ライフサイエンスコーパス: glutamine

1 tyl-glutamic acid (NAAG) and their precursor glutamine.

2 t that does not contain millimolar levels of glutamine.

3 es condensation of ammonia with glutamate to glutamine.

4 arving the hexosamine pathway of glucose and glutamine.

5 ted T cells requires increased metabolism of glutamine.

6 carbon metabolism to promote utilization of glutamine.

7 fructose, and lower levels of potassium and glutamine.

8 cal nucleotide binding site 2 was mutated to glutamine.

9 ylation and degradation of GS in response to glutamine.

10 a-conglycinin and glycinin fragments rich in glutamine.

11 human ataxin-3 protein containing either 23 glutamines (23Q, wild-type) or 84Q (MJD-causing) within

12 SNAT7 is the primary permeation pathway for glutamine across the lysosomal membrane and it is requir

13 an interpretation of the Warburg effect and glutamine addiction as features of a growth state that p

14 Driven by oncogenic signaling, glutamine addiction exhibited by cancer cells often lead

15 73 isoform TAp73 as a crucial factor causing glutamine addiction in aggressive medulloblastomas.

16 or viral replication, and, importantly, that glutamine addiction is a hallmark of tumor cells.

17 can be converted into an MPnS by mutation of glutamine-adjacent residues, identifying the molecular r

18 ence of PD fluid supplementation with alanyl-glutamine (AlaGln) in 6 patients in an open-label, rando

19 ne, methionine, phenylalanine, valine, GABA, glutamine, alanine, glycine and taurine were separated a

20 Both DMG and glutamine alone elicited GLP-1 secretion in GLUTag cells

21 Mice treated with glutamine also had higher numbers of HSV-specific IFN-ga

22 aracterization of over 30 cognate and hybrid glutamine amidotransferase complexes in combination with

23 tP search of GenBank sequences revealed five glutamine amidotransferase-QueC homologs in Enterobacter

24 , we investigated the anti-tumor effect of a glutamine analog (6-diazo-5-oxo-L-norleucine) as an adju

25 tabolism, defining important determinants of glutamine anaplerosis and glutaminase dependence in canc

26 glutamine catabolism and reduced reliance on glutamine anaplerosis compared to cells cultured in stan

27 However, some cell lines that depend on glutamine anaplerosis in culture rely less on glutamine

28 in type 1 conditions (Th1) were regulated by glutamine and alpha-ketoglutarate (alphaKG)-induced even

29 ings reveal a novel link between endothelial glutamine and asparagine metabolism in vessel sprouting.

30 a lysosomal transporter highly selective for glutamine and asparagine.

31 mpaired EC sprouting even in the presence of glutamine and asparagine.

32 The combined glutamate and glutamine and choline showed no changes in drug-off or d

33 percentage of (13)C enrichment of glutamate, glutamine and GABA (gamma-aminobutyric acid).

34 andomly mutated cells simulated at different glutamine and glucose uptake rates.

35 g is mediated by Idh1 and Fasn, supported by glutamine and HIF-2alpha increments.

36 However, l-glutamine and l-alanine model reactions showed the same

37 ing aqueous d-glucose model reactions with l-glutamine and l-alanine yielded similar colored solution

38 s to formation of an isopeptide bond between glutamine and lysine residues found on the surface of pr

39 ble damage product formed spontaneously from glutamine and other sources.

40 Metabolism of glutamine and related analogs by GDH in the L cell may e

41 The three primary uptake pathways, glucose, glutamine and serine, are each characterized by three fe

42 rsity of biosynthetic and regulatory uses of glutamine and their role in proliferation, stress resist

43 MM cells are reliant on glucose and glutamine and withdrawal of either nutrient is associate

44 quickly and directly with glutamic acid and glutamine, and further with peptides, in A. thaliana cel

45 Glutamate, glutamine, and GABA were measured cortically and subcort

46 his hypothesis by measuring GABA, glutamate, glutamine, and the sum of glutamine plus glutamate conce

47 d whether altered levels of GABA, glutamate, glutamine, and the sum of glutamine plus glutamate refle

48 mprising the N17 domain, a polyQ tract of 17 glutamines, and a short hexameric polyProline region tha

49 The glutamine antagonist 6-diazo-5-oxo-l-norleucine (DON, 14

50 granule cell activation could be restored by glutamine application, implicating compromised GABA synt

51 thylated derivatives of lysine, arginine and glutamine are readily accessible.

52 Many mammalian cancer cell lines depend on glutamine as a major tri-carboxylic acid (TCA) cycle ana

53 ine for cataplerotic processes; the need for glutamine as a nitrogen source for generation of biomass

54 th (13)C stable isotope-labelled glucose and glutamine as metabolic tracers, we probed the phenotypic

55 Many prion-forming proteins contain glutamine/asparagine (Q/N) rich domains, and there are c

56 nine at 156) and baleen whales or Mysticeti (glutamine at 156).

57 An amino acid substitution, lysine to glutamine, at position 166 (H3 numbering) in the major a

58 eas an uncommon betaine, valine betaine, and glutamine betaine were present only in flours of barley,

59 Valine betaine and glutamine betaine, the latter never reported before in p

60 also exhibited increased serine/glycine and glutamine biosynthesis.

61 The dependence of glutamine-bound ammonia disposal to urea on the rate of

62 ng stable isotopes, we show that disposal of glutamine-bound ammonia to urea (through mitochondrial g

63 that normal mammary epithelial cells consume glutamine, but do not secrete glutamate.

64 Glutamine can also generate aspartate, the carbon source

65 vailable to cells in vivo, exhibit decreased glutamine catabolism and reduced reliance on glutamine a

66 cluding that in pericentral hepatocytes) and glutamine catabolism in (periportal) hepatocytes represe

67 The first step in glutamine catabolism is catalysis by the mitochondrial e

68 ndii depends on cooperativity of glucose and glutamine catabolism to meet biosynthetic demands.

69 lutamine anaplerosis in culture rely less on glutamine catabolism to proliferate in vivo.

70 ine, is necessary and sufficient to increase glutamine catabolism, defining important determinants of

71 n mice of glutaminase, the initial enzyme in glutamine catabolism, markedly blunts angiogenesis.

72 Without glutamine catabolism, there is near complete loss of TCA

73 taminolysis, markedly increasing glucose and glutamine catabolism.

74 Rather, lower subiculum volumes and glutamine concentrations correlated with impaired verbal

75 in [4-(13)C]glutamate but unaltered [4-(13)C]glutamine concentrations in the VMH of RH animals.

76 o cancer cell survival and adaptation to low-glutamine conditions.

77 The structures of glutamate and glutamine conjugates were confirmed using synthesized st

78 ells, as well as a metabolic switch favoring glutamine consumption through IGF1 receptor (IGF1R) acti

79 tumor cells often experience, the effect of glutamine deficiency on cellular responses to DNA damage

80 Here, we show that glutamine deficiency, through the reduction of alpha-ket

81 Further, we show that cystine levels dictate glutamine dependence via the cystine/glutamate antiporte

82 Our data suggest that HCV establishes glutamine dependence, which is required for viral replic

83 peutic targets in cancer subtypes exhibiting glutamine dependency.

84 aired respiratory capacity while providing a glutamine-dependent cell survival advantage, strongly su

85 e activity of a branched TCA cycle, in which glutamine-dependent reductive carboxylation cooperates t

86 Importantly, the results that glutamine-dependent survival and sensitivity to ER stres

87 These findings raise the possibility that glutamine depletion can be used as an adjuvant treatment

88 ibited by cancer cells often leads to severe glutamine depletion in solid tumors.

89 Here, we demonstrate that glutamine deprivation and hypoxia result in inhibition o

90 ed mutp53 promotes cancer cell survival upon glutamine deprivation both in vitro and in vivo.

91 As a result, glutamine deprivation or glutaminase inhibitor treatment

92 In cell culture, glutamine deprivation or inhibition of glutaminase preve

93 essing mutp53 proteins are more resistant to glutamine deprivation than cells with wild-type p53.

94 er-transactivate p53-target gene CDKN1A upon glutamine deprivation, thus triggering cell cycle arrest

95 Beclin1 S30 phosphorylation are required for glutamine deprivation- and hypoxia-induced autophagy and

96 3 in p53 null cells results in resistance to glutamine deprivation.

97 errations and proliferation defect caused by glutamine deprivation.

98 Asparagine further proved crucial in glutamine-deprived ECs to restore protein synthesis, sup

99 e apply this assay to quantitatively measure glutamine-derived ammonia in lung cancer cell lines with

100 onditional mutant revealed defective flux of glutamine-derived carbon into RNA-bound ribose sugar as

101 asparagine synthetase (ASNS, which converts glutamine-derived nitrogen and aspartate to asparagine)

102 mine uptake doubled, but ATP production from glutamine did not significantly change.

103 rexpression of a membrane-localized protein (GLUTAMINE DUMPER 1 (GDU1)) that requires a ubiquitin lig

104 w concentrations of peritoneal extracellular glutamine during PD may contribute to this immune defici

105 red for growth of cancer cells in a low free-glutamine environment, when macropinocytosis and lysosom

106 s a neurodegenerative disease caused by poly-glutamine expansion in the Htt protein, resulting in Htt

107 duced increase in hippocampal Glx (glutamate+glutamine; F=3.76; P=0.04), a decrease in fronto-tempora

108 Cancer cells increase glucose and glutamine flux to provide energy needs and macromolecula

109 rences that cause differential dependence on glutamine for anaplerosis.

110 these data outline the dependence of ECs on glutamine for cataplerotic processes; the need for gluta

111 ne biosynthetic pathway requires glucose and glutamine for de novo synthesis of UDP-GlcNAc, a sugar-n

112 al cell carcinoma (ccRCC), require exogenous glutamine for growth and exhibit reprogrammed glutamine

113 e-negative breast cancers (TNBC), to utilize glutamine for survival and growth.

114 The H85Q mutant substitutes a glutamine found in several peroxygenases that favor fatt

115 This PrD is unique in size and composition: glutamine free, asparagine rich, and the smallest define

116 in metabolism by catalyzing the synthesis of glutamine from glutamate and ammonia.

117 anterior cingulate (AC) glutamate (Glu) and glutamine (Gln) and arterial spin labeling evaluation fo

118 red to normal cells, including dependence on glutamine (GLN) for survival, known as GLN addiction.

119 ber of adaptations including a non-canonical glutamine (Gln) metabolic pathway and that inhibition of

120 dditional genes, ybaS and ybaT, which confer glutamine (Gln)-dependent acid tolerance and contribute

121 le nucleotide polymorphism substitution from glutamine (Gln, Q) to arginine (Arg, R) at codon 460 of

122 2 in Tsc2-null cells decreased intracellular glutamine, glutamate, and glutathione (GSH).

123 ich have been suggested as being involved in glutamine/glutamate and GABA cycles of metabolism in exc

124 The glutamine/glutamate increase in the pgACC caused by keta

125 the improvement is mirrored by the change of glutamine/glutamate ratio and if such effects show a reg

126 Post-hoc analyses revealed that the glutamine/glutamate ratio increased significantly in the

127 ime, region, and treatment was found for the glutamine/glutamate ratios (placebo, n=14; ketamine, n=1

128 ignificant temporal and regional response in glutamine/glutamate ratios to a single subanesthetic dos

129 olateral prefrontal cortex (DLPFC) glutamate+glutamine (Glx) were measured using a clinician-administ

130 of the combined resonances of glutamate and glutamine (Glx), were measured by 1H MRS in the left dor

131 Glutamine had no effect on granule cell activation earli

132 Reliance on glutamine has long been considered a hallmark of cancer

133 Polar residues (tyrosine and glutamine) have been previously demonstrated to be criti

134 licited similar alterations in metabolism as glutamine in both cell lines.

135 Thus the requirements for glutamine in cancer are overall highly heterogeneous.

136 hysiology collectively influence the role of glutamine in cancer.

137 omass; and the distinct roles of glucose and glutamine in EC biology.

138 In vivo infusion of (15)N-glutamine in obese mouse models of PDA demonstrates enha

139 A constant amount of asparagine and glutamine in palm olein and soy bean oils was heated up

140 Not only are the levels of glutamine in standard tissue culture media at least ten-

141 study of ketamine, we measured glutamate and glutamine in the pregenual ACC (pgACC) and the anterior

142 A glutamine in the selectivity filter may be an important

143 accounts for the differential dependence on glutamine in these different environmental contexts.

144 e is ample evidence of an essential role for glutamine in tumors and that a variety of factors, inclu

145 Withdrawal of glucose or glutamine induced G1 and G2/M arrest without increasing

146 In addition, low glutamine-induced DNA damage is abolished in ALKBH defic

147 sformed cell line we experimentally assessed glutamine-induced metabolic changes.

148 eta-oxidation and the likely re-directing of glutamine into biosynthetic rather than energy-generatin

149 acid transporter 1 (SNAT1), which transports glutamine into neurons, was also upregulated.

150 ith calmodulin via its N-terminal isoleucine-glutamine (IQ) motif.

151 iscover that it has an unusual 2-histidine-1-glutamine iron-coordinating triad.

152 Despite the fact that glutamine is a nonessential amino acid that can be synth

153 Although the amino acid glutamine is a potent elicitor of GLP-1 secretion, the r

154 Glutamine is a significant source of energy for cells an

155 ten-fold higher than other amino acids, but glutamine is also the most abundant amino acid in the hu

156 ion in which the alpha amino group of mono-l-glutamine is covalently linked to the side chain of glut

157 Q237N, Q328N, and Q366N demonstrated that no glutamine is dependent on another to react first in the

158 oliferation and manage oxidative stress, yet glutamine is often depleted at tumor sites owing to exce

159 th alanine (K265A), glutamic acid (K265E) or glutamine (K265Q), and the functional and kinetic proper

160 Site directed mutagenesis of lysine 68 to glutamine (K68Q), mimicking acetylation, decreased MnSOD

161 that this newly discovered enzyme be named l-glutamine kinase.

162 When Glu(73) was mutated to a glutamine, KK174 no longer photolabeled this residue, bu

163 mouse mitochondrial IDH2), we used lysine-to-glutamine (KQ) mutants to mimic acetylated lysines and s

164 of metastatic cells to utilize extracellular glutamine, leading to cytosolic accumulation of NADH and

165 abolite concentrations, most showing reduced glutamine levels (62.5%).

166 ofibroblasts compared with controls, whereas glutamine levels were decreased, suggesting enhanced glu

167 tivity with concomitantly reduced intestinal glutamine levels.

168 and Glx (combined estimate of glutamate and glutamine) levels using magnetic resonance spectroscopy.

169 isms that cells utilize in order to adapt to glutamine limitation.

170 intermediates exceeds that of glucose, with glutamine making a larger contribution than lactate in p

171 g experiments with the alga showed that host glutamine may be utilized by the algal endosymbiont as a

172 Thus, glutamine may enhance the IFN-gamma-associated immune re

173 We demonstrate that disruption of glutamine metabolic pathways improves the efficacy of ge

174 e downregulated in response to disruption of glutamine metabolic pathways.

175 at SIRT1 dose-dependently regulates cellular glutamine metabolism and apoptosis, which in turn differ

176 Herein we demonstrate that DON inhibits glutamine metabolism and provides antitumor efficacy in

177 promotes antioxidant defence, it antagonizes glutamine metabolism and restricts nutrient flexibility.

178 of Sirt1 induces c-Myc expression, enhancing glutamine metabolism and subsequent proliferation, autop

179 Together, the crosstalk between glutamine metabolism and the DNA repair pathway identifi

180 We finally show that inhibiting glutamine metabolism attenuates HCV infection and the ox

181 ons both for basic science and for targeting glutamine metabolism in cancer therapy.

182 ed for further clarifications on the role of glutamine metabolism in cancer.

183 Inhibition of glutamine metabolism in ECs did not cause energy distres

184 tor of angiogenesis, but the precise role of glutamine metabolism in ECs is unknown.

185 Glutamine metabolism in endothelial cells (ECs) has been

186 is well-established, but the involvement of glutamine metabolism in invasive processes is yet to be

187 tions and (13)C tracing approaches to define glutamine metabolism in these cells.

188 ates the transcript levels of key enzymes of glutamine metabolism in vitro and in liver biopsies of c

189 With the recent renewed understanding of glutamine metabolism involvement in drug resistance and

190 ark of human cancers, and the glycolytic and glutamine metabolism pathways were shown to be deregulat

191 Reductive glutamine metabolism was highly dependent on cytosolic i

192 inhibitors of metabolism (e.g., glycolysis, glutamine metabolism, and fatty acid oxidation) can regu

193 on of D-2HG and reactive oxygen, a reductive glutamine metabolism, and modifications of the epigeneti

194 lutamine for growth and exhibit reprogrammed glutamine metabolism, at least in part due to the glutat

195 has been associated with altered glucose and glutamine metabolism.

196 ng glycolysis, mitochondrial respiration and glutamine metabolism.

197 s accompanied by changes in both glucose and glutamine metabolism.

198 l growth and proliferation via regulation of glutamine metabolism.

199 ermine absolute concentrations of glutamate, glutamine, myo-inositol, NAA, creatine and choline.

200 ites containing trimethylamine oxide (TMAO), glutamine, N-acetyl-glycoproteins, citrate, tyrosine, ph

201 and carbon substrates (a mix of substrates, glutamine, N-acetylglucosamine, or pyruvate) revealed co

202 e for alanine or more conservative residues, glutamine or asparagine, in the GERAMT-binding site.

203 Here, we show that depriving ECs of glutamine or inhibiting glutaminase 1 (GLS1) caused vess

204 asparagine residues to structurally similar glutamines or alanines.

205 Glutamine (or acetylated lysine) was neutral and thus ca

206 At high utilization rates of glutamine, oxidative utilization of glucose was decrease

207 hich the RR motif was replaced with a lysine-glutamine pair.

208 uding acetate and the amino acids glutamate, glutamine, phenylalanine and tyrosine.

209 The l-glutamine-phosphate product was characterized using (31)

210 Glutamine plays a significant role in local synthesis of

211 g GABA, glutamate, glutamine, and the sum of glutamine plus glutamate concentrations in vivo in patie

212 f GABA, glutamate, glutamine, and the sum of glutamine plus glutamate reflect genetic vulnerability t

213 vity in TNBC tumors resulted in low cellular glutamine pool size assayed via high-resolution (1)H mag

214 nclusion, [(18)F]4F-Gln PET tracked cellular glutamine pool size in breast cancers with differential

215 GLS inhibition significantly increased glutamine pool size in TNBC tumors.

216 activity and detected increases in cellular glutamine pool size induced by GLS inhibitors.

217 ive correlation between T/B values and tumor glutamine pool size measured using MRS (r(2) = 0.71).

218 pared with TNBC, displayed a larger baseline glutamine pool size that did not change as much in respo

219 [(18)F]4F-Gln) PET to measure tumor cellular glutamine pool size, whose change might reveal the pharm

220 (18)F]4F-Gln PET images matched the distinct glutamine pool sizes of both tumor models at baseline.

221 six amino acids namely (alanine, asparagine, glutamine, proline, serine and valine) for Sudanese food

222 Mechanistically, glutamine provided nitrogen for asparagine synthesis to

223 ity of oxidizing specific substrates, namely glutamine, pyruvate, glucose, or palmitate, in mitochond

224 on the "conditionally essential" amino acid glutamine (Q) as an anaplerotic carbon source for TCA cy

225 ation that substituted glutamic acid (E) for glutamine (Q) at amino acid position 623 (E623Q) display

226 s a codon, replacing the genomically encoded glutamine (Q) with arginine (R); thus this editing site

227 17), an amyloidogenic segment of consecutive glutamines (QN), and a proline-rich segment.

228 ere, we found that supplementation with oral glutamine reduced virus reactivation in latently HSV-1-i

229 NAT7 may, thus, represent a novel target for glutamine-related anticancer therapies.

230 Reduced cortical glutamine relative to healthy control subjects was obser

231 pores, but mutating these glutamic acids to glutamines rendered the toxin pH-insensitive.

232 nvolved the gain or loss of an asparagine or glutamine residue.

233 rough mutational analysis, we identified two glutamine residues and a beta-hairpin within this putati

234 Above a threshold of 37 glutamine residues, htt(e1) starts to aggregate in a nuc

235 Their findings pave the way for the use of glutamine restriction as an adjuvant treatment for TAp73

236 ed an increase in survival time in mice on a glutamine restriction diet.

237 r nutrient signaling, and the histidine- and glutamine-rich domain of TCP20, which is conserved acros

238 is mainly due to the "glue-like" behavior of glutamine's side chains with significantly more side cha

239 Glutamine serves, with alanine, as a major nontoxic inte

240 Mutation of E73 to either alanine or glutamine severely reduces oligomerization, demonstratin

241 The orientation of the glutamine side chains also tend to be "buried" inside, e

242 Notably, glutamine starvation has a synergistic effect with cispl

243 Glutamine starvation rendered tumour cells more resistan

244 bitor-induced DNA damage and reversal of the glutamine starvation restored the sensitivity of tumour

245 However, glutamine substitution did not substantially change thes

246 Here, we report that glutamine substitutions of these residues, which preserv

247 We show that glutamine supplementation is not sufficient to prevent l

248 Glutamine supplies the majority of carbons in the tricyc

249 nt things about the significance of external glutamine supply for mammalian cell growth and prolifera

250 phosphate synthetase) depends on the rate of glutamine synthesis and increases from approximately 7%

251 Glutamine synthesis in the periphery (including that in

252 synthesis suggests that enhancing peripheral glutamine synthesis is a promising strategy to treat hyp

253 ound ammonia disposal to urea on the rate of glutamine synthesis suggests that enhancing peripheral g

254 g a number of regulators, genes required for glutamine synthesis, NADH/NAD(P)H metabolism, as well as

255 ause total urea synthesis does not depend on glutamine synthesis, we hypothesize that glutamate dehyd

256 ate amino acid degradation, ureagenesis, and glutamine synthesis.

257 toxification of ammonium via ureagenesis and glutamine synthesis.

258 Glutamine synthetase (GS) catalyzes condensation of ammo

259 ere correlated with changes in expression in glutamine synthetase (GS) in astrocyte-like glia and in

260 Glutamine synthetase (GS) plays an essential role in met

261 d up-regulation of beta-catenin targets like glutamine synthetase (GS), leukocyte cell-derived chemot

262 hydrolyzing carboxylate-amine ligases of the glutamine synthetase type.

263 tion of several transcripts, including XDH1, glutamine synthetase, alanine aminotransferase, catalase

264 The model predicts the responses of glutamine synthetase, GlnB, and GlnK under time-varying

265 pression of glial fibrillary acidic protein, glutamine synthetase, glutamate transporter 1 (GLT1), aq

266 how they conjointly modulate the activity of glutamine synthetase, the key enzyme for nitrogen assimi

267 ill for HTT exon 1 fragments having 20 or 30 glutamines, the aggregation landscape for fragments with

268 at proposed phospholipid-binding sites with glutamines, the two sites have been identified.

269 , leads to increased dependency on exogenous glutamine through increased consumption of glutamate for

270 1 generates malate with carbons derived from glutamine, thus enabling utilization of glucose carbons

271 ine synthetase (ASNS) converts aspartate and glutamine to asparagine and glutamate in an ATP-dependen

272 lic pathways are used to convert glucose and glutamine to balanced energy and biomass production, we

273 ippel-Lindau (VHL) tumor suppressor gene use glutamine to generate citrate and lipids through reducti

274 utamate level (P = .05), and higher ratio of glutamine to glutamate (P = .003).

275 ures of invasive breast cancer cells convert glutamine to glutamate which is released from the cell t

276 ove normal, probably due to the breakdown of glutamine to glutamate.

277 For rat Glut5, a change of glutamine to glutamic acid at codon 166 (p.Q166E) has be

278 Due to a fast occurring cyclization of l-glutamine to pyroglutamic acid, the typical amino-carbon

279 Cancer cells depend on glutamine to sustain their increased proliferation and m

280 gtin (HTT) gene, translating to an elongated glutamine tract in the huntingtin protein.

281 p62 positively regulated the glutamine transporter Slc1a5 and increased glutamine upt

282 eminal ganglia from latently HSV-1-infected, glutamine-treated WT mice showed upregulation of several

283 Under euglycemic conditions glutamine uptake doubled, but ATP production from glutam

284 ar surface competition assay for quantifying glutamine uptake from single cells.

285 e glutamine transporter Slc1a5 and increased glutamine uptake in Tsc2-null cells.

286 Consistently, HCV infection increases glutamine use and dependence.

287 ate from glucose (Warburg effect), extensive glutamine utilization and impaired mitochondrial electro

288 theory that metastatic progression increases glutamine utilization and the inhibition of glutaminolys

289 Aerobic glycolysis and enhanced reliance on glutamine utilization are prime examples of such rewirin

290 een these two cell lines, we found increased glutamine utilization in the metastatic PC3M subline tha

291 reased, while the production of lactate from glutamine was enhanced.

292 In contrast to WT mice, supplemental glutamine was ineffective in reducing the rate of HSV-1

293 All starved cells could oxidize exogenous glutamine, whereas the capacity for oxidizing palmitate

294 cer cells preferentially utilize glucose and glutamine, which provide macromolecules and antioxidants

295 re partially rescued by supplementation with glutamine, which requires CARD11 for import into T cells

296 the proliferating cancer cells' appetite for glutamine-which goes far beyond satisfying their protein

297 PEPCKmt in linking catabolism of glucose and glutamine with anabolic pathways.

298 t phosphorylation of the amide nitrogen of l-glutamine with ATP by the catalytic activity of Cj1418.

299 Glucose or glutamine withdrawal resulted in a 5- to 10-fold protect

300 lymphoma cells leads to cell sensitivity to glutamine withdrawal, whereas expression of mutp53 in p5