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1 nd Kreb's cycle intermediates (succinate and alpha-ketoglutarate).
2 cumulation of 2-hydroxyglutarate and reduced alpha-ketoglutarate.
3 ehydrogenases, efficiently oxidized D-2HG to alpha-ketoglutarate.
4 reductive carboxylation of glutamine-derived alpha-ketoglutarate.
5 glutamate to pyruvate, yielding alanine and alpha-ketoglutarate.
6 potency compared with that of KDM5B at 1 mm alpha-ketoglutarate.
7 rs, JIB-04 is not a competitive inhibitor of alpha-ketoglutarate.
8 nce on the concentration of its co-substrate alpha-ketoglutarate.
9 y of producing 2-hydroxyglutarate (2HG) from alpha-ketoglutarate.
10 levels of O(2)-regulated metabolites such as alpha-ketoglutarate.
11 her converted to 3-deoxy-2-keto-hexarate and alpha-ketoglutarate.
12 tor vs 4PE and a noncompetitive inhibitor vs alpha-ketoglutarate.
13 increase in GDH affinity for its substrate, alpha-ketoglutarate.
14 ination of saccharopine to give l-lysine and alpha-ketoglutarate.
15 r is sequentially converted to glutamate and alpha-ketoglutarate.
16 hile Arg428 contributes mainly to binding of alpha-ketoglutarate.
17 altering stimulation by glucose, leucine, or alpha-ketoglutarate.
18 type PII, and this effect was antagonized by alpha-ketoglutarate.
19 supplementation with TCA cycle intermediate alpha-ketoglutarate.
20 atios of succinate to glutamate, fumarate to alpha-ketoglutarate, 2HG to glutamate, and D-2HG to L-2H
21 xpression due to the increased production of alpha-ketoglutarate, a critical substrate for prolyl hyd
22 glutamate export and that supplementation of alpha-ketoglutarate, a key downstream metabolite of glut
23 omote transcription and, thus, production of alpha-ketoglutarate, a key metabolite in the regulation
24 Loss of Nrd1 or Ogdh leads to an increase in alpha-ketoglutarate, a substrate for OGDH, which in turn
25 low and NADPH production, an accumulation of alpha-ketoglutarate, aconitate, and citrate that is asso
26 ell pairs to demonstrate that treatment with alpha-ketoglutarate (aKG) esters elicits rapid death of
28 astic cells leads to increased production of alpha-ketoglutarate (aKG) within mesenchymal stem cells
29 was present, the antagonism between ADP and alpha-ketoglutarate allowed each of these effectors to i
31 , IDH1 and IDH2, decarboxylate isocitrate to alpha-ketoglutarate (alpha-KG) and reduce NADP to NADPH.
32 The mechanism is steady state ordered with alpha-ketoglutarate (alpha-Kg) binding prior to acetyl-C
33 (d-2-HG) is an oncometabolite generated from alpha-ketoglutarate (alpha-KG) by mutant isocitrate dehy
34 ate synthase (HOAS), the E1 component of the alpha-ketoglutarate (alpha-KG) dehydrogenase complex (KD
36 atory genes necessary for the utilization of alpha-ketoglutarate (alpha-KG) in Pseudomonas aeruginosa
37 rption was also activated by induction of an alpha-ketoglutarate (alpha-KG) paracrine signaling syste
39 ino group from branched-chain amino acids to alpha-ketoglutarate (alpha-KG) thereby regenerating glut
45 Ten-eleven-translocation (TET) proteins are alpha-ketoglutarate (alpha-KG)-dependent dioxygenases th
46 yclization is catalyzed by the non-heme iron alpha-ketoglutarate (alpha-KG)-dependent SnoK in the bio
51 ranslocation (TET) family enzymes, which are alpha-ketoglutarate (alpha-KG)/Fe(II)-dependent dioxygen
52 ity or mitochondrial Ca(2+) uptake increased alpha-ketoglutarate (alphaKG) abundance and the NAD(+)/N
53 ative decarboxylation of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) and the NADPH/CO(2)-depend
55 at the tricarboxylic acid cycle intermediate alpha-ketoglutarate (alphaKG) can both sustain naive mou
56 -dependent conversion of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) in the cytosol and peroxis
58 hether a physiologic plasma concentration of alpha-ketoglutarate (alphaKG) influences the kinetic int
60 ukoencephalopathy and a urinary excretion of alpha-ketoglutarate (alphaKG) that was markedly increase
61 enzymatic activity allowing them to convert alpha-ketoglutarate (alphaKG) to 2-hydroxyglutarate (2HG
62 Aliphatic halogenases activate O(2), cleave alpha-ketoglutarate (alphaKG) to CO(2) and succinate, an
63 family of enzymes that use Fe(2+), O(2) and alpha-ketoglutarate (alphaKG) to perform a variety of ha
64 me activity that catalyzes the conversion of alpha-ketoglutarate (alphaKG) to the oncometabolite D-(2
65 ase load can reverse the direction of apical alpha-ketoglutarate (alphaKG) transport in the proximal
67 y, belongs to a recently discovered class of alpha-ketoglutarate (alphaKG), non-heme Fe(II)-dependent
68 anaerobic conditions containing iron(II) and alpha-ketoglutarate (alphaKG), to dioxygen initiates oxi
69 to catalyze the conversion of isocitrate to alpha-ketoglutarate (alphaKG), whereas conferring a gain
70 activates anaplerotic flux from glutamine to alpha-ketoglutarate (alphaKG), which subsequently enters
71 rial the citric acid(TCA) cycle intermediate alpha-ketoglutarate (alphaKG), which via its OXGR1 recep
72 ted mouse models to ask if inhibition of the alpha-ketoglutarate (alphaKG)-dependent dioxygenase Egln
74 al (2-His-1-carboxylate) facial triad in the alpha-ketoglutarate (alphaKG)-dependent dioxygenases cla
75 xylases (P4Hs) are mononuclear non-heme iron alpha-ketoglutarate (alphaKG)-dependent dioxygenases tha
76 factor (HIF) prolyl hydroxylases (PHDs) are alpha-ketoglutarate (alphaKG)-dependent dioxygenases tha
78 ibiting hypoxia-inducible factor (FIH) is an alpha-ketoglutarate (alphaKG)-dependent enzyme which cat
79 ently discovered class of nonheme Fe(II) and alpha-ketoglutarate (alphaKG)-dependent halogenases, cat
81 itions (Th1) were regulated by glutamine and alpha-ketoglutarate (alphaKG)-induced events, in part th
86 models of PDAC leads to the accumulation of alpha-ketoglutarate (alphaKG, also known as 2-oxoglutara
87 tricarboxylic acid cycle (TCA) intermediate, alpha-ketoglutarate, also blocks the transcriptional act
88 socitrate pathway, which generates cytosolic alpha-ketoglutarate, also known as 2-oxoglutarate (2OG).
90 This is a cell-permeable prodrug form of alpha-ketoglutarate, an important intermediate in the tr
91 and IDH2 and reduces levels of intracellular alpha-ketoglutarate, an obligatory cofactor for various
94 toglutarate alone, and HPV in the absence of alpha-ketoglutarate and cysteine was not attenuated by a
95 djustments would ensure the replenishment of alpha-ketoglutarate and glutamate, which provide the car
96 depleted in all TCA cycle substrates between alpha-ketoglutarate and malate despite high rates of glu
97 ecrease in cell proliferation was rescued by alpha-ketoglutarate and overexpression of IDH2, whereas
99 the ternary complex of HygX with cosubstrate alpha-ketoglutarate and putative product hygromycin B id
100 ling the intracellular levels of its product alpha-ketoglutarate and subsequent metabolite fumarate.
102 n to citric acid cycle intermediates such as alpha-ketoglutarate and succinate, NaDC3 transports othe
104 ycle activity to IDH2-mediated production of alpha-ketoglutarate and through it, the activity of key
105 to IDH1 R132H competitively with respect to alpha-ketoglutarate and uncompetitively with respect to
107 s the substrate required addition of Fe(2+), alpha-ketoglutarate, and ascorbic acid, confirming that
108 ndent mitochondrial enzymes, mainly lactate, alpha-ketoglutarate, and branched chain keto-acids.
109 ponent (E3) is associated with the pyruvate, alpha-ketoglutarate, and glycine dehydrogenase complexes
111 (H), the enzyme in a complex with NAD(H) and alpha-ketoglutarate, and the enzyme in a complex with NA
112 x redox enzymes are involved, including four alpha-ketoglutarate- and iron(II)-dependent dioxygenases
113 e levels, but causes a drop in the levels of alpha-ketoglutarate, another output of the pathway and a
114 ells (BMDACs) with dimethyloxalylglycine, an alpha-ketoglutarate antagonist that induces hypoxia-indu
115 nt in its physiological concentration range, alpha-ketoglutarate apparently played a role in only the
116 e: levels of TCA-cycle metabolites including alpha-ketoglutarate are high, and levels of the key regu
119 glutamate production from either pyruvate or alpha-ketoglutarate as potential translatable metabolic
120 d by prolyl 4-hydroxylases that use O(2) and alpha-ketoglutarate as substrates to hydroxylate conserv
121 e specific activity of DapL using ll-DAP and alpha-ketoglutarate as substrates was 24.3 + or - 2.0 nm
122 r was used for GC-MS/MS analysis of alanine, alpha-ketoglutarate, asparagine, aspartic acid, cystathi
123 alytic JmjC domain with conserved Fe(II) and alpha-ketoglutarate binding sites, and displays H3K9me1/
124 ly reconstitutes the cofactor (metal ion and alpha-ketoglutarate) binding characteristics of other st
125 as rescued with exogenous membrane-permeable alpha-ketoglutarate, but not pyruvate or oxaloacetate, s
126 The product, l-lyxonate, is catabolized to alpha-ketoglutarate by a previously characterized pathwa
127 In addition, reductive carboxylation of alpha-ketoglutarate by isocitrate dehydrogenase 1 (IDH1)
129 this report we demonstrate that derivatized alpha-ketoglutarate can be used as a strategy for mainta
131 this proof-of-concept study, that [1-(13)C] alpha-ketoglutarate can serve as a metabolic imaging age
132 reductive carboxylation of glutamine-derived alpha-ketoglutarate (catalyzed by reverse flux through i
133 entify several cellular conditions where the alpha-ketoglutarate/citrate ratio is changed due to an a
135 lglycine (DMOG, 200 mug/g), an antagonist of alpha-ketoglutarate cofactor and inhibitor for HIF PHD,
136 of KIC/glutamine (10/2 mM) did not influence alpha-ketoglutarate concentrations but caused 120 and 33
137 hen ATP was the sole adenylylate nucleotide, alpha-ketoglutarate controlled the extent of PII activat
139 (via the gamma-aminobutyric acid pathway or alpha-ketoglutarate decarboxylase/succinic semialdehyde
142 , we found an increase in phosphorylation of alpha-ketoglutarate dehydrogenase (alphaKGDH) in female
144 lexes, such as pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase (KGDH), and the glycin
145 ial chaperones and assists in the folding of alpha-ketoglutarate dehydrogenase (OGDH), a rate-limitin
146 acid cofactor of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase and other mitochondria
147 ributions of regulation of the activities of alpha-ketoglutarate dehydrogenase and the aspartate-glut
148 ltiple proteins, including the E2 subunit of alpha-ketoglutarate dehydrogenase and the glutathione S-
149 complexes, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and the glycine cleava
151 oxymethyl transferase, and components of the alpha-ketoglutarate dehydrogenase complex in conjunction
152 d its target DLST-the E2 subcomponent of the alpha-ketoglutarate dehydrogenase complex, a rate-contro
154 oteins, we demonstrate that the pyruvate and alpha-ketoglutarate dehydrogenase complexes directly cat
155 osttranslational lipoylation of pyruvate and alpha-ketoglutarate dehydrogenase complexes, resulting i
157 complexes, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and branched-chain ke
160 methylation was changed in 1797 genes [e.g., alpha-ketoglutarate dependent dioxygenase (FTO), interle
161 ibitor treatment promoted GBM survival in an alpha-ketoglutarate-dependent (alphaKG-dependent) manner
162 Two functional subtypes of nonheme Fe(II)/alpha-ketoglutarate-dependent aspartyl beta-hydroxylases
163 n of R172K mutant IDH2 resulted in increased alpha-ketoglutarate-dependent consumption of NADPH compa
166 ies its lipid-A by hydroxylation by the Fe2+/alpha-ketoglutarate-dependent dioxygenase enzyme (LpxO).
167 Moreover, we applied a key biosynthetic alpha-ketoglutarate-dependent dioxygenase enzyme in a bi
170 lation didomain protein, DdaD, and an Fe(II)/alpha-ketoglutarate-dependent dioxygenase homologue, Dda
172 metal ions or substrate taurine to TauD, an alpha-ketoglutarate-dependent dioxygenase, alters its UV
177 mO3 and PtmO6 are two functionally redundant alpha-ketoglutarate-dependent dioxygenases that generate
179 even-translocation) proteins are Fe(ii)- and alpha-ketoglutarate-dependent dioxygenases that modify t
180 o serine synthesis, which in turn stimulates alpha-ketoglutarate-dependent dioxygenases that remove t
181 to epigenetic effects through inhibition of alpha-ketoglutarate-dependent dioxygenases that require
182 droxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases' by Xu and co
183 the active-site plasticity of these Fe(II) /alpha-ketoglutarate-dependent dioxygenases, and suggest
184 et-dependent methyltransferases, Fe(II)- and alpha-ketoglutarate-dependent dioxygenases, base excisio
185 e TET proteins, a family of AlkB-like Fe(II)/alpha-ketoglutarate-dependent dioxygenases, can oxidize
186 es inhibit a superfamily of enzymes known as alpha-ketoglutarate-dependent dioxygenases, leading to e
187 unit and establish the role of an iron- and alpha-ketoglutarate-dependent enzyme (Fe/alphaKG) in the
188 stically distinct bifunctional non-heme iron alpha-ketoglutarate-dependent enzyme responsible for the
191 e function and genomic localization of these alpha-ketoglutarate-dependent enzymes in the maintenance
192 alternatively activated macrophages require alpha-ketoglutarate-dependent epigenetic reprogramming t
196 iggered in vivo by hyperammonemia through an alpha-ketoglutarate-dependent inhibition of the mammalia
197 Aspergillus fumigatus is the first reported alpha-ketoglutarate-dependent mononuclear non-haem iron
203 e residue, the inclusion of a non-heme iron, alpha-ketoglutarate-dependent oxygenase for hydroxylatio
204 dentified a conserved group of nonheme iron, alpha-ketoglutarate-dependent oxygenases likely responsi
205 family of histone demethylases are Fe2+- and alpha-ketoglutarate-dependent oxygenases that are essent
206 The enzymatic function of many of these alpha-ketoglutarate-dependent proteins is required for p
208 Alkb homolog 7 (ALKBH7) is a mitochondrial alpha-ketoglutarate dioxygenase required for DNA alkylat
209 ely, blocking serine synthesis or repressing alpha-ketoglutarate-driven demethylation facilitates mal
212 -D via a pathway initiated by the Fe(II) and alpha-ketoglutarate (Fe/alphaKG)-dependent aryloxyalkano
217 tulate that steric constraints could prevent alpha-ketoglutarate from undergoing an "off-line"-to-"in
221 dependent carboxylation of glutamine-derived alpha-ketoglutarate in hypoxia is associated with a conc
222 to convert glutamine-derived glutamate into alpha-ketoglutarate in the mitochondria to fuel the tric
223 erated tricarboxylic acid cycle intermediate alpha-ketoglutarate, in turn, serves as the cofactor for
224 by an increase in reductive carboxylation of alpha-ketoglutarate (increased concentrations of 2-hydro
225 ion of the tricarboxyclic acid cycle product alpha-ketoglutarate, indicating the critical function of
226 utamine deficiency, through the reduction of alpha-ketoglutarate, inhibits the AlkB homolog (ALKBH) e
227 Four minireviews deal with aspects of the alpha-ketoglutarate/iron-dependent dioxygenases in this
230 e metabolic fate of hyperpolarized [1-(13)C] alpha-ketoglutarate is studied in isogenic glioblastoma
231 actions with the alpha-carboxylate moiety of alpha-ketoglutarate, is also uniquely positioned to best
233 inate (suc(2-)) through glutarate (glu(2-)), alpha-ketoglutarate (kglu(2-)), adipate (adi(2-)), pimel
234 nscription factor RTG1 Furthermore, elevated alpha-ketoglutarate levels also suppress 2HG-mediated re
235 ubunit of the IDH3 heterotetramer, decreased alpha-ketoglutarate levels and increased the stability a
238 However, enhanced glutamine flux increases alpha-ketoglutarate levels, which in turn increases prol
240 from a virtual screen of RsbU revealed that alpha-ketoglutarate, malate and oxaloacetate bound to th
241 termediates with good sensitivity, including alpha-ketoglutarate, malate, fumarate, succinate, 2-hydr
242 other tricarboxylic acid cycle metabolites (alpha-ketoglutarate, malic acid, and glutamate) in froze
243 of a novel pathogenicity island involved in alpha-ketoglutarate metabolism under anaerobic condition
244 of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and
245 tivity, carried by Dld3, to convert D-2HG to alpha-ketoglutarate, namely an FAD-dependent transhydrog
247 Although two enzymes that catalyze Fe(2+)/alpha-ketoglutarate/O(2)-dependent hydroxylation of deox
248 upying three coordination sites, a bidentate alpha-ketoglutarate occupying two sites, and an aquo lig
249 strate phosphoenolpyruvate and the inhibitor alpha-ketoglutarate, on the structure and dynamics of EI
250 on with an NAD(+) precursor or its substrate alpha-ketoglutarate or treatment with a poly(ADP ribose)
251 lexes it forms with either the co-substrate (alpha-ketoglutarate) or the substrate (fumitremorgin B).
252 hosphate (SerC and PdxA), we have found that alpha-ketoglutarate, oxaloacetic acid, and pyruvate are
253 ons included an unexpected pathway bypassing alpha-ketoglutarate-oxidizing steps in the tricarboxylic
256 Accordingly, serine starvation or enforced alpha-ketoglutarate production antagonizes squamous cell
257 aling by fueling serine biosynthesis-derived alpha-ketoglutarate production in breast-cancer-derived
258 xygen atoms of N-oxalylglycine (an analog of alpha-ketoglutarate) provide four coordinations in the e
259 Idh, the enzyme that converts isocitrate to alpha-ketoglutarate, providing mechanistic explanation f
261 ous type I IFN controls the cellular citrate/alpha-ketoglutarate ratio and inhibits expression and ac
262 we have characterized the stereochemistry of alpha-ketoglutarate reduction by showing that d-2-HGA, b
268 ession was dependent on the concentration of alpha-ketoglutarate substrate in glioma cell lines and c
269 tricarboxylic acid (TCA) cycle intermediate, alpha-ketoglutarate, suggesting that exogenous glutamine
271 to the tricarboxylic acid cycle intermediate alpha-ketoglutarate through glutaminase and alanine amin
272 s is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate" by Ward and c
274 morphic enzymatic activity: the reduction of alpha-ketoglutarate to d-2-hydroxyglutaric acid, which i
275 ine biosynthesis pathway, in addition reduce alpha-ketoglutarate to D-2HG using NADH and represent ma
277 SRC-2 stimulated reductive carboxylation of alpha-ketoglutarate to generate citrate via retrograde T
278 ted leucine catabolism and transamination of alpha-ketoglutarate to glutamate, with impaired TCA anap
279 zes reversible transamination of leucine and alpha-ketoglutarate to KIC and glutamate, the first step
280 utaminolysis, the conversion of glutamine to alpha-ketoglutarate to maintain the TCA cycle (anapleros
281 n of a combination of 1 mm cysteine and 1 mm alpha-ketoglutarate to promote sulphide synthesis via th
282 CRCs convert substantially more glutamine to alpha-ketoglutarate to replenish the tricarboxylic acid
283 ase (OOR), which catalyzes the conversion of alpha-ketoglutarate to succinyl coenzyme A (succinyl-CoA
284 that human cells use reductive metabolism of alpha-ketoglutarate to synthesize AcCoA for lipid synthe
285 ctural alteration that leads to catalysis of alpha-ketoglutarate to the oncometabolite D-2-hydroxyglu
286 nfer gain-of-function activity by converting alpha-ketoglutarate to the oncometabolite R-2-hydroxyglu
287 Last, addition of the TCA cycle intermediate alpha-ketoglutarate to the Rb TKO MEFs reversed the inhi
288 duced iron and 2-oxoglutarate (also known as alpha-ketoglutarate) to function, although their affinit
290 stimulation, net synthesis of glutamate from alpha-ketoglutarate was impaired in GDH-deficient islets
291 The apparent K(m)s of MJ1391 for ll-DAP and alpha-ketoglutarate were 82.8 + or - 10 microM and 0.42
292 ed [1-(13)C]glutamate produced from [1-(13)C]alpha-ketoglutarate were significantly higher in temozol
293 s of glutaminolysis catabolites particularly alpha-ketoglutarate, which are generated in an mTORC2-de
294 sm by increasing production of glutamate and alpha-ketoglutarate, which in turn results in enhanced m
295 hydrogenase expression and the production of alpha-ketoglutarate, which negatively regulate hypoxia-i
296 ing the metabolism of glutamine/glutamate to alpha-ketoglutarate, which, in turn, is metabolized to p
297 n of the enzyme (conversion of isocitrate to alpha-ketoglutarate) while conferring a new enzymatic fu
298 ementation with the mitochondrial metabolite alpha-ketoglutarate, whose synthesis is regulated by RIP
300 whereby Q-derived glutamate is converted to alpha-ketoglutarate with the concomitant conversion of o