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1 b's cycle intermediates (succinate and alpha-ketoglutarate).
2 B-04 is not a competitive inhibitor of alpha-ketoglutarate.
3  the concentration of its co-substrate alpha-ketoglutarate.
4 roducing 2-hydroxyglutarate (2HG) from alpha-ketoglutarate.
5  of O(2)-regulated metabolites such as alpha-ketoglutarate.
6 nverted to 3-deoxy-2-keto-hexarate and alpha-ketoglutarate.
7 hlorite oxidation afforded the 1-monooctyl 2-ketoglutarate.
8  4PE and a noncompetitive inhibitor vs alpha-ketoglutarate.
9 er than that towards the natural substrate 2-ketoglutarate.
10 ase in GDH affinity for its substrate, alpha-ketoglutarate.
11 n of saccharopine to give l-lysine and alpha-ketoglutarate.
12 equentially converted to glutamate and alpha-ketoglutarate.
13 rg428 contributes mainly to binding of alpha-ketoglutarate.
14 ng stimulation by glucose, leucine, or alpha-ketoglutarate.
15 II, and this effect was antagonized by alpha-ketoglutarate.
16 o catalyse conversion of isocitrate to alpha-ketoglutarate.
17 itric acid cycle intermediates, mostly alpha-ketoglutarate.
18 pyridine dicarboxylate, an analogue of alpha-ketoglutarate.
19 ementation with TCA cycle intermediate alpha-ketoglutarate.
20 tion of 2-hydroxyglutarate and reduced alpha-ketoglutarate.
21 genases, efficiently oxidized D-2HG to alpha-ketoglutarate.
22 ive carboxylation of glutamine-derived alpha-ketoglutarate.
23 mate to pyruvate, yielding alanine and alpha-ketoglutarate.
24 cy compared with that of KDM5B at 1 mm alpha-ketoglutarate.
25 ioxygenases using the essential metabolite 2-ketoglutarate (2KG) as a cofactor.
26 ion due to the increased production of alpha-ketoglutarate, a critical substrate for prolyl hydroxyla
27 ate export and that supplementation of alpha-ketoglutarate, a key downstream metabolite of glutamate,
28 transcription and, thus, production of alpha-ketoglutarate, a key metabolite in the regulation of ESC
29 f Nrd1 or Ogdh leads to an increase in alpha-ketoglutarate, a substrate for OGDH, which in turn leads
30                                        alpha-Ketoglutarate (AKG) is a key intermediate of tricarboxyl
31 resent, the antagonism between ADP and alpha-ketoglutarate allowed each of these effectors to influen
32 However, HPV was not increased by 1 mm alpha-ketoglutarate alone, and HPV in the absence of alpha-ket
33  and IDH2, decarboxylate isocitrate to alpha-ketoglutarate (alpha-KG) and reduce NADP to NADPH.
34 mechanism is steady state ordered with alpha-ketoglutarate (alpha-Kg) binding prior to acetyl-CoA (Ac
35 G) is an oncometabolite generated from alpha-ketoglutarate (alpha-KG) by mutant isocitrate dehydrogen
36 nthase (HOAS), the E1 component of the alpha-ketoglutarate (alpha-KG) dehydrogenase complex (KDHC), d
37   Mononuclear nonheme Fe(II) (MNH) and alpha-ketoglutarate (alpha-KG) dependent halogenases activate
38 genes necessary for the utilization of alpha-ketoglutarate (alpha-KG) in Pseudomonas aeruginosa PAO1.
39  was also activated by induction of an alpha-ketoglutarate (alpha-KG) paracrine signaling system.
40 oup from branched-chain amino acids to alpha-ketoglutarate (alpha-KG) thereby regenerating glutamate,
41 osphate (NADPH)-dependent reduction of alpha-ketoglutarate (alpha-KG) to 2-HG.
42 condensation of acetyl-CoA (AcCoA) and alpha-ketoglutarate (alpha-KG) to give homocitrate and CoA.
43 hed-chain amino acids while converting alpha-ketoglutarate (alpha-KG) to glutamate.
44       Glutaminolysis converts Gln into alpha-ketoglutarate (alpha-KG), a critical intermediate in the
45                      Here we show that alpha-ketoglutarate (alpha-KG), a tricarboxylic acid cycle int
46                            Fe(II)- and alpha-ketoglutarate (alpha-KG)-dependent dioxygenases are a la
47 tion is catalyzed by the non-heme iron alpha-ketoglutarate (alpha-KG)-dependent SnoK in the biosynthe
48  of D-2-hydroxyglutarate (D-2-HG) from alpha-ketoglutarate (alpha-KG).
49 roduces 2-hydroxyglutarate (2-HG) from alpha-ketoglutarate (alpha-KG).
50 levels of the Krebs cycle intermediate alpha-ketoglutarate (alpha-KG).
51 drogenases (IDH) convert isocitrate to alpha-ketoglutarate (alpha-KG).
52 decarboxylation of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) and the NADPH/CO(2)-dependent re
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 atic activity allowing them to convert alpha-ketoglutarate (alphaKG) to 2-hydroxyglutarate (2HG), whi
57 atic halogenases activate O(2), cleave alpha-ketoglutarate (alphaKG) to CO(2) and succinate, and form
58 y of enzymes that use Fe(2+), O(2) and alpha-ketoglutarate (alphaKG) to perform a variety of halogena
59 ivity that catalyzes the conversion of alpha-ketoglutarate (alphaKG) to the oncometabolite D-(2)-hydr
60 ad can reverse the direction of apical alpha-ketoglutarate (alphaKG) transport in the proximal tubule
61            Glutamine is catabolyzed to alpha-ketoglutarate (alphaKG), a tricarboxylic acid (TCA) cycl
62 alphaKG oxygenases and require Fe(II), alpha-ketoglutarate (alphaKG), and O(2) for activity.
63 ongs to a recently discovered class of alpha-ketoglutarate (alphaKG), non-heme Fe(II)-dependent halog
64 bic conditions containing iron(II) and alpha-ketoglutarate (alphaKG), to dioxygen initiates oxidation
65 talyze the conversion of isocitrate to alpha-ketoglutarate (alphaKG), whereas conferring a gain of a
66 he citric acid(TCA) cycle intermediate alpha-ketoglutarate (alphaKG), which via its OXGR1 receptor pl
67 use models to ask if inhibition of the alpha-ketoglutarate (alphaKG)-dependent dioxygenase Egln1, whi
68              FIH is a non-heme Fe(II), alpha-ketoglutarate (alphaKG)-dependent dioxygenase that inhib
69 His-1-carboxylate) facial triad in the alpha-ketoglutarate (alphaKG)-dependent dioxygenases clavamina
70 s (P4Hs) are mononuclear non-heme iron alpha-ketoglutarate (alphaKG)-dependent dioxygenases that cata
71 r (HIF) prolyl hydroxylases (PHDs) are alpha-ketoglutarate (alphaKG)-dependent dioxygenases that func
72 g hypoxia-inducible factor (FIH) is an alpha-ketoglutarate (alphaKG)-dependent enzyme which catalyzes
73 discovered class of nonheme Fe(II) and alpha-ketoglutarate (alphaKG)-dependent halogenases, catalyzes
74 nase (tauD) is one of the best-studied alpha-ketoglutarate (alphaKG)-dependent nonheme iron oxygenase
75  (Th1) were regulated by glutamine and alpha-ketoglutarate (alphaKG)-induced events, in part through
76 hrough reductive carboxylation (RC) of alpha-ketoglutarate (alphaKG).
77 DH1) reversibly converts isocitrate to alpha-ketoglutarate (alphaKG).
78 ive decarboxylation of isocitrate into alpha-ketoglutarate (alphaKG).
79 maintain a high level of intracellular alpha-ketoglutarate (alphaKG).
80 boxylic acid cycle (TCA) intermediate, alpha-ketoglutarate, also blocks the transcriptional activity
81 ate pathway, which generates cytosolic alpha-ketoglutarate, also known as 2-oxoglutarate (2OG).
82                             The use of alpha-ketoglutarate (alternatively termed 2-oxoglutarate) as a
83 is is a cell-permeable prodrug form of alpha-ketoglutarate, an important intermediate in the tricarbo
84  (CD) studies using a non-decarboxylatable 2-ketoglutarate analog and determined the distribution of
85 tes to mtDNA loss by acting as a toxic alpha-ketoglutarate analog.
86            By increasing intracellular alpha-ketoglutarate and activating PHDs we trigger PHD-depende
87 ; these proteins are direct sensors of alpha-ketoglutarate and adenylylate energy charge and control
88                           Signaling of alpha-ketoglutarate and adenylylate energy charge by these het
89            PII proteins are sensors of alpha-ketoglutarate and adenylylate energy charge that regulat
90 he role of the three binding sites for alpha-ketoglutarate and adenylylate nucleotide in the PII trim
91 ate conditions, the antagonism between alpha-ketoglutarate and ADP allowed each of these effectors to
92 re also used to examine the effects of alpha-ketoglutarate and ADP on PII activation of the adenylylt
93 arate alone, and HPV in the absence of alpha-ketoglutarate and cysteine was not attenuated by asparta
94 ents would ensure the replenishment of alpha-ketoglutarate and glutamate, which provide the carbon ba
95 yme, produces 2-hydroxy-3-oxoadipate using 2-ketoglutarate and glyoxylate.
96                               P4H uses alpha-ketoglutarate and O2 as cosubstrates, and forms succinat
97 e in cell proliferation was rescued by alpha-ketoglutarate and overexpression of IDH2, whereas prolif
98 a-keto analog of asparagine), yielding alpha-ketoglutarate and oxaloacetate, respectively.
99 rnary complex of HygX with cosubstrate alpha-ketoglutarate and putative product hygromycin B identifi
100 he intracellular levels of its product alpha-ketoglutarate and subsequent metabolite fumarate.
101 re flushed in situ with histidine-tryptophan-ketoglutarate and subsequently preserved either by simpl
102 itric acid cycle intermediates such as alpha-ketoglutarate and succinate, NaDC3 transports other comp
103                                   Both alpha-ketoglutarate and the UDP-linked sugar bind in the WlbA
104 H1 R132H competitively with respect to alpha-ketoglutarate and uncompetitively with respect to NADPH.
105 lows to succinate both through citrate/alpha-ketoglutarate and via malate/fumarate.
106 substrate required addition of Fe(2+), alpha-ketoglutarate, and ascorbic acid, confirming that KdoO i
107 mitochondrial enzymes, mainly lactate, alpha-ketoglutarate, and branched chain keto-acids.
108  (E3) is associated with the pyruvate, alpha-ketoglutarate, and glycine dehydrogenase complexes.
109   EI(Ntr) activity was not affected by alpha-ketoglutarate, and no binding between the EIGAF and alph
110 he enzyme in a complex with NAD(H) and alpha-ketoglutarate, and the enzyme in a complex with NAD(H) a
111 x enzymes are involved, including four alpha-ketoglutarate- and iron(II)-dependent dioxygenases that
112 ls, but causes a drop in the levels of alpha-ketoglutarate, another output of the pathway and a trica
113 BMDACs) with dimethyloxalylglycine, an alpha-ketoglutarate antagonist that induces hypoxia-inducible
114 its physiological concentration range, alpha-ketoglutarate apparently played a role in only the latte
115 els of TCA-cycle metabolites including alpha-ketoglutarate are high, and levels of the key regulatory
116      This enzyme has been shown to use alpha-ketoglutarate as an oxidant to regenerate the oxidized d
117 e phenazine reduction with pyruvate or alpha-ketoglutarate as electron donors.
118 rolyl 4-hydroxylases that use O(2) and alpha-ketoglutarate as substrates to hydroxylate conserved pro
119 ific activity of DapL using ll-DAP and alpha-ketoglutarate as substrates was 24.3 + or - 2.0 nmol min
120 vitro in the presence of Fe (2+), O 2, alpha-ketoglutarate, ascorbate, and Triton X-100.
121 used for GC-MS/MS analysis of alanine, alpha-ketoglutarate, asparagine, aspartic acid, cystathionine,
122  JmjC domain with conserved Fe(II) and alpha-ketoglutarate binding sites, and displays H3K9me1/2 deme
123 onstitutes the cofactor (metal ion and alpha-ketoglutarate) binding characteristics of other structur
124 n addition, reductive carboxylation of alpha-ketoglutarate by isocitrate dehydrogenase 1 (IDH1) and 2
125   Homocitrate synthase (acetyl-coenzyme A: 2-ketoglutarate C-transferase; E.C. 2.3.3.14) (HCS) cataly
126 pe IDH1, only hyperpolarized [1-(13)C] alpha-ketoglutarate can be detected.
127 report we demonstrate that derivatized alpha-ketoglutarate can be used as a strategy for maintaining
128          We also show that derivatized alpha-ketoglutarate can permeate multiple layers of cells, red
129 proof-of-concept study, that [1-(13)C] alpha-ketoglutarate can serve as a metabolic imaging agent for
130 ive carboxylation of glutamine-derived alpha-ketoglutarate (catalyzed by reverse flux through isocitr
131  several cellular conditions where the alpha-ketoglutarate/citrate ratio is changed due to an altered
132 ions that result in an increase in the alpha-ketoglutarate/citrate ratio.
133 ne (DMOG, 200 mug/g), an antagonist of alpha-ketoglutarate cofactor and inhibitor for HIF PHD, on pos
134 /glutamine (10/2 mM) did not influence alpha-ketoglutarate concentrations but caused 120 and 33% incr
135 P was the sole adenylylate nucleotide, alpha-ketoglutarate controlled the extent of PII activation bu
136 , and no binding between the EIGAF and alpha-ketoglutarate could be detected.
137 the gamma-aminobutyric acid pathway or alpha-ketoglutarate decarboxylase/succinic semialdehyde dehydr
138                  Here we show that the alpha-ketoglutarate dehydrogenase (alpha-KGDH) complex is loca
139 rganization of the multienzyme complex alpha-ketoglutarate dehydrogenase (alpha-KGDH).
140 ound an increase in phosphorylation of alpha-ketoglutarate dehydrogenase (alphaKGDH) in female hearts
141 in amino acid dehydrogenase (BCDH) and alpha-ketoglutarate dehydrogenase (KDH).
142  such as pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase (KGDH), and the glycine clea
143 aperones and assists in the folding of alpha-ketoglutarate dehydrogenase (OGDH), a rate-limiting enzy
144 cofactor of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase and other mitochondrial targ
145 ons of regulation of the activities of alpha-ketoglutarate dehydrogenase and the aspartate-glutamate
146  proteins, including the E2 subunit of alpha-ketoglutarate dehydrogenase and the glutathione S-transf
147                    The activity of the alpha-ketoglutarate dehydrogenase complex (KGDHC), an arguably
148 hyl transferase, and components of the alpha-ketoglutarate dehydrogenase complex in conjunction with
149 target DLST-the E2 subcomponent of the alpha-ketoglutarate dehydrogenase complex, a rate-controlling
150 A to the reduction of NAD(+) using the alpha-ketoglutarate dehydrogenase complex.
151 , we demonstrate that the pyruvate and alpha-ketoglutarate dehydrogenase complexes directly catalyze
152 nslational lipoylation of pyruvate and alpha-ketoglutarate dehydrogenase complexes, resulting in dimi
153 nent of the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes.
154 xes, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and branched-chain ketoacid
155 subunits of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, and Gcv3, the H protein of
156 le enzymes, pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase.
157 ation was changed in 1797 genes [e.g., alpha-ketoglutarate dependent dioxygenase (FTO), interleukin 6
158  treatment promoted GBM survival in an alpha-ketoglutarate-dependent (alphaKG-dependent) manner.
159 172K mutant IDH2 resulted in increased alpha-ketoglutarate-dependent consumption of NADPH compared to
160  The KDM5/JARID1 family of Fe(II)- and alpha-ketoglutarate-dependent demethylases remove methyl group
161 s lipid-A by hydroxylation by the Fe2+/alpha-ketoglutarate-dependent dioxygenase enzyme (LpxO).
162 emethylation are members of the Fe(II)/alpha-ketoglutarate-dependent dioxygenase family.
163                 Inactivation of Fe(II)/alpha-ketoglutarate-dependent dioxygenase gene fr9P led to los
164  didomain protein, DdaD, and an Fe(II)/alpha-ketoglutarate-dependent dioxygenase homologue, DdaC.
165 for the archetypal non-heme Fe(II) and alpha-ketoglutarate-dependent dioxygenase TauD.
166 , which encodes a putative Fe (2+)/O 2/alpha-ketoglutarate-dependent dioxygenase, abolishes S-2-hydro
167  ions or substrate taurine to TauD, an alpha-ketoglutarate-dependent dioxygenase, alters its UV absor
168 demethylation of thebaine by an Fe(II)/alpha-ketoglutarate-dependent dioxygenase.
169         The AlkB family of Fe(II)- and alpha-ketoglutarate-dependent dioxygenases is a class of ubiqu
170     Fumarate has been shown to inhibit alpha-ketoglutarate-dependent dioxygenases that are involved i
171                           The PHDs are alpha-ketoglutarate-dependent dioxygenases that have low K(m)
172 ranslocation) proteins are Fe(ii)- and alpha-ketoglutarate-dependent dioxygenases that modify the met
173 igenetic effects through inhibition of alpha-ketoglutarate-dependent dioxygenases that require iron a
174 lutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases' by Xu and colleagu
175 endent methyltransferases, Fe(II)- and alpha-ketoglutarate-dependent dioxygenases, base excision glyc
176 proteins, a family of AlkB-like Fe(II)/alpha-ketoglutarate-dependent dioxygenases, can oxidize 5mC to
177 ly distinct bifunctional non-heme iron alpha-ketoglutarate-dependent enzyme responsible for the termi
178  by Cur halogenase, a non-haem Fe(ii), alpha-ketoglutarate-dependent enzyme.
179             DdaC catalyzes Fe(II)- and alpha-ketoglutarate-dependent epoxidation of the covalently bo
180               We show that Fe(II)- and alpha-ketoglutarate-dependent fat mass and obesity-associated
181                                    The alpha-ketoglutarate-dependent hydroxylases and halogenases emp
182 d in vivo by hyperammonemia through an alpha-ketoglutarate-dependent inhibition of the mammalian targ
183 gillus fumigatus is the first reported alpha-ketoglutarate-dependent mononuclear non-haem iron enzyme
184           Notably, we characterized an alpha-ketoglutarate-dependent non-heme Fe(II) dioxygenase that
185 5caC in three consecutive, Fe(II)- and alpha-ketoglutarate-dependent oxidation reactions.
186 caC) in three consecutive, Fe(II)- and alpha-ketoglutarate-dependent oxidation reactions.
187 om nucleic acids by a unique iron- and alpha-ketoglutarate-dependent oxidation strategy.
188 ied a conserved group of nonheme iron, alpha-ketoglutarate-dependent oxygenases likely responsible fo
189  of histone demethylases are Fe2+- and alpha-ketoglutarate-dependent oxygenases that are essential co
190 hich can be overcome by treatment with alpha-ketoglutarate derivatives.
191                Residue F159 in taurine alpha-ketoglutarate dioxygenase (TauD) is demonstrated to play
192                                Taurine alpha-ketoglutarate dioxygenase (tauD) is one of the best-stud
193 uctive metabolism of glutamine-derived alpha-ketoglutarate even in normoxic conditions.
194            The Jumonji C domain Fe(II) alpha-ketoglutarate family of proteins performs the majority o
195             PHF2 belongs to a class of alpha-ketoglutarate-Fe(2)(+)-dependent dioxygenases.
196  The sequential activities of PhnY, an alpha-ketoglutarate/Fe(II)-dependent dioxygenase, and PhnZ, a
197 y 'ancient' CoA-dependent pyruvate and alpha-ketoglutarate ferredoxin oxidoreductases.
198 ive carboxylation of glutamine-derived alpha-ketoglutarate for de novo lipogenesis.
199 e and an assay procedure that measures alpha-ketoglutarate formation from alpha-ketoglutaramate in a
200  that steric constraints could prevent alpha-ketoglutarate from undergoing an "off-line"-to-"in-line"
201                   AMPKalpha2 regulates alpha-ketoglutarate generation, hypoxia-inducible factor-1alph
202                        Uniquely, after alpha-ketoglutarate has bound to the mononuclear iron centre i
203     Reducing O-GlcNAcylation increases alpha-ketoglutarate, HIF-1 hydroxylation, and interaction with
204 ylation covalent intermediate derived from 2-ketoglutarate; however, it decreases the abundance of th
205 olled trials (RCTs) and histidine-tryptophan-ketoglutarate (HTK) in two RCTs.
206 osomolar citrate (HOC), histidine-tryptophan-ketoglutarate (HTK), or University of Wisconsin (UW) sol
207 n solutions such as new histidine-tryptophan-ketoglutarate (HTK-N) and TiProtec on the individual tis
208  oxidative deamination of glutamate to alpha-ketoglutarate in a limited number of tissues in humans,
209 ent carboxylation of glutamine-derived alpha-ketoglutarate in hypoxia is associated with a concomitan
210 atalyze the oxidation of isocitrate to alpha-ketoglutarate in the citric acid cycle.
211 nvert glutamine-derived glutamate into alpha-ketoglutarate in the mitochondria to fuel the tricarboxy
212 increase in reductive carboxylation of alpha-ketoglutarate (increased concentrations of 2-hydroxyglut
213  the tricarboxyclic acid cycle product alpha-ketoglutarate, indicating the critical function of GLS1
214 e deficiency, through the reduction of alpha-ketoglutarate, inhibits the AlkB homolog (ALKBH) enzymes
215 ethanolamine, 2,4-diaminobutyrate, and alpha-ketoglutarate into achromobactin.
216 r minireviews deal with aspects of the alpha-ketoglutarate/iron-dependent dioxygenases in this eighth
217                      Glutamine-derived alpha-ketoglutarate is reductively carboxylated by the NADPH-l
218 bolic fate of hyperpolarized [1-(13)C] alpha-ketoglutarate is studied in isogenic glioblastoma cells
219 s with the alpha-carboxylate moiety of alpha-ketoglutarate, is also uniquely positioned to bestow spe
220 (suc(2-)) through glutarate (glu(2-)), alpha-ketoglutarate (kglu(2-)), adipate (adi(2-)), pimelate (p
221 tion factor RTG1 Furthermore, elevated alpha-ketoglutarate levels also suppress 2HG-mediated respirat
222  of the IDH3 heterotetramer, decreased alpha-ketoglutarate levels and increased the stability and tra
223                  Genetic modulation of alpha-ketoglutarate levels demonstrates a key regulatory role
224 DHs, which correlated with the reduced alpha-ketoglutarate levels.
225 iates with good sensitivity, including alpha-ketoglutarate, malate, fumarate, succinate, 2-hydroxyglu
226 novel pathogenicity island involved in alpha-ketoglutarate metabolism under anaerobic conditions.
227  increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH l
228 , carried by Dld3, to convert D-2HG to alpha-ketoglutarate, namely an FAD-dependent transhydrogenase
229 acid, confirming that KdoO is a Fe(2+)/alpha-ketoglutarate/O(2)-dependent dioxygenase.
230 hough two enzymes that catalyze Fe(2+)/alpha-ketoglutarate/O(2)-dependent hydroxylation of deoxyuridi
231  three coordination sites, a bidentate alpha-ketoglutarate occupying two sites, and an aquo ligand in
232 s to investigate the effect of ADP and alpha-ketoglutarate on the binding of PII to ATase and NRII.
233  phosphoenolpyruvate and the inhibitor alpha-ketoglutarate, on the structure and dynamics of EI using
234 h an NAD(+) precursor or its substrate alpha-ketoglutarate or treatment with a poly(ADP ribose) polym
235  or 30 hr CI in saline, histidine-tryptophan-ketoglutarate or University of Wisconsin preservation so
236 it forms with either the co-substrate (alpha-ketoglutarate) or the substrate (fumitremorgin B).
237 starved cells by the TCA intermediates alpha-ketoglutarate, oxaloacetate, and pyruvate, confirming th
238 te (SerC and PdxA), we have found that alpha-ketoglutarate, oxaloacetic acid, and pyruvate are equall
239 cluded an unexpected pathway bypassing alpha-ketoglutarate-oxidizing steps in the tricarboxylic acid
240 One such enzyme is the 2-oxoglutarate (alpha-ketoglutarate) oxidoreductase (OOR), which catalyzes the
241 k could be relieved by addition of the alpha-ketoglutarate precursor glutamate.
242                         Histidine-tryptophan-ketoglutarate preservation solution slightly decreased i
243 atoms of N-oxalylglycine (an analog of alpha-ketoglutarate) provide four coordinations in the equator
244 the enzyme that converts isocitrate to alpha-ketoglutarate, providing mechanistic explanation for TCA
245            Glucose, galacturonic acid, alpha-ketoglutarate, pyruvate, acetoin and acetaldehyde were d
246 e characterized the stereochemistry of alpha-ketoglutarate reduction by showing that d-2-HGA, but not
247              Prior studies showed that alpha-ketoglutarate regulated the ability of PII to control th
248 ere, we show that a similar pattern of alpha-ketoglutarate regulation was obtained with another PII r
249 Mechanistically, addition of exogenous alpha-ketoglutarate replenishes TCA intermediates and rescues
250 on of KIC and glutamate to leucine and alpha-ketoglutarate, respectively.
251 ochondria via glutamate synthesis from alpha-ketoglutarate resulting in cataplerosis.
252              A cell-permeable ester of alpha-ketoglutarate reversed the low TCA cycle intermediates a
253 inhibitor Meloxicam via histidine-tryptophan-ketoglutarate showed the best graft-protective attribute
254 NEVKP or in 4 degrees C histidine-tryptophan-ketoglutarate solution (SCS), followed by kidney autotra
255                         Histidine-Tryptophan-Ketoglutarate solution could have an economically superi
256 ither preserved in cold histidine-tryptophan-ketoglutarate solution for 8 hours (n = 5), or subjected
257  of Wisconsin solution, histidine-tryptophan-ketoglutarate solution, and Belzer-machine perfusion sol
258 3 hr of cold storage in histidine-tryptophan-ketoglutarate solution.
259 ersity of Wisconsin and Histidine-Tryptophan-Ketoglutarate solutions are clinically equivalent.
260  was dependent on the concentration of alpha-ketoglutarate substrate in glioma cell lines and could b
261 , which is suppressed by glutamate and alpha-ketoglutarate supplementation.
262  tricarboxylic acid cycle intermediate alpha-ketoglutarate through glutaminase and alanine aminotrans
263      Variation of the concentration of alpha-ketoglutarate through its physiological range provided d
264  neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate" by Ward and colleag
265  neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate".
266  acquisition of the ability to convert alpha-ketoglutarate to 2HG.
267 c enzymatic activity: the reduction of alpha-ketoglutarate to d-2-hydroxyglutaric acid, which is prop
268 osynthesis pathway, in addition reduce alpha-ketoglutarate to D-2HG using NADH and represent major in
269 ion of E78A, which exhibits binding of alpha-ketoglutarate to E and E.NADH.
270 enzymes needed to convert glutamine to alpha-ketoglutarate to enter the TCA cycle.
271  stimulated reductive carboxylation of alpha-ketoglutarate to generate citrate via retrograde TCA cyc
272 ucine catabolism and transamination of alpha-ketoglutarate to glutamate, with impaired TCA anaplerosi
273 versible transamination of leucine and alpha-ketoglutarate to KIC and glutamate, the first step of le
274 olysis, the conversion of glutamine to alpha-ketoglutarate to maintain the TCA cycle (anaplerosis) an
275  combination of 1 mm cysteine and 1 mm alpha-ketoglutarate to promote sulphide synthesis via the cyst
276 alyse the NADPH-dependent reduction of alpha-ketoglutarate to R(-)-2-hydroxyglutarate (2HG).
277 onvert substantially more glutamine to alpha-ketoglutarate to replenish the tricarboxylic acid cycle
278 OR), which catalyzes the conversion of alpha-ketoglutarate to succinyl coenzyme A (succinyl-CoA) and
279 uman cells use reductive metabolism of alpha-ketoglutarate to synthesize AcCoA for lipid synthesis.
280  alteration that leads to catalysis of alpha-ketoglutarate to the oncometabolite D-2-hydroxyglutarate
281 ain-of-function activity by converting alpha-ketoglutarate to the oncometabolite R-2-hydroxyglutarate
282 addition of the TCA cycle intermediate alpha-ketoglutarate to the Rb TKO MEFs reversed the inhibitory
283 ears to be increased by Histidine-Tryptophan-Ketoglutarate-use (p = 0.018), this effect could not be
284          The ammonia is transferred to alpha-ketoglutarate via glutamate dehydrogenase, yielding glut
285       Only Meloxicam in histidine-tryptophan-ketoglutarate was demonstrated to be a safe drug without
286                            Apparently, alpha-ketoglutarate was generated from unlabeled glutamate via
287 ation, net synthesis of glutamate from alpha-ketoglutarate was impaired in GDH-deficient islets.
288                               Although alpha-ketoglutarate was required for the binding of PII to NRI
289 I equally well as the concentration of alpha-ketoglutarate was varied through its physiological range
290   Subsequent binding of the substrate, alpha-ketoglutarate, was characterized by a rapid equilibrium
291 pparent K(m)s of MJ1391 for ll-DAP and alpha-ketoglutarate were 82.8 + or - 10 microM and 0.42 + or -
292 lutaminolysis catabolites particularly alpha-ketoglutarate, which are generated in an mTORC2-dependen
293 increasing production of glutamate and alpha-ketoglutarate, which in turn results in enhanced mitocho
294 enase expression and the production of alpha-ketoglutarate, which negatively regulate hypoxia-inducib
295 e metabolism of glutamine/glutamate to alpha-ketoglutarate, which, in turn, is metabolized to produce
296 he enzyme (conversion of isocitrate to alpha-ketoglutarate) while conferring a new enzymatic function
297 tion with the mitochondrial metabolite alpha-ketoglutarate, whose synthesis is regulated by RIP1/RIP3
298 outcomes when comparing histidine-tryptophan-ketoglutarate with either of the University of Wisconsin
299 s a Stetter-like conjugate addition of alpha-ketoglutarate with isochorismate.
300 by Q-derived glutamate is converted to alpha-ketoglutarate with the concomitant conversion of oxaloac

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