コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 GLS2 isoforms (glutaminase B and liver-type glutaminase).
2 as 2 orders of magnitude higher than that of glutaminase.
3 ly, they are more sensitive to inhibition of glutaminase.
4 t cancer at baseline and after inhibition of glutaminase.
5 thereby decreasing the flux through GDH and glutaminase.
6 t human airway epithelium could also express glutaminase.
7 s characterization of Glu-AdT as a Ser-based glutaminase.
8 an increased synthesis of the mitochondrial glutaminase.
9 r cell lines with differential expression of glutaminase.
10 ed through the pharmacological inhibition of glutaminase.
12 hat depriving ECs of glutamine or inhibiting glutaminase 1 (GLS1) caused vessel sprouting defects due
20 analysis and in vitro experiments confirmed glutaminase 2 (GLS2) as a key gene associated with the f
23 s, including two involved in metabolism:Gls2(glutaminase 2) and Sco2 We also show that human and mous
25 o Glu-AdT, none of the ATP analogues induced glutaminase activation except ATP-gammaS, which stimulat
27 midotransferase, which produces ammonia in a glutaminase active site and channels it through a 30-A i
29 channel indicate that NaAD(+) stimulates the glutaminase active site in the k(cat) term by a synergis
32 (alphaS,5R) diastereomer were modeled in the glutaminase active site of GMPS and CPS to confirm that
33 structure of a ternary complex in which the glutaminase active site was inactivated by a glutamine a
34 eading from the effector binding site to the glutaminase active site, forming conserved communication
35 PS with a Michaelis-like intermediate in the glutaminase active site, the first covalent intermediate
39 uncoupling between ATP-gammaS hydrolysis and glutaminase activities suggests that the activation of g
40 nal enzyme couples the NAD(+) synthetase and glutaminase activities through an ammonia tunnel but fre
41 were twofold greater and phosphate-activated glutaminase activities were fourfold greater in the schi
42 shows completely preserved asparaginase and glutaminase activities, long-term storage stability, imp
45 e hydrolysis were examined: (a) an enzymatic glutaminase activity and (b) a non-enzymatic mechanism.
46 dues (Lys(52), Ser(128), Ser(152)) abolished glutaminase activity and consequently the amidotransfera
47 cells in vitro have biochemical evidence for glutaminase activity and express mRNA for two glutaminas
52 e activities suggests that the activation of glutaminase activity by ATP or ATP-gammaS, together with
53 e, interface mutations controlling secondary glutaminase activity demonstrated the importance of this
54 position 121 (WoA-P121) was found to have L-glutaminase activity in contrast to Uniprot entry P50286
61 re a common glutaminase domain for which the glutaminase activity is tightly regulated by an acceptor
62 d that this inhibition correlates with their glutaminase activity levels and produces a strong apopto
63 consequence, combined targeting of eIF4A and glutaminase activity more effectively inhibits PDA cell
65 NA(Gln) but not tRNA(Gln) could activate the glutaminase activity of GatD suggests that glutamine hyd
66 ibition of the Glu-tRNA(Gln)/ATP-independent glutaminase activity of Glu-AdT by gamma-Glu boronic aci
73 JHU-083 normalized CSDS-induced increases in glutaminase activity specifically in microglia-enriched
74 WoA-S121 was confirmed to have much lower L-glutaminase activity than WoA-P121, yet both showed comp
77 tivation except ATP-gammaS, which stimulates glutaminase activity to the same level as ATP, but witho
78 generated through increased small intestinal glutaminase activity with concomitantly reduced intestin
79 ssay method that measures the stimulation of glutaminase activity, a K(d) of 2 microm was measured fo
80 glial activation), serum ammonia, intestinal glutaminase activity, and cecal glutamine content were c
82 oxicity of L-ASP is thought to stem from its glutaminase activity, these findings suggest the hypothe
83 Y176F and Y176S exhibited greatly decreased glutaminase activity, whereas K288S/Y176F, a variant mut
84 d l-asparaginases also possess significant l-glutaminase activity, which correlates with many of the
85 Ser254(ErA), may correlate with significant glutaminase activity, while their substitution by Gln an
96 glutarate dehydrogenase, phosphate-activated glutaminase, alanine aminotransferase, aspartate aminotr
97 cle intermediate alpha-ketoglutarate through glutaminase and alanine aminotransferase is essential fo
100 bound ammonia to urea (through mitochondrial glutaminase and carbamoylphosphate synthetase) depends o
101 further identified that increased levels of glutaminase and connexin 32 in Mecp2-null microglia are
106 High glucose inhibited flux through both glutaminase and GDH, and leucine was unable to override
108 ected replacement of Ser176 by Ala abolishes glutaminase and Gln-dependent transamidase activities of
109 in infected cells, as did the activities of glutaminase and glutamate dehydrogenase, the enzymes nee
113 needed to (i) coordinate, albeit weakly, the glutaminase and synthetase activities of the enzyme and
114 nitoring of ATP or ATP-gammaS hydrolysis and glutaminase and transamidase activities reveals tight co
116 on of vascular endothelial growth factor and glutaminase, and is likely mediated by reduced expressio
117 tissue pH, inhibition of phosphate-activated glutaminase, and medication effects could not account fo
118 ns the ATP and FGAR binding sites, PurQ is a glutaminase, and the function of PurS is just now becomi
123 learly show that the reaction catalyzed by L-glutaminase-asparaginases proceeds through formation of
127 ermobacter thermautotrophicus GatD acts as a glutaminase but only in the presence of both Glu-tRNA(Gl
128 pathways, including effective inhibition of glutaminase by nanoparticle drug delivery, holds promise
129 neous repression of pyruvate carboxylase and glutaminase by selecting all seed matches shared by thei
132 ve transcripts: the kidney isoform (KGA) and glutaminase C (GAC) for GLS, and the liver isoform (LGA)
136 enzyme glutaminase, with a specific isoform, glutaminase C (GAC), being highly expressed in cancer ce
137 ied splice variant of the gene gls, known as Glutaminase C (GAC), is important for tumor metabolism.
138 ppearance of the most active enzyme isoform, glutaminase C (GAC), which is expressed in many cancers,
141 zole-4-carboxamide ribonucleotide) activates glutaminase catalysis at a distance of 25 A from the glu
147 sition states during catalysis, and validate glutaminase-directed inhibition of Glu-AdT as a route fo
149 classes of Qns1 mutants that fall within the glutaminase domain and the synthetase domain selectively
152 of the enzymes in this family share a common glutaminase domain for which the glutaminase activity is
155 esence of a partially structured loop in the glutaminase domain, whose sequence is present in eukaryo
156 domain, the FGAM synthetase domain, and the glutaminase domain, with a putative ammonia channel loca
160 lution, is organized as a hexamer, where the glutaminase domains adopt an inactive conformation.
161 s of the two complexes are superimposed, the glutaminase domains are rotated by about 180 degrees wit
163 udy 4-13 wk after initiation of therapy with glutaminase, dual TORC1/2, or programmed death-1 inhibit
170 asparaginase (WoA) has been reported to be L-glutaminase free, suggesting it would have fewer side ef
178 mal inhibition lowered the expression of the glutaminases GLS and GLS2, which support glutamine metab
180 ective enzymes producing glutamate and GABA, glutaminase (Gls) and glutamate decarboxylase 1 and 2 (G
181 tabolomic studies in GBM cells revealed that glutaminase (GLS) and glutamate levels are elevated foll
182 screen has revealed that the combination of glutaminase (GLS) and heat shock protein 90 (Hsp90) inhi
184 mplex fine-tunes the alternative splicing of Glutaminase (GLS) by selecting the poly(A) site in intro
188 ted with TGF-beta1-induced expression of the glutaminase (GLS) isoform, GLS1, which converts Gln into
191 a panel of 19 GBM BTSC lines, inhibition of glutaminase (GLS) showed a variable response from comple
192 elective allosteric inhibitor of kidney-type glutaminase (GLS) that has served as a molecular probe t
193 5' untranslated region of the gene encoding glutaminase (GLS) that was identified through detailed c
194 o deamination reactions, the first requiring glutaminase (GLS) to generate glutamate and the second o
195 void microRNA-mediated repression, including glutaminase (GLS), a key metabolic enzyme for tumour pro
196 ort that ovarian cancer cells overexpressing glutaminase (GLS), a target of MYC and a key enzyme in g
200 ibited significantly increased expression of glutaminase (GLS), which catalyzes the first step in the
202 est whether recently developed inhibitors of glutaminase (GLS), which mediates an early step in Gln m
207 ation modulated metabolic enzymes, including glutaminase (GLS1), to coordinate glutaminolysis and gly
208 atter with markers for glutamate production (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT
209 t strain, Ty21a-AR-Ss, by inserting Shigella glutaminase-glutamate decarboxylase systems coexpressed
210 the thioester intermediate formed during the glutaminase half-reaction by accessing the N-terminal ac
211 metabolism via pharmacological inhibition of glutaminase has been translated into clinical trials as
212 monstrate that, of the three major mammalian glutaminases identified to date, the lesser studied spli
214 ies observed in the CSDS model, and identify glutaminase in microglia-enriched CD11b(+) cells as a ph
215 GP synthase shows a 4900-fold stimulation of glutaminase in the presence of the substrate acceptor PR
217 ssion of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 pro
219 the HypoxCR reporter in vivo, we found that glutaminase inhibition reduced tumor growth by specifica
221 evealed that surviving tumor cells following glutaminase inhibition were reliant on glycolysis and gl
224 U-083, our recently developed prodrug of the glutaminase inhibitor 6-diazo-5-oxo-L-norleucine (DON) a
225 ckage of microglial glutamate synthesis by a glutaminase inhibitor abolished the neurotoxic activity,
226 ministration of a KV1.3 channel blocker or a glutaminase inhibitor ameliorated disability in experime
229 effect and glutamine dependence, making the glutaminase inhibitor CB-839 therapeutically promising f
231 ormed at baseline and after treatment with a glutaminase inhibitor or a vehicle solution for 4 mouse
234 ls of liver enzymes in contrast to CB-839, a glutaminase inhibitor that is currently in clinical tria
236 1,3,4-thiadiazol-2-yl)ethyl sulfide, a known glutaminase inhibitor, completely disrupted the higher o
238 igms will lead to new treatment options with glutaminase inhibitors and the utility of PET to identif
241 d-deprived cells with exogenous glutamine or glutaminase inhibitors restores tRNA(Gln) charging and t
249 glutaminase C (GAC) isoform of mitochondrial glutaminase is overexpressed in many cancer cells and th
250 catalyzing glutaminolysis, human kidney-type glutaminase isoform (KGA) is becoming an attractive targ
251 egulation of the glutamate-generating enzyme glutaminase isoform glutaminase C in HIV-1-infected micr
254 d the activity levels of the three mammalian glutaminase isozymes was established, with GAC being the
255 eat-containing C termini of both kidney-type glutaminase (KGA) and GLS2 isoforms (glutaminase B and l
256 ng is confirmed by significant reductions in glutaminase kinetic activity and allosteric ligand bindi
259 ce within the 3'-nontranslated region of the glutaminase mRNA binds a unique protein with high affini
260 art, by a cell-specific stabilization of the glutaminase mRNA that leads to an increased synthesis of
261 , these findings suggest the hypothesis that glutaminase-negative variants of L-ASP would provide lar
262 retion could be blocked by inhibiting either glutaminase or KV1.3 channels, which are known to be lin
263 epletion or pharmacologic inhibition of Rho, glutaminase, or fatty acid synthase abrogated the increa
265 te early gene c-fos) and phosphate activated glutaminase (PAG; the rate-limiting enzyme in the synthe
269 raction and enzymatic deamidation by protein-glutaminase (PG) on evening primrose seed cake (EPSC) pr
270 ture, glutamine deprivation or inhibition of glutaminase prevents EC proliferation, but does not prev
272 ty MCEM(2) to data from the endogenous mouse glutaminase promoter reveals nearly deterministic promot
273 understanding how this residue impacts the L-glutaminase property, kinetic analysis was coupled with
275 r inflammatory neurologic diseases displayed glutaminase reactivity, whereas normals and noninflammat
277 Binding of PRPP is required to activate the glutaminase site (termed interdomain signaling) to preve
278 ely accepted view that ammonia released in a glutaminase site is channeled efficiently into a separat
279 ase is that the transfer of ammonia from the glutaminase site occurs through the (beta/alpha)(8) core
280 or Gln hydrolysis, as is common in all other glutaminases: some Glu-AdT lack Cys, but all contain a c
285 S and PdxT appear to encode the synthase and glutaminase subunits, respectively, of a glutamine amido
287 iptional signature and tended to overexpress glutaminase, suggestive of a functional relationship bet
288 h in cells with IDH1 mutations by inhibiting glutaminase suggests a unique reprogramming of intermedi
289 ely, these results provide information about glutaminases that may aid in the design of isoform-speci
291 ects neutrophil function at rest and whether glutaminase, the major enzyme that metabolizes glutamine
294 The unique means by which Myc regulates glutaminase uncovers a previously unsuspected link betwe
295 with flow cytometry and confocal microscopy, glutaminase was shown to be present on the surface of hu
300 ism is catalysis by the mitochondrial enzyme glutaminase, with a specific isoform, glutaminase C (GAC