synthase sequences, and the importance of that r

265 e carbon units entering the TCA cycle at the citrate synthase step.

266 thod based on inner membrane permeability to citrate synthase substrates, TG induced MPT in a concent

267 in expression of Cit2, the cytosolic form of citrate synthase that functions in the glyoxylate pathwa

268 5% Re-type stereospecific), i.e., a novel Re-citrate synthase that is apparently different from the o

269 anced low-temperature activity for A. pernix citrate synthase that is synthesized during leucine to m

270 vered between aspartate aminotransferase and citrate synthase that only come to light in the context

271 ediately adjacent to CIT1, which encodes the citrate synthase that performs a key regulated step in t

272 For luciferase and citrate synthase, the efficiency of substrate protection

273 Citrate synthase, the first and rate-limiting enzyme of

274 Corroborated by data referring to citrate synthase, these results confirm the transitory (

275 but not ATP citrate synthase, work opposite citrate synthase to control the direction of carbon flow

276 However, the ratio of citrate synthase to cytochrome c oxidase was higher in t

277 significantly reduced thermal aggregation of citrate synthase to levels 36% to 44% of control levels.

278 analysis of site-directed mutants of the two citrate synthases to investigate the contribution of the

279 action performed by Thermoplasma acidophilum citrate synthase (TpCS) with the natural thioester subst

280 Citrate synthase Vmax and citrate levels were lowered 45

281 lowered level of G-6-P and 50% reductions in citrate synthase Vmax and the citrate content.

282 As predicted, citrate synthase Vmax was lowered and PFK Vmax was incre

283 drial markers transcription factor A (TFAM), citrate synthase, voltage-dependent anion channel (VDAC)

284 aperone substrates and decreased to 66% when citrate synthase was the chaperone substrate.

285 rt to the in vivo data, which suggested that citrate synthase was the source of a toxic metabolite.

286 and chaperone test substrates (rhodanese or citrate synthase) was inhibited by CK2 phosphorylation.

287 asmic reticulum calcium ATPase isoform 2 and citrate synthase, was evident in GW7647-treated hearts.

288 gene, encoding Sinorhizobium meliloti 104A14 citrate synthase, was isolated by complementing an Esche

289 showed that only L-lactate dehydrogenase and citrate synthase were inhibited but only by two specific

290 f both ICDH, found to be NAD+ dependent, and citrate synthase were measured in cell extracts of wild-

291 activities of respiratory chain enzymes and citrate synthase were measured in cortical mitochondria

292 were swapped; (b) mutants of the P. furiosus citrate synthase where the inter-subunit ionic network i

293 ignificant cell death, whereas mitochondrial citrate synthase, which is oxidative stress insensitive,

294 The production of acetyl-CoA was coupled to citrate synthase, which produced citrate and coenzyme A.

295 The catalytic strategies of enzymes (such as citrate synthase) whose reactions require the abstractio

296 rate synthase) and in isolated mitochondria (citrate synthase) with increasing age, indicating declin

297 ppears to be essentially the same as that of citrate synthase, with the electrophile activated for nu

298 AMP-forming acetate:CoA ligase, but not ATP citrate synthase, work opposite citrate synthase to cont

299 (Y(TR) 92 +/- 4% versus O(TR) 140 +/- 25%); citrate synthase (Y(TR) 37 +/- 8% versus O(TR) 97 +/- 33

300 SbnG is structurally distinct from TCA cycle citrate synthases yet similar to metal-dependent class I