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1 fixation and increased ATP yield (1 ATP per oxaloacetate).
2 ion of malate supplied from the cytoplasm to oxaloacetate.
3 e capacity to accommodate the TCA metabolite oxaloacetate.
4 but only AOX1A is additionally activated by oxaloacetate.
5 ysed reversible interconversion of malate to oxaloacetate.
6 l-CoA to pyruvate to yield propionyl-CoA and oxaloacetate.
7 -CoA to pyruvate, yielding propionyl-CoA and oxaloacetate.
8 ear high enough to abolish any channeling of oxaloacetate.
9 ehydrogenase specifically oxidizes malate to oxaloacetate.
10 izing 2-methylcitrate from propionyl-CoA and oxaloacetate.
11 ghly specific for the oxidation of malate to oxaloacetate.
12 itself or its temperature-labile substrate, oxaloacetate.
13 drogenase does not exhibit any channeling of oxaloacetate.
14 citrate, succinate, alpha-ketoglutarate, and oxaloacetate.
15 etyl-coenzyme A, in its ternary complex with oxaloacetate.
16 ent the negatively charged carboxyl group in oxaloacetate.
17 ibution from either plasma glucose or muscle oxaloacetate.
18 activity and was blocked by the CS substrate oxaloacetate.
19 m and an active site variant in complex with oxaloacetate.
20 action mechanism promotes decarboxylation of oxaloacetate.
21 miting step in the biosynthesis of AcCoA and oxaloacetate.
22 tamate abrogated inhibition of Complex II by oxaloacetate.
23 K) kinetic isotope effect observed on C-4 of oxaloacetate [(13)(V/K) = 1.0117 +/- 0.0005] indicates t
24 ic enzyme (275%); elevated concentrations of oxaloacetate (150%), malate (250%), citrate (140%), and
26 ne with (k(cat)/K(m)(pyruvate))/(k(cat)/K(m)(oxaloacetate)) = 6.1 x 10(-9) to one with that ratio = 2
27 cosubstrates, 2-oxoglutarate, pyruvate, and oxaloacetate, Ab-ArAT4 possesses strong substrate prefer
28 mino acid sequence identity to the confirmed oxaloacetate acetyl hydrolase (OAH), an enzyme that belo
29 ough several different biochemical pathways, oxaloacetate acetylhydrolase (OAH)-catalyzed hydrolytic
31 exhibited a 52 +/- 7% reduction in cytosolic oxaloacetate, an 83 +/- 4% reduction in malonyl-CoA leve
32 MgATP-dependent carboxylation of pyruvate to oxaloacetate, an important anaplerotic reaction in mamma
33 tate with pyruvate, alpha-ketoglutarate, and oxaloacetate and (ii) mercaptopicolinate and pyruvate.
35 bisubstrate adduct indicate that each of the oxaloacetate and acetyl-CoA substrates is bound to an in
36 routes glutamine metabolism to generate both oxaloacetate and acetyl-CoA, enabling persistent tricarb
37 and MgATP-dependent cleavage of citrate into oxaloacetate and acetyl-CoA, representing a key step in
41 ates determined at varying concentrations of oxaloacetate and fixed concentrations of oxamate reveale
44 es the cell with only one pathway, involving oxaloacetate and l-glutamate, for de novo synthesis of h
45 ve determined the ternary complex bound with oxaloacetate and magnesium, revealing some of the conser
46 ed production of the TCA cycle intermediates oxaloacetate and NADPH, and impaired oxygen consumption.
47 complex ferricyanide, and 3) the keto-acids oxaloacetate and pyruvate (and phosphoenolpyruvate, a me
48 malate or that cannot convert malate to both oxaloacetate and pyruvate are also avirulent and protect
49 s and identified a high futile cycle between oxaloacetate and pyruvate, indicating a highly active in
51 nitor the PC-catalyzed formation of [4-(13)C]oxaloacetate and subsequent transfer of (13)CO(2) from o
52 oor or moderate KDM5B inhibitors, except for oxaloacetate and succinate, which were shown to compete
53 0 forms a hydrogen bond with the carbonyl of oxaloacetate and the alcohols of the citryl-coenzyme A a
54 led pyruvate leads to formation of [1,2-13C2]oxaloacetate and to multiply labeled glutamate and succi
55 Structural analyses of the complexes with oxaloacetate and with a bisubstrate adduct indicate that
56 d vesicles catalyzed the exchange of malate, oxaloacetate, and aspartate for phosphate plus a proton
57 y the TCA intermediates alpha-ketoglutarate, oxaloacetate, and pyruvate, confirming that in infected
59 olase (OAH)-catalyzed hydrolytic cleavage of oxaloacetate appears to be an especially important route
60 In the aerobic regime, 75% of mitochondrial oxaloacetate arises from anaplerotic carboxylation of py
62 is essential for the conversion of malate to oxaloacetate as part of the proper functioning of the Kr
65 iet, HFD-fed mice displayed higher levels of oxaloacetate, aspartate, and malate, along with increase
66 ubsite, and uncouples the decarboxylation of oxaloacetate at subsite 2 from the formation of ATP at s
67 dehydrogenase (MDH) to assess the chances of oxaloacetate being channeled between the MDH and CS acti
68 d with the specific example of channeling of oxaloacetate between Escherichia coli aspartate aminotra
71 through carbonyl bond polarization, not just oxaloacetate binding in the active site, is required for
74 the enzyme fumarase and further oxidized to oxaloacetate by malate dehydrogenase with the accompanyi
79 olpyruvate carboxylase [PEPC; orthophosphate:oxaloacetate carboxy-lyase (phosphorylating), EC 4.1.1.3
80 olpyruvate carboxylase [PEPC; orthophosphate:oxaloacetate carboxy-lyase (phosphorylating), EC 4.1.1.3
82 athway for the interconversion of malate and oxaloacetate catalyzed by the enzyme malate dehydrogenas
83 ated by a carbamylated lysine, except in the oxaloacetate complex in which the product's carboxylate
85 on the enzymatic conversion of glyoxylate to oxaloacetate coupled to the reduction of oxidized nicoti
87 ervation with carboxyltransferase domains in oxaloacetate decarboxylase and transcarboxylase, the str
88 ceptor domain from the Klebsiella pneumoniae oxaloacetate decarboxylase are extracted with 5 M urea o
90 ge amounts of aspartate aminotransferase and oxaloacetate decarboxylase, as competing enzymes for the
93 bject to enzymatic decarboxylation; however, oxaloacetate decarboxylases (ODx) were so far not identi
95 n of the two enzymes required are described; oxaloacetate decarboxylating malic dehydrogenase is also
96 atase to convert fumarate to malate and uses oxaloacetate decarboxylating malic dehydrogenase to conv
98 indicative of a glyoxylate-induced state of oxaloacetate deficiency, acetate overload, and ketoacido
99 ansfer preceding hydride transfer (malate to oxaloacetate direction), (2) the existence of two transi
100 xpressed to access the one-step synthesis of oxaloacetate directly from phosphoenolpyruvate without p
101 (alpha)-H cleavage, ketimine hydrolysis, and oxaloacetate dissociation to the rate limitation with th
102 cetyl cysteine or the TCA cycle intermediate oxaloacetate efficiently rescues Gln starvation-induced
103 tterns of Asp and Thr suggested formation of oxaloacetate exclusively via the phosphoenolpyruvate car
104 as a complete, albeit bifurcated, TCA cycle; oxaloacetate flows to succinate both through citrate/alp
105 erate reductive power (NADPH) and to restore oxaloacetate for continued TCA cycle function (anapleros
106 ter, respectively, whereas those for GTP and oxaloacetate (for the phosphoenolpyruvate formation acti
107 bound PEP, brought subtle effects, lowering oxaloacetate formation rate but enhancing PEP formation
109 phorylation), substrate channeling (e.g., of oxaloacetate from malate dehydrogenase to citrate syntha
111 ial pyruvate metabolism; (e) the transfer of oxaloacetate from the cytosol to the mitochondria is lar
114 ed, and that for the physiological substrate oxaloacetate has been diminished, through the replacemen
115 ces the rate of enzymatic decarboxylation of oxaloacetate in the carboxyl transferase domain of pyruv
116 etyl-CoA (3 micromol/l), which combines with oxaloacetate in the citrate synthase reaction and lowers
119 ow that the glucose metabolites pyruvate and oxaloacetate inactivate HIF-1alpha decay in a manner sel
122 AP as well as glyceraldehyde 3-phosphate and oxaloacetate inhibited activity of both yeast and human
127 Synthesis of phosphoenolpyruvate (PEP) from oxaloacetate is an absolute requirement for gluconeogene
128 d (ii) intrinsic inhibition of Complex II by oxaloacetate is an inherent mechanism that protects agai
129 e presence of oxamate, the apparent K(m) for oxaloacetate is artificially suppressed (from 15 to 4-5
131 ation rate, which suggests that an excess of oxaloacetate is converted to aspartate and reintroduced
133 H) catalyzed oxidation/reduction of L-malate/oxaloacetate is pH-dependent due to the proton generated
135 lycolysis; (c) the majority of the cytosolic oxaloacetate is synthesized via anaplerotic carboxylatio
136 random, suggesting that the enol tautomer of oxaloacetate is the product; this expectation was confir
137 to the discovery that PA4872 decarboxylates oxaloacetate (kcat = 7500 s(-1) and Km = 2.2 mM) and 3-m
139 dentified (2R)-ethyl, (3S)-methylmalate, and oxaloacetate [likely to bind as the hydrate, C(2)(OH)(2)
140 tabolic end products of lignin (pyruvate and oxaloacetate) must enter the tricarboxylic acid (TCA) cy
142 he crystal structure of AaCS, complexed with oxaloacetate (OAA) and the inhibitor carboxymethyldethia
143 recognition of phosphoenolpyruvate (PEP) and oxaloacetate (OAA) by cytosolic phosphoenolpyruvate carb
145 y intriguing condensation of acetyl-CoA with oxaloacetate (OAA) to form citryl-CoA and the subsequent
146 uconeogenesis by conversion of mitochondrial oxaloacetate (OAA) to phosphoenolpyruvate, regulates glu
151 gative charge of the substrate side-chain of oxaloacetate or alpha-ketomalonate, charge repulsion wou
153 talysis, such as the conversion of malate to oxaloacetate or the activation of the toxin 3-nitropropi
156 zes of amino acids derived from pyruvate and oxaloacetate, polyamine precursors, and compatible solut
157 pathways, including pyruvate, glutamate and oxaloacetate pools, and urea production from arginine, w
159 analyses with succinate, fumarate, L-malate, oxaloacetate, pyruvate and D- and L-2HG support the kine
160 ate, succinate, 2-hydroxyglutarate, citrate, oxaloacetate, pyruvate, isocitrate, and lactate using a
162 catalyzes the readily reversible reaction of oxaloacetate reversible malate using either NADH or NADP
164 that in glucose grown cells, both the malate/oxaloacetate shuttle and a glycerol-3-phosphate dehydrog
168 es identified in PCS, destabilization of the oxaloacetate substrate carbonyl and stabilization of the
169 ained decarboxylase activity for the smaller oxaloacetate substrate, which is not inhibited by excess
170 Burkholderia species utilize acetyl-CoA and oxaloacetate, substrates for citrate synthase in the TCA
171 decrease in malic acid, and lower amounts of oxaloacetate, suggesting that malate metabolism plays an
172 In Methanothermobacter thermautotrophicus, oxaloacetate synthesis is a major and essential CO(2)-fi
173 is presented that, in Methanosarcina barkeri oxaloacetate synthesis, an essential and major CO(2) fix
176 results and the existence of an alternative oxaloacetate synthesizing enzyme phosphoenolpyruvate car
177 This methanogenic archaeon possesses two oxaloacetate-synthesizing enzymes, pyruvate carboxylase
179 tenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, d
181 gATP, the oxamate-induced decarboxylation of oxaloacetate, the phosphorylation of MgADP by carbamoyl
182 determined for the forward reaction to form oxaloacetate, the reverse reaction to form MgATP, the ox
183 sion reduced TCA cycle activity and diverted oxaloacetate, the substrate of CS, into production of th
184 gest that activation of the first substrate, oxaloacetate, through carbonyl bond polarization, not ju
186 th the portion of the citric acid cycle from oxaloacetate to alpha-ketoglutarate via cis-aconitate.
188 e base, its failure to further condense with oxaloacetate to form a sulfur-less analog of citryl-coen
190 (PEPCK), forward TCA cycle flux of [4-(13)C]oxaloacetate to generate (13)CO(2) at isocitrate dehydro
191 rease the rate of the coupled L-aspartate to oxaloacetate to malate sequence only if the direct metab
192 f the enzymatic conversion of hyperpolarized oxaloacetate to malate, the two signal components are se
193 atalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase
197 can be productively metabolized by glutamate oxaloacetate transaminase (GOT) to maintain cellular ene
198 s work demonstrated the ability of glutamate oxaloacetate transaminase (GOT) to metabolize neurotoxic
199 uced significant increase in serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruva
201 C-transformed cells depend on both glutamate-oxaloacetate transaminase and glutamate dehydrogenase to
204 to the mitochondria and cytoplasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogena
205 ansported via malate, which when oxidized to oxaloacetate, transfers an electron pair to reduce NAD t
206 t understanding would not have predicted the oxaloacetate transforming activity of Ser101Leu102 or th
207 ing cataplerotic decarboxylation of [4-(13)C]oxaloacetate via phosphoenolpyruvate carboxykinase (PEPC
208 se (DET0724-0727) and pyruvate conversion to oxaloacetate via pyruvate carboxylase (DET0119-0120).
211 bstrate analog: the gem-diol of 3,3-difluoro-oxaloacetate) was determined for the purpose of identify
213 protein could account for the channeling of oxaloacetate we observed with the yeast fusion protein.
214 late through protocatechuate to pyruvate and oxaloacetate were demonstrated in cells or cell extracts
215 oglutarate, succinate, fumarate, malate, and oxaloacetate) were tested for their influence on AOX1A,
216 boxylase were less effective competitors for oxaloacetate when precipitated citrate synthase and mito
218 liberated enzymatically by transamination to oxaloacetate with aspartate aminotransferase and then de
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