ライフサイエンスコーパス: glutaminase

1 GLS2 isoforms (glutaminase B and liver-type glutaminase).

2 thereby decreasing the flux through GDH and glutaminase.

3 t human airway epithelium could also express glutaminase.

4 s characterization of Glu-AdT as a Ser-based glutaminase.

5 an increased synthesis of the mitochondrial glutaminase.

6 r cell lines with differential expression of glutaminase.

7 MPS), strongly implicating the mitochondrial glutaminase.

8 ed through the pharmacological inhibition of glutaminase.

9 as 2 orders of magnitude higher than that of glutaminase.

10 metric assay for high-throughput analysis of glutaminases.

11 hat depriving ECs of glutamine or inhibiting glutaminase 1 (GLS1) caused vessel sprouting defects due

12 Glutaminase 1 (GLS1) inhibitors depleted pyrimidines and

13 he activity of pyruvate carboxylase (PC) and glutaminase 1 (GLS1), respectively.

14 tamine transporter ASCT2 and the activity of glutaminase 1 (GLS1).

15 analysis and in vitro experiments confirmed glutaminase 2 (GLS2) as a key gene associated with the f

16 Here, we identify glutaminase 2 (GLS2) as a previously uncharacterized p53

17 Additionally, we found that glutaminase 2 (GLS2), a modulator of p73-dependent antio

18 s, including two involved in metabolism:Gls2(glutaminase 2) and Sco2 We also show that human and mous

19 lly controls a key enzyme of glutaminolysis, glutaminase-2 (GLS-2).

20 o Glu-AdT, none of the ATP analogues induced glutaminase activation except ATP-gammaS, which stimulat

21 has long been the accepted mechanism for the glutaminase activation.

22 midotransferase, which produces ammonia in a glutaminase active site and channels it through a 30-A i

23 The N-terminal domain lacks the glutaminase active site found in AS-B, and an extended l

24 channel indicate that NaAD(+) stimulates the glutaminase active site in the k(cat) term by a synergis

25 The glutaminase active site is stimulated by NaAD(+) more th

26 Upregulation of the glutaminase active site occurs when these competitive in

27 (alphaS,5R) diastereomer were modeled in the glutaminase active site of GMPS and CPS to confirm that

28 structure of a ternary complex in which the glutaminase active site was inactivated by a glutamine a

29 eading from the effector binding site to the glutaminase active site, forming conserved communication

30 PS with a Michaelis-like intermediate in the glutaminase active site, the first covalent intermediate

31 ein-protein interface, and ultimately at the glutaminase active site.

32 lase domain to the substrate analogue in the glutaminase active site.

33 with engagement of a Ser nucleophile in the glutaminase active site.

34 uncoupling between ATP-gammaS hydrolysis and glutaminase activities suggests that the activation of g

35 were twofold greater and phosphate-activated glutaminase activities were fourfold greater in the schi

36 shows completely preserved asparaginase and glutaminase activities, long-term storage stability, imp

37 in part because of its dual asparaginase and glutaminase activities.

38 esence of Asp-tRNA(Asn) and ATP enhances the glutaminase activity about 22-fold.

39 e hydrolysis were examined: (a) an enzymatic glutaminase activity and (b) a non-enzymatic mechanism.

40 dues (Lys(52), Ser(128), Ser(152)) abolished glutaminase activity and consequently the amidotransfera

41 cells in vitro have biochemical evidence for glutaminase activity and express mRNA for two glutaminas

42 Pdx2 has been shown to have glutaminase activity and most likely channels ammonia to

43 Therefore, l-asparaginases with reduced l-glutaminase activity are predicted to be safer.

44 transfer reaction while fully activating the glutaminase activity at the hydrolase domain.

45 the synthase activity without inhibiting the glutaminase activity at the hydrolase domain.

46 e activities suggests that the activation of glutaminase activity by ATP or ATP-gammaS, together with

47 Although glutaminase activity decreases in the central ischemic a

48 e, interface mutations controlling secondary glutaminase activity demonstrated the importance of this

49 The glutaminase activity from damaged neurons is sufficient

50 ichia coli exhibits a basal PRPP-independent glutaminase activity having a kcat/Km that is 0.3% of fu

51 position 121 (WoA-P121) was found to have L-glutaminase activity in contrast to Uniprot entry P50286

52 enzymes and serves to explain the lack of L-glutaminase activity in the guinea pig enzyme.

53 ayed as PLP synthase, whereas PdxT exhibited glutaminase activity in vitro.

54 Glutaminase activity increased in response to acidic str

55 Glutaminase activity is impaired in the resting enzyme,

56 Here, we show that L-ASP's glutaminase activity is not always required for the enzy

57 re a common glutaminase domain for which the glutaminase activity is tightly regulated by an acceptor

58 d that this inhibition correlates with their glutaminase activity levels and produces a strong apopto

59 PurQ had a glutaminase activity of 0.002 s(-1), and smPurL had an a

60 NA(Gln) but not tRNA(Gln) could activate the glutaminase activity of GatD suggests that glutamine hyd

61 ibition of the Glu-tRNA(Gln)/ATP-independent glutaminase activity of Glu-AdT by gamma-Glu boronic aci

62 Those observations indicate that the glutaminase activity of L-ASP is necessary for anticance

63 However, Glu-tRNA(Gln) activates the glutaminase activity of the enzyme about 10-fold; additi

64 The essential glutaminase activity of the enzyme is a property of the

65 By diminishing the l-glutaminase activity of these highly active l-asparagina

66 Pharmacologic inhibition of glutaminase activity reduced tumor growth in both ephrin

67 In sum, significant mitochondrial glutaminase activity remains in the periphery of the isc

68 In analogy to the conditional glutaminase activity seen in IGPS and GMPS, the rates of

69 WoA-S121 was confirmed to have much lower L-glutaminase activity than WoA-P121, yet both showed comp

70 cceptor, Glu-tRNA(Gln), the enzyme has basal glutaminase activity that is unaffected by ATP.

71 ATP-gammaS stimulates the glutaminase activity to an extent similar to that with A

72 tivation except ATP-gammaS, which stimulates glutaminase activity to the same level as ATP, but witho

73 Despite an increase in transport, glutaminase activity was diminished and glutamine oxidat

74 le of the enzyme in neuronal injury in vivo, glutaminase activity was measured in central and periphe

75 generated through increased small intestinal glutaminase activity with concomitantly reduced intestin

76 ssay method that measures the stimulation of glutaminase activity, a K(d) of 2 microm was measured fo

77 glial activation), serum ammonia, intestinal glutaminase activity, and cecal glutamine content were c

78 ast, ATP and HCO(3)(-) did not stimulate the glutaminase activity, indicating that the interdomain li

79 BPTES inhibited glutaminase activity, lowered glutamate and alpha-KG lev

80 oxicity of L-ASP is thought to stem from its glutaminase activity, these findings suggest the hypothe

81 Y176F and Y176S exhibited greatly decreased glutaminase activity, whereas K288S/Y176F, a variant mut

82 d l-asparaginases also possess significant l-glutaminase activity, which correlates with many of the

83 Ser254(ErA), may correlate with significant glutaminase activity, while their substitution by Gln an

84 l-ase) is an anticancer agent also harboring glutaminase activity.

85 tructure has not been reported, contains the glutaminase activity.

86 raphy and apparently form a complex that has glutaminase activity.

87 tro, whereas the latter mutants retain basal glutaminase activity.

88 or their ability to stimulate tRNA-dependent glutaminase activity.

89 and Asn, respectively, may lead to minimal L-glutaminase activity.

90 mate are highly correlated with decreases in glutaminase activity.

91 nases have been related to their secondary L-glutaminase activity.

92 were attributed to increased RhoA-dependent glutaminase activity.

93 ng leads to elevated GLS gene expression and glutaminase activity.

94 asparaginase activity but shows undetectable glutaminase activity.

95 glutarate dehydrogenase, phosphate-activated glutaminase, alanine aminotransferase, aspartate aminotr

96 cle intermediate alpha-ketoglutarate through glutaminase and alanine aminotransferase is essential fo

97 An up-regulation of two key enzymes (glutaminase and alanine aminotransferase) provided a mec

98 -AT is proposed to channel ammonia between a glutaminase and AT domain.

99 With both mutants, the glutaminase and bicarbonate-dependent ATPase reactions h

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

102 Glutamine is converted to glutamate by glutaminase and further metabolized to alpha-KG.

103 High glucose inhibited both glutaminase and GDH flux, and leucine could not override

104 High glucose inhibited flux through both glutaminase and GDH, and leucine was unable to override

105 augmenting glutaminolysis through activating glutaminase and GDH.

106 ected replacement of Ser176 by Ala abolishes glutaminase and Gln-dependent transamidase activities of

107 in infected cells, as did the activities of glutaminase and glutamate dehydrogenase, the enzymes nee

108 Differences in phosphate-activated glutaminase and glutamic acid decarboxylase activities i

109 Greater phosphate-activated glutaminase and glutamic acid decarboxylase activities,

110 In IGP synthase the glutaminase and PRFAR binding sites are separated by 30

111 needed to (i) coordinate, albeit weakly, the glutaminase and synthetase activities of the enzyme and

112 nitoring of ATP or ATP-gammaS hydrolysis and glutaminase and transamidase activities reveals tight co

113 ree proteins: PurS (10 kDa), PurQ (25 kDa, a glutaminase), and smPurL (80 kDa, an AT).

114 extracellular glutamine by the mitochondrial glutaminase, and 2) the glutaminase in damaged neurons i

115 on of vascular endothelial growth factor and glutaminase, and is likely mediated by reduced expressio

116 tissue pH, inhibition of phosphate-activated glutaminase, and medication effects could not account fo

117 ns the ATP and FGAR binding sites, PurQ is a glutaminase, and the function of PurS is just now becomi

118 We found that the glutaminase ANK repeats form unique intramolecular conta

119 In conclusion, these findings support glutaminase as a potential component of the HAND pathoge

120 Pseudomonas 7A glutaminase-asparaginase (PGA) catalyzes the hydrolysis

121 Pseudomonas 7A glutaminase-asparaginase (PGA) catalyzes the hydrolysis

122 AC) for GLS, and the liver isoform (LGA) and glutaminase B (GAB) for GLS2.

123 ey-type glutaminase (KGA) and GLS2 isoforms (glutaminase B and liver-type glutaminase).

124 tifs employed in our interaction studies are glutaminase, beta-catenin and FAS.

125 ermobacter thermautotrophicus GatD acts as a glutaminase but only in the presence of both Glu-tRNA(Gl

126 pathways, including effective inhibition of glutaminase by nanoparticle drug delivery, holds promise

127 neous repression of pyruvate carboxylase and glutaminase by selecting all seed matches shared by thei

128 domain interface is proposed to activate the glutaminase by unblocking the oxyanion hole.

129 The mitochondrial enzyme glutaminase C (GAC) catalyzes the hydrolysis of glutamin

130 ve transcripts: the kidney isoform (KGA) and glutaminase C (GAC) for GLS, and the liver isoform (LGA)

131 Glutaminase C (GAC) is the GA isoform that is most abund

132 Here, we demonstrate that activated glutaminase C (GAC) self-assembles into a helical, fiber

133 enzyme glutaminase, with a specific isoform, glutaminase C (GAC), being highly expressed in cancer ce

134 ied splice variant of the gene gls, known as Glutaminase C (GAC), is important for tumor metabolism.

135 ppearance of the most active enzyme isoform, glutaminase C (GAC), which is expressed in many cancers,

136 tamate-generating enzyme glutaminase isoform glutaminase C in HIV-1-infected microglia.

137 The glutaminase C levels in the brain tissues of HIV dementi

138 zole-4-carboxamide ribonucleotide) activates glutaminase catalysis at a distance of 25 A from the glu

139 GLS2 encodes a mitochondrial glutaminase catalyzing the hydrolysis of glutamine to gl

140 Glutaminase converts glutamine to glutamate, which is fu

141 The glutaminase, CPS.A, and CPS.B homologs from A. aeolicus

142 mulated during the reaction catalyzed by the glutaminase-deficient mutants or by GatE alone.

143 nt determinants of glutamine anaplerosis and glutaminase dependence in cancer.

144 sition states during catalysis, and validate glutaminase-directed inhibition of Glu-AdT as a route fo

145 The amidotransferase or glutaminase domain (GLN domain) of mammalian carbamyl-ph

146 classes of Qns1 mutants that fall within the glutaminase domain and the synthetase domain selectively

147 tamylthioester intermediate was found in the glutaminase domain at Cys1135.

148 Analysis of enzymes with mutations in the glutaminase domain C-terminal helix and a 404-420 peptid

149 of the enzymes in this family share a common glutaminase domain for which the glutaminase activity is

150 lving these catalytic residues resembles the glutaminase domain of glucosamine 6-phosphate synthase,

151 osphorylation of this site may influence the glutaminase domain of hCTPS2.

152 neling of NH(3) from a site in an N-terminal glutaminase domain to a distal phosphoribosylpyrophospha

153 hannel through which ammonia passes from the glutaminase domain to the FGAM synthetase domain.

154 71-492) reported fluorescence changes in the glutaminase domain upon binding of PRPP and glutamine.

155 domain, the FGAM synthetase domain, and the glutaminase domain, with a putative ammonia channel loca

156 leotide synthetase (PurM) dimer, and a triad glutaminase domain.

157 de of the cyclase domain in signaling to the glutaminase domain.

158 luorescence reporter in key positions in the glutaminase domain.

159 d to activate the reaction at the N-terminal glutaminase domain.

160 , and ammonia usually produced by a separate glutaminase domain.

161 The HisH (glutaminase) domain of imidazole glycerol phosphate synt

162 lution, is organized as a hexamer, where the glutaminase domains adopt an inactive conformation.

163 s of the two complexes are superimposed, the glutaminase domains are rotated by about 180 degrees wit

164 Distinctions in the glutaminase domains of IGPS from E. coli, the bifunction

165 tilize glutamine and possess the appropriate glutaminase enzyme for metabolizing glutamine.

166 Significantly, an ultra-low l-glutaminase ErA variant maintained its cell killing abil

167 Correlation between glutaminase expression and axonal damage was confirmed e

168 Active MS lesions showed high-level glutaminase expression in macrophages and microglia in c

169 ncentrations partly as a result of decreased glutaminase expression.

170 asparaginase (WoA) has been reported to be L-glutaminase free, suggesting it would have fewer side ef

171 ally used) or Wolinella succinogenes (novel, glutaminase-free form).

172 of the frog enzyme, K258L, yields a gain of glutaminase function.

173 es of an oxyanion hole that are required for glutaminase function.

174 pH-responsive stabilization of the rat renal glutaminase (GA) mRNA during metabolic acidosis is media

175 of the 3'-nontranslated region of the renal glutaminase (GA) mRNA were tested for their ability to e

176 lism involves its conversion to glutamate by glutaminase (GA).

177 , we targeted the glutamate-recycling enzyme glutaminase (gene Gls1).

178 Humans have two glutaminase genes, GLS (GLS1) and GLS2, each of which ha

179 nd the ammonium-evolving periplasmic enzymes glutaminase (Ggt) and asparaginase (AsnB).

180 synthetase (CPSase) is comprised of a 40-kDa glutaminase (GLN) and a 120-kDa synthetase (CPS) subunit

181 nthesis requires the concerted action of the glutaminase (GLN) and carbamoyl-phosphate synthetase dom

182 High glutaminase (GLS) activity in TNBC tumors resulted in lo

183 ective enzymes producing glutamate and GABA, glutaminase (Gls) and glutamate decarboxylase 1 and 2 (G

184 tabolomic studies in GBM cells revealed that glutaminase (GLS) and glutamate levels are elevated foll

185 screen has revealed that the combination of glutaminase (GLS) and heat shock protein 90 (Hsp90) inhi

186 We identify glutaminase (GLS) as a critical enzyme for optimal adeno

187 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

189 ene JUN, is a key regulator of mitochondrial glutaminase (GLS) levels.

190 elective allosteric inhibitor of kidney-type glutaminase (GLS) that has served as a molecular probe t

191 o deamination reactions, the first requiring glutaminase (GLS) to generate glutamate and the second o

192 void microRNA-mediated repression, including glutaminase (GLS), a key metabolic enzyme for tumour pro

193 Silencing of glutaminase (GLS), which catalyzes the first step in glu

194 Glutaminase (GLS), which converts glutamine to glutamate

195 est whether recently developed inhibitors of glutaminase (GLS), which mediates an early step in Gln m

196 ration of cancer cells through up-regulating glutaminase (GLS).

197 yzed by GAC, a splice variant of kidney-type glutaminase (GLS).

198 tumor sensitivity to inhibitors of SIRT1 and glutaminase GLS1.

199 Interestingly, HMCLs expressed glutaminase (GLS1) and were sensitive to its inhibition,

200 ation modulated metabolic enzymes, including glutaminase (GLS1), to coordinate glutaminolysis and gly

201 atter with markers for glutamate production (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT

202 t strain, Ty21a-AR-Ss, by inserting Shigella glutaminase-glutamate decarboxylase systems coexpressed

203 the thioester intermediate formed during the glutaminase half-reaction by accessing the N-terminal ac

204 metabolism via pharmacological inhibition of glutaminase has been translated into clinical trials as

205 monstrate that, of the three major mammalian glutaminases identified to date, the lesser studied spli

206 Inactivation of the glutaminase in central areas of the ischemic lesion does

207 by the mitochondrial glutaminase, and 2) the glutaminase in damaged neurons is sufficient to cause ne

208 GP synthase shows a 4900-fold stimulation of glutaminase in the presence of the substrate acceptor PR

209 first demonstrated the existence of multiple glutaminases in mammals.

210 ssion of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 pro

211 on, whereas pharmacologic and siRNA-mediated glutaminase inhibition reduced 2HG levels.

212 the HypoxCR reporter in vivo, we found that glutaminase inhibition reduced tumor growth by specifica

213 evealed that surviving tumor cells following glutaminase inhibition were reliant on glycolysis and gl

214 Upon glutaminase inhibition with CB-839 or BPTES, the RCC cel

215 2-mutant lung tumors as likely to respond to glutaminase inhibition.

216 ckage of microglial glutamate synthesis by a glutaminase inhibitor abolished the neurotoxic activity,

217 subline that led directly to sensitivity to glutaminase inhibitor CB-839.

218 Treatment of cells with a glutaminase inhibitor phenocopies glutamine restriction,

219 In contrast, a glutaminase inhibitor reduced conversion of (13)C-pyruva

220 ls of liver enzymes in contrast to CB-839, a glutaminase inhibitor that is currently in clinical tria

221 As a result, glutamine deprivation or glutaminase inhibitor treatment triggers DNA damage accu

222 1,3,4-thiadiazol-2-yl)ethyl sulfide, a known glutaminase inhibitor, completely disrupted the higher o

223 BPTES), a selective but relatively insoluble glutaminase inhibitor, in nanoparticles.

224 igms will lead to new treatment options with glutaminase inhibitors and the utility of PET to identif

225 ents with ccRCC who are likely to respond to glutaminase inhibitors in the clinic.

226 Importantly, we show that glutaminase inhibitors, 6-Diazo-5-oxo-L-norleucine (DON)

227 at may aid in the design of isoform-specific glutaminase inhibitors.

228 Human glutaminase interacting protein (GIP), also known as tax

229 Glutaminase interacting protein (GIP), also known as Tax

230 YaaE shows similarity to HisH, a glutaminase involved in histidine biosynthesis.

231 The mitochondrial enzyme glutaminase is a significant contributor to extracellula

232 These data demonstrate that glutaminase is expressed and active in the human airway

233 rmat for high-throughput kinetic analysis of glutaminases is demonstrated for Escherichia coli carbam

234 catalyzing glutaminolysis, human kidney-type glutaminase isoform (KGA) is becoming an attractive targ

235 egulation of the glutamate-generating enzyme glutaminase isoform glutaminase C in HIV-1-infected micr

236 lutaminase activity and express mRNA for two glutaminase isoforms (KGA and GAC).

237 uman genes are known to encode at least four glutaminase isoforms.

238 d the activity levels of the three mammalian glutaminase isozymes was established, with GAC being the

239 eat-containing C termini of both kidney-type glutaminase (KGA) and GLS2 isoforms (glutaminase B and l

240 ng is confirmed by significant reductions in glutaminase kinetic activity and allosteric ligand bindi

241 siveness, and they were able to adjust their glutaminase level to suit glutamine availability.

242 This interdomain contact modulates the glutaminase loop containing the histidine and glutamic a

243 Western blots show no detectable change in glutaminase molecular weight or total immunoreactivity,

244 ce within the 3'-nontranslated region of the glutaminase mRNA binds a unique protein with high affini

245 art, by a cell-specific stabilization of the glutaminase mRNA that leads to an increased synthesis of

246 , these findings suggest the hypothesis that glutaminase-negative variants of L-ASP would provide lar

247 epletion or pharmacologic inhibition of Rho, glutaminase, or fatty acid synthase abrogated the increa

248 The brain/kidney phosphate-activated glutaminase (PAG), the product of the GLS1 gene, produce

249 te early gene c-fos) and phosphate activated glutaminase (PAG; the rate-limiting enzyme in the synthe

250 Analysis of the glutaminase partial reaction demonstrated that the hydro

251 y affect the bicarbonate-dependent ATPase or glutaminase partial reactions.

252 r was used to predict a docking site for the glutaminase partner, PdxT.

253 Flux through phosphate-dependent glutaminase (PDG) and [15N]urea synthesis were stimulate

254 e and its metabolism via phosphate-dependent glutaminase (PDG) to form U(m+1) and U(m+2) (urea contai

255 ng pyridoxine synthase (PDX1) and pyridoxine glutaminase (PDX2).

256 ture, glutamine deprivation or inhibition of glutaminase prevents EC proliferation, but does not prev

257 In renal tubular epithelium, glutaminase produces ammonia to buffer urinary acid excr

258 e an enzyme known as the phosphate-activated glutaminase produces glutamate for release as a neurotra

259 ty MCEM(2) to data from the endogenous mouse glutaminase promoter reveals nearly deterministic promot

260 understanding how this residue impacts the L-glutaminase property, kinetic analysis was coupled with

261 Glutaminase protein was expressed in the human airway in

262 For the glutaminase reaction catalyzed by AS-B at pH 8.0, substi

263 The glutaminase reaction that is catalyzed by the enzyme was

264 r inflammatory neurologic diseases displayed glutaminase reactivity, whereas normals and noninflammat

265 Inhibition of glutaminase reduced glutamate staining.

266 Using prokaryotic and eukaryotic glutaminase sequences, we built a phylogenetic tree whos

267 Binding of PRPP is required to activate the glutaminase site (termed interdomain signaling) to preve

268 ely accepted view that ammonia released in a glutaminase site is channeled efficiently into a separat

269 ase is that the transfer of ammonia from the glutaminase site occurs through the (beta/alpha)(8) core

270 zed to glutamate plus NH(3) at an N-terminal glutaminase site, and NH(3) is transferred through a 20-

271 or Gln hydrolysis, as is common in all other glutaminases: some Glu-AdT lack Cys, but all contain a c

272 In a novel finding using glutaminase-specific antibodies in combination with flow

273 Perfusion of the glutaminase substrate glutamine and the enzyme activator

274 rms a stable and functional complex with the glutaminase subunit (HisH) of an extant ImGP-S.

275 The glutaminase subunit is a glutamine amidotransferase that

276 The inclusion of the glutaminase subunit resulted in the formation of a 171-k

277 S and PdxT appear to encode the synthase and glutaminase subunits, respectively, of a glutamine amido

278 he intact enzyme includes 12 synthase and 12 glutaminase subunits.

279 iptional signature and tended to overexpress glutaminase, suggestive of a functional relationship bet

280 h in cells with IDH1 mutations by inhibiting glutaminase suggests a unique reprogramming of intermedi

281 ely, these results provide information about glutaminases that may aid in the design of isoform-speci

282 mbrane, breakdown of glutamine by the enzyme glutaminase (the first step in oxidation), glutamine and

283 EC-specific deletion in mice of glutaminase, the initial enzyme in glutamine catabolism,

284 ects neutrophil function at rest and whether glutaminase, the major enzyme that metabolizes glutamine

285 also immunoreactive for phosphate-activated glutaminase, the major source of neurotransmitter glutam

286 redness, drug prescriptions and tissue-Trans-Glutaminase (tTG) serum levels.

287 The unique means by which Myc regulates glutaminase uncovers a previously unsuspected link betwe

288 sure to 500 microM N-methyl-D-aspartate, the glutaminase was localized to fragments of damaged neuron

289 with flow cytometry and confocal microscopy, glutaminase was shown to be present on the surface of hu

290 When glutaminase was subsequently inhibited by siRNA or by a

291 The fluxes via GDH and glutaminase were measured by tracing 15N flux from [2-15

292 The ankyrin (ANK) repeats in the glutaminases were acquired early in their evolution.

293 Therefore, we inhibited glutaminase with siRNA or the small molecule inhibitor b

294 ism is catalysis by the mitochondrial enzyme glutaminase, with a specific isoform, glutaminase C (GAC