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1 dehydrogenase (carboxylation of alpha-KG to isocitrate).
2 uppressed by providing the aconitase product isocitrate.
3 is much more sensitive to concentrations of isocitrate.
5 arboxylic acid cycle intermediates (citrate, isocitrate, 2-oxoglutarate, succinate, fumarate, malate,
7 f the erythroid iron restriction response by isocitrate administration corrected anemia and erythropo
9 extension in C. elegans, reversibly converts isocitrate and acetyl-CoA to succinate, malate, and CoA.
10 ttributed to the competitive binding between isocitrate and alphaKG, which is made more favorable for
12 se assays demonstrated the presence of eight isocitrate and four AMP binding sites for the wild-type
13 Mtb's ICLs are catalytically bifunctional isocitrate and methylisocitrate lyases required for grow
15 the chiral imidazolium hosts toward citrate, isocitrate and the two enantiomers of malate have been s
17 mmonly found in AML reduces the affinity for isocitrate, and increases the affinity for NADPH and alp
18 yglutarate, citrate, oxaloacetate, pyruvate, isocitrate, and lactate using a 8-min run time in cancer
19 noise for citrate and an 8-fold increase for isocitrate as compared to detection of the untagged anal
22 dictions that the enzyme would contain eight isocitrate binding sites, four NAD(+) binding sites, and
23 Cys-150 residues and to half-site binding of isocitrate, but that a form of negative cooperativity ma
24 pathway, involving the mitochondrial citrate/isocitrate carrier and the cytosolic NADP-dependent isoc
25 siRNA-mediated suppression of ICDc, citrate/isocitrate carrier, or Kv2.2 expression impaired GSIS, a
26 Isotope tracing revealed that in spheroids, isocitrate/citrate produced reductively in the cytosol c
27 odel in which a key function of the pyruvate-isocitrate cycle is to maintain levels of Kv2.2 expressi
28 Recent studies have shown that the pyruvate-isocitrate cycling pathway, involving the mitochondrial
31 direction of the normal reaction (alphaKG to isocitrate), dead-end inhibition studies suggest that wi
33 tion cryo-EM structures of the cancer target isocitrate dehydrogenase (93 kDa) and identify the natur
34 ase and to stimulate the reverse reaction of isocitrate dehydrogenase (carboxylation of alpha-KG to i
35 of isocitrate and engagement with cytosolic isocitrate dehydrogenase (ICDc) may be one key pathway,
36 ate carrier and the cytosolic NADP-dependent isocitrate dehydrogenase (ICDc), is involved in control
37 (via isocitrate lyase) or the TCA cycle (via isocitrate dehydrogenase (ICDH) activity) and we sought
39 1 and aminopeptidase), inhibitors of mutated isocitrate dehydrogenase (IDH) 1 and IDH2, antibody-base
40 associated with disease progression such as isocitrate dehydrogenase (IDH) 1, IDH2, EZH2, serine/arg
41 Cit2 and reduced expression of NAD-specific isocitrate dehydrogenase (Idh) and aconitase (Aco1) in p
44 activity for grading and characterization of isocitrate dehydrogenase (IDH) gene mutation status of g
45 ne promoter and the mutational status of the isocitrate dehydrogenase (IDH) gene were determined.
48 expression of ATP-citrate synthase (ACS) and isocitrate dehydrogenase (IDH) genes in cold-treated tom
49 discovery of mutations in the genes encoding isocitrate dehydrogenase (IDH) has uncovered a critical
50 terozygous mutations in the metabolic enzyme isocitrate dehydrogenase (IDH) in subsets of cancers, in
53 stigation of metabolic pathways disturbed in isocitrate dehydrogenase (IDH) mutant tumors revealed th
54 er, accuracy was poorer when tumors harbored isocitrate dehydrogenase (IDH) mutations (91% in IDH-wil
56 s caused by recurrent mutations, such as the isocitrate dehydrogenase (IDH) mutations found in 15% of
58 ation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic
59 associated with MYC signaling, but not with isocitrate dehydrogenase (IDH) mutations, suggesting a d
60 that shows how robust behavior arises in the isocitrate dehydrogenase (IDH) regulatory system of Esch
61 ally available MRI parameters for predicting isocitrate dehydrogenase (IDH) status in patients with g
62 drogenase (SDH), fumarate hydratase (FH) and isocitrate dehydrogenase (IDH), advancing and challengin
63 role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carbo
65 determine whether MRI/CT analysis identifies isocitrate dehydrogenase (IDH)-mutant gliomas misassigne
67 ide adenine dinucleotide phosphate-dependent isocitrate dehydrogenase (IDH)1 and IDH2 frequently aris
69 y, we explored the function of mitochondrial isocitrate dehydrogenase (IDH)2, a tricarboxylic acid cy
70 atio and inhibits expression and activity of isocitrate dehydrogenase (IDH); and, via 13C-labeling st
71 imaging-defined invasive phenotypes of both isocitrate dehydrogenase (IDH-1)-mutated and IDH-1 wild-
73 utarate (2HG), generated by mutated forms of isocitrate dehydrogenase (IDH1 and IDH2), reduces the ex
74 Mutations in the cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDH1) occur in several types o
75 rboxylated by the NADPH-linked mitochondrial isocitrate dehydrogenase (IDH2) to form isocitrate, whic
77 tive carboxylation of alpha-ketoglutarate by isocitrate dehydrogenase 1 (IDH1) and 2 (IDH2) was recen
80 1 was exclusive to tumors carrying wild-type isocitrate dehydrogenase 1 (IDH1) and IDH2 genes and was
82 sue of Blood, Shi et al describe the role of isocitrate dehydrogenase 1 (idh1) and idh2 in developmen
83 Mutations in metabolic enzymes, including isocitrate dehydrogenase 1 (IDH1) and IDH2, in cancer st
87 Mutations at the arginine residue (R132) in isocitrate dehydrogenase 1 (IDH1) are frequently identif
90 in HuR-deficient PDAC cell lines identified isocitrate dehydrogenase 1 (IDH1) as the sole antioxidan
95 vosidenib is an oral inhibitor of the mutant isocitrate dehydrogenase 1 (IDH1) enzyme, approved for t
96 grade gliomas are driven by mutations in the isocitrate dehydrogenase 1 (IDH1) gene and are less aggr
106 se dependent, acted synergistically with the isocitrate dehydrogenase 1 (IDH1) mutation, and resemble
110 Arg132 of the cytoplasmic NADP(+)-dependent isocitrate dehydrogenase 1 (IDH1) occur frequently in gl
111 letion) and mutations in the metabolic genes isocitrate dehydrogenase 1 (IDH1) or IDH2(1,2), were sha
113 dromes, at least one tumor has a mutation in isocitrate dehydrogenase 1 (IDH1) or in IDH2, 65% of whi
117 Here we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), establishes G-CIMP by
126 zygously expressed single-point mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2, respect
130 aking is that patients with mutations in the isocitrate dehydrogenase 1 and 2 (IDH1/2) oncogenes are
134 ers of gliomagenesis, including mutations in isocitrate dehydrogenase 1 and the NF-kappaB pathway, an
136 rganization 2007 tumor grade, histology, and isocitrate dehydrogenase 1 R132H mutational status.
137 ssigned NF1-glioma to LGm6, a poorly defined Isocitrate Dehydrogenase 1 wild-type subgroup enriched w
138 ade gliomas with mutations in IDH1 (encoding isocitrate dehydrogenase 1), we studied paired tumor sam
140 D-2-hydroxyglutarate imaging is possible in isocitrate dehydrogenase 1-mutated human glioma by using
142 e (R-2HG), produced at high levels by mutant isocitrate dehydrogenase 1/2 (IDH1/2) enzymes, was repor
144 d hematopoietic differentiation in AML after isocitrate dehydrogenase 1/2 mutation and 2-hydroxygluta
147 pecies (ROS) by deacetylating and activating isocitrate dehydrogenase 2 (IDH2) and superoxide dismuta
151 cute myeloid leukemia (AML) treated with the isocitrate dehydrogenase 2 (IDH2) mutant-specific inhibi
152 ochondrial superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2) observed in untreated
154 Recurrent mutations at R140 and R172 in isocitrate dehydrogenase 2 (IDH2) occur in many cancers,
155 ons in isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) occur in most grade 2
157 and colleagues demonstrate the mutations in isocitrate dehydrogenase 2 (IDH2), commonly found in acu
158 tly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased
160 of unfavorable outcome, such as mutations in isocitrate dehydrogenase 2 (IDH2-R172) and overexpressio
161 rate-limiting tricarboxylic acid cycle (TCA) isocitrate dehydrogenase 2 and superoxide dismutase 2, c
162 findings demonstrate that MitEpac1 inhibits isocitrate dehydrogenase 2 via the mitochondrial recruit
164 nd that the aberrant expression of wild-type isocitrate dehydrogenase 3alpha (IDH3alpha), a subunit o
165 rogenase, 2-oxoxglutarate dehydrogenase, and isocitrate dehydrogenase activities of the Krebs cycle i
168 ssion changes of some metabolic genes (e.g., isocitrate dehydrogenase and fumarate hydratase) may enh
169 lternative CAM cycle involving mitochondrial isocitrate dehydrogenase as a potential contributor to i
171 al water-saving effect of carbon fixation by isocitrate dehydrogenase can reach 11% total water savin
172 e production of 2-hydroxyglutarate by mutant isocitrate dehydrogenase enzymes, we can observe metabol
174 with glioma harbor specific mutations in the isocitrate dehydrogenase gene IDH1 that associate with a
176 glioma-associated mutations into the NADP(+ )isocitrate dehydrogenase genes (IDP1, IDP2, IDP3) in Sac
178 occurring mutations in the NADP(+)-dependent isocitrate dehydrogenase genes IDH1 and IDH2 These mutat
179 e chromatin architecture at the promoters of isocitrate dehydrogenase genes to promote transcription
181 .35 million compounds against mutant (R132H) isocitrate dehydrogenase IDH1 led to the identification
182 Ps harbored hotspot mutations at R172 of the isocitrate dehydrogenase IDH2, of which 8 of 10 displaye
185 hosphorylation catalyzed by the bifunctional isocitrate dehydrogenase kinase/phosphatase (IDHKP), and
187 anine-DNA methyltransferase-methylation, and isocitrate dehydrogenase mutation status, the proportion
188 prognostic and therapeutic consequences: (a) isocitrate dehydrogenase mutation; (b) the combined loss
189 features or genetic alterations, except for isocitrate dehydrogenase mutations (IDH(mut)) that were
190 t developments and implications in regard to isocitrate dehydrogenase mutations in chondrosarcoma, a
192 tumor morphologic characteristics predicted isocitrate dehydrogenase status in World Health Organiza
194 glutarate in cells results from mutations to isocitrate dehydrogenase that correlate with cancer.
195 hat specifically binds an epitope of mutated isocitrate dehydrogenase type 1 (IDH1R132H), which is fr
196 c MRI were retrospectively selected (36 with isocitrate dehydrogenase wild-type [IDH(wt)], 16 with mu
197 ylic acid cycle (oxoglutarate dehydrogenase, isocitrate dehydrogenase) and glycine decarboxylase.
198 ytosolic isoforms of NADP(+)/NADPH-dependent isocitrate dehydrogenase, and subsequent metabolism of g
199 hydrogenase alpha levels and lower levels of isocitrate dehydrogenase, both proteins involved in the
200 ccinate dehydrogenase, fumarate hydratase or isocitrate dehydrogenase, can dysregulate specific 2OGDD
202 search terms were used: IDH, IDH1, IDH2, and isocitrate dehydrogenase, in conjunction with glioma or
203 -(13)C]oxaloacetate to generate (13)CO(2) at isocitrate dehydrogenase, or decarboxylation of [1-(13)C
205 rom alpha-ketoglutarate (alpha-KG) by mutant isocitrate dehydrogenase, whereas l-(S)-2-HG is generate
206 tly map to genes for aconitate hydratase and isocitrate dehydrogenase, which are expected to alter ce
211 metabolism was highly dependent on cytosolic isocitrate dehydrogenase-1 (IDH1), because the activity
214 lignancies owing to somatic mutations in the isocitrate dehydrogenase-1 or -2 (IDH1 or IDH2) genes, o
217 ients with acute myeloid leukemia (AML) have isocitrate dehydrogenase-2 (IDH2) mutations, which occur
219 pment of acquired isocitrate dehydrogenase-1/isocitrate dehydrogenase-2 mutations has been described
220 ticipation of concurrent NADPH sources (i.e. isocitrate dehydrogenase-2, malic enzymes, and glutamate
221 insulin secretion is amplified by cytosolic isocitrate dehydrogenase-dependent transfer of reducing
225 scribed metabolic oncogenic factors: mutated isocitrate dehydrogenases (IDH), succinate dehydrogenase
228 in arginine N-methyltransferases (PRMTs) and isocitrate dehydrogenases (IDHs), and highlight the most
229 e FGFR2 gene and mutations in genes encoding isocitrate dehydrogenases (in approximately 60% of iCCAs
232 Point mutations of the NADP(+)-dependent isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2) occur
234 n the tricarboxylic acid (TCA) cycle enzymes isocitrate dehydrogenases 1 and 2 (IDH1/2) highlights th
235 tions in IDH1 and IDH2, the genes coding for isocitrate dehydrogenases 1 and 2, are common in several
237 lic point mutations of the NADP(+)-dependent isocitrate dehydrogenases IDH1 and IDH2 occur frequently
238 d outcome of mutations in IDH genes encoding isocitrate dehydrogenases in adult de novo cytogenetical
239 and the expression and activity of TETs and isocitrate dehydrogenases in primary human chondrocytes.
242 expressing R172K mutant IDH2 did not display isocitrate-dependent NADPH production above vector contr
244 DP(+)-dependent oxidative decarboxylation of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) and th
245 e reversible NADP(+)-dependent conversion of isocitrate (ICT) to alpha-ketoglutarate (alphaKG) in the
247 of aconitase, which isomerizes citrate into isocitrate, is controlled by several transcriptional reg
252 at the first enzyme of the glyoxylate shunt, isocitrate lyase (ICL), may mediate survival of Mtb duri
254 ose-1,6-bisphosphatase 1) and ICL1 (encoding isocitrate lyase 1) are under control of the Mig1 repres
256 eling is mediated by the bifunctional enzyme isocitrate lyase acting in a noncanonical role distinct
257 ssion of the latent infection genes encoding isocitrate lyase and alpha-crystallin, respectively.
262 ve expression of the glyoxylate shunt genes (isocitrate lyase and malate synthase) was >300-fold high
263 Previous studies reported the activities of isocitrate lyase and malate synthase, the key enzymes of
264 ural rearrangement, substantially increasing isocitrate lyase and methylisocitrate lyase activities.
265 w that two additional gluconeogenic enzymes, isocitrate lyase and phosphoenolpyruvate carboxykinase,
266 with PR genes and highest expression of the isocitrate lyase gene coinciding with highest solar irra
268 three enzymes are: trace levels of OGDH, the isocitrate lyase of the glyoxylate shunt and an unantici
269 , a member of the phosphoenolpyruvate mutase/isocitrate lyase superfamily, catalyzes the hydrolysis o
270 tumefaciens BlcR is a member of the emerging isocitrate lyase transcription regulators that negativel
271 Mutants of the glyoxylate shunt gene for isocitrate lyase were able to grow in the presence of oi
272 n feed into either the glyoxylate shunt (via isocitrate lyase) or the TCA cycle (via isocitrate dehyd
273 sphosphatase (FBPase), malate dehydrogenase, isocitrate lyase, and phosphoenolpyruvate carboxykinase
274 s in central carbon metabolism, specifically isocitrate lyase, malate synthase, transaldolase, fructo
275 d inhibits the growth of bacteria expressing isocitrate lyase, such as Salmonella enterica and Mycoba
276 Methylobacterium extorquens AM1, which lacks isocitrate lyase, the key enzyme in the glyoxylate cycle
277 ic acid is an organic compound that inhibits isocitrate lyase, the key enzyme of the glyoxylate shunt
280 all three drugs trigger activation of Mtb's isocitrate lyases (ICLs), metabolic enzymes commonly ass
284 c malate than with the trianionic citrate or isocitrate, suggesting that the smaller guest is better
285 dehydrogenases, IDH1 and IDH2, decarboxylate isocitrate to alpha-ketoglutarate (alpha-KG) and reduce
287 IDH1 and IDH2 to catalyze the conversion of isocitrate to alpha-ketoglutarate (alphaKG), whereas con
289 ldtype function of the enzyme (conversion of isocitrate to alpha-ketoglutarate) while conferring a ne
290 bolic break at Idh, the enzyme that converts isocitrate to alpha-ketoglutarate, providing mechanistic
291 is prevents the oxidative decarboxylation of isocitrate to alpha-KG, and facilitates the conversion o
293 we have detailed the kinetics of the normal (isocitrate to alphaKG) and neomorphic (alphaKG to alphaH
294 onitase-mediated isomerization of citrate to isocitrate; trans-aconitate, but not its methyl ester, i
295 t enzyme) demonstrated half-site binding for isocitrate (two sites) in the absence of dithiothreitol
296 lactate, alanine, glycerol-3 phosphate, and isocitrate were significantly associated with higher T2D
297 biomarkers-formate, citrulline, taurine, and isocitrate-were identified as markers of SSB intake.
298 strate the present approach with citrate and isocitrate, which are isomeric metabolites each containi
299 ng by TamR, as do citrate, cis-aconitate and isocitrate, which are the substrate, intermediate and pr
300 rial isocitrate dehydrogenase (IDH2) to form isocitrate, which can then be isomerized to citrate.