ライフサイエンスコーパス: glutamine

1 spectrometric quantification of brain tissue glutamine.

2 the proliferation of tumor cells reliant on glutamine.

3 render colorectal cancers more dependent on glutamine.

4 tamine synthase, converting glutamic acid to glutamine.

5 arburg's effects on other nutrients, such as glutamine.

6 and menhaden oils heated in the presence of glutamine.

7 o the latter by a combination of cystine and glutamine.

8 ed by flux studies with isotopically labeled glutamine.

9 ly toxic ammonia to the valuable amino acid, glutamine.

10 metabolism from production to consumption of glutamine.

11 ct between alanine 53 of alpha-synuclein and glutamine 111 in the catalytic pocket of CypA.

12 Glutamine-148->histidine (Q148H) and glycine-140->serine

13 We found that histone H3 glutamine 5 dopaminylation (H3Q5dop) plays a critical ro

14 ystem responses to aaRS depletion, the yeast glutamine aaRS gene (GLN4) was transcriptionally regulat

15 In contrast, glutamine activates mTORC1 through a Rag GTPase-independ

16 Our integrative approach thus links glutamine addiction to glutamate excretion in cancer and

17 e to heat shock or in the presence of a poly-glutamine aggregation protein cell-based model of Huntin

18 Conversely, L-glutamine, agmatine, and uridine 5-monophosphate are pro

19 incipal component analysis, we observed that glutamine, alanine, glutathione, and lactate were positi

20 It was demonstrated that glutamine amide 1 could select an optimal aldehyde compo

21 A simple self-assembling glutamine amide derivative 1 was initially found to cata

22 trogen status modulates phosphorylation when glutamine, an abundant amino acid when nitrogen is avail

23 utamine-utilizing enzyme by a small molecule glutamine analog (6-diazo-5-oxo-l-norleucine [DON]).

24 centas, reduced initial rate uptake of (14)C-glutamine and (14)C-glutamate (per mg placental protein)

25 spartic acid/asparagine (Asx), glutamic acid/glutamine and alanine are positively correlated with sea

26 subjects, CHR individuals had high glutamate/glutamine and elevated focal cerebral blood volume on fu

27 d fibroblasts migrate and invade toward free glutamine and facilitate invasion of tumor epithelial ce

28 tabolomics would identify increased glucose, glutamine and fatty acid uptake and utilization in human

29 In TGF-beta-treated PASMCs, glucose, glutamine and fatty acids all contributed carbons to the

30 FXR deficiency increased the contribution of glutamine and fatty acids toward respiration and enhance

31 g activation of AMPK, the PPP, and reductive glutamine and folate metabolism.

32 ne-fructose amidotransferase 1 (GFAT1), uses glutamine and fructose 6-phosphate to eventually synthes

33 n levels and reportedly depends on exogenous glutamine and GLS activity for survival.

34 d cell viability in MDV-infected cells, both glutamine and glucose were required for virus replicatio

35 The amino acids glutamine and glutamate are essential for normal placent

36 hat FGR is associated with reduced placental glutamine and glutamate transporter activity and express

37 ort our hypothesis and suggest that abnormal glutamine and glutamate transporter activity is part of

38 ro exposure to rapamycin inhibited placental glutamine and glutamate uptake (24 h, uncomplicated preg

39 and, unexpectedly, little glucose; secreted glutamine and other nitrogen-rich amino acids, indicatin

40 Lyso.PC.a.C18.0, PC.ae.C34.2, C3.DC..C4.OH, glutamine and SM.C16.1, being the most significant metab

41 MRS) to measure glutamate (Glx = glutamate + glutamine) and GABA+ (GABA + macromolecules) levels in 3

42 oxygenase for hydroxylation of the C3 of the glutamine, and a thioesterase.

43 Targeted metabolites (e.g., lactate, glutamine, and citrate) were mapped to pathways of glyco

44 ntose shunt flux, increased anaplerosis from glutamine, and decreased fatty acid beta-oxidation.

45 drial respiration, feed the Krebs cycle with glutamine, and favor the accumulation of oxaloacetate in

46 (glucose uptake, and intracellular- lactate, glutamine, and glutamate).

47 een the levels of ATP, ADP, 2-OG, PII-sensed glutamine, and NAD(+), representing a metabolic hub that

48 amma-glutamylalanine, gamma-glutamylglycine, glutamine, and pyridoxate) identified treatment response

49 lerant of spectating tryptophan, asparagine, glutamine, and threonine residues.

50 n tracing analyses (U-(13)C-glucose, U-(13)C-glutamine, and U-(13)C-palmitic acid) demonstrated enhan

51 5) substituted derivatives did not methylate glutamine (another potentially methylated amino acid).

52 sue of the JCI, Sharma et al. employ a broad glutamine antagonist, 6-diazo-5-oxo-l-norleucine (DON),

53 ntext dependent, but (13)C-glucose and (13)C-glutamine are often applied because they feed a large nu

54 ts motivate further in vivo investigation of glutamine as a biomarker for tumor progression and treat

55 NAD(+) Some members of the NadE family use l-glutamine as a nitrogen donor and are named NadE(Gln) Pr

56 human glioma samples and explore the use of glutamine as a potential biomarker.

57 inflammation, can lead to an upregulation of glutamine as an energy source for cancer cells.

58 Like glutamine, asparagine signals to mTORC1 through Arf1 in

59 Many cancer cells consume glutamine at high rates; counterintuitively, they simult

60 s 125 (A125T) and 151 (A151T) and leucine to glutamine at residue 217 (L217Q) in the hemagglutinin (H

61 Mechanistically, decreased glutamine availability attenuated S-glutathionylation of

62 encoding transcripts serve as key sensors of glutamine availability in mammalian cells.

63 alpha)-independent manner, thereby promoting glutamine-based anaplerosis.

64 Comparison of glutamine binding in the presence or absence of the BPTE

65 ide competed with the substrate peptide, and glutamine bound in the active site, but too far away fro

66 ated by MDV-infected cells in vitro Although glutamine, but not glucose, deprivation significantly re

67 or glutamate, we revealed that ammonium and glutamine, but not glutamate promote the growth of S. au

68 Deprivation of glutamine by glutamine-withdrawal, GLS knockdown, or exp

69 In hyperoxia, anaplerotic catabolism of glutamine by Muller cells increased ammonium release two

70 The elevated consumption of glutamine can lead to intratumoral nutrient depletion, c

71 This suggests that besides ammonium also glutamine can serve as a nitrogen source under these con

72 tion to stimulating the entry of glucose and glutamine carbon into the TCA cycle, TGFbeta induced the

73 g the mitochondrial oxidation of glucose and glutamine carbons to support the bioenergetic demand of

74 nduced increase in mitochondrial glucose and glutamine catabolism from generating damaging reactive o

75 d elevated levels of metabolites involved in glutamine catabolism, such as glutamic acid, alanine, gl

76 ables and a singular response variable, e.g. glutamine chromatogram area, was developed by statistica

77 consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells

78 isual glutathione-glutamate component; and a glutamine component.

79 s also invaded a Matrigel matrix following a glutamine concentration gradient and enhanced the invasi

80 AlsT and hence likely a higher intracellular glutamine concentration inhibited c-di-AMP production, w

81 through RelA-SpoT homolog enzymes, detecting glutamine concentration using a nitrogen phosphotransfer

82 Glutamine concentrations across the three voxels were si

83 We measured glutathione, glutamate and glutamine concentrations in the anterior cingulate corte

84 nts: n = 22), we also measured glutamate and glutamine concentrations in the left putamen using ultra

85 toward this amino acid when cultured in low glutamine conditions.

86 Glutamine consumption has been linked to replenishment o

87 cle in Muller cells accompanied by increased glutamine consumption in response to hyperoxia.

88 ethyl sulfide (BPTES), which curtails cells' glutamine consumption, may inhibit HNSCC cell growth.

89 However, the glutamine-containing peptide competed with the substrate

90 icular for the attachment of alkyl amines to glutamine-containing peptides and proteins.

91 Polar residues, such as glutamine, contribute significantly to the stability of

92 sotope tracing revealed that glucose but not glutamine contributed to increased biosynthesis of aspar

93 pectroscopy of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, and choline compoun

94 rmal levels of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, or choline compound

95 ); however, only 4 therapies (hydroxyurea, l-glutamine, crizanlizumab, and voxeletor) are currently a

96 tion of genes involved in the glutamate/GABA/glutamine cycle in glia to control neurotransmitter leve

97 supporting a central imbalance of glutamate-glutamine cycling in depression, our results suggest tha

98 s caused by outcompeting D-serine for a dual glutamine-D-serine transport system.

99 served behaviour was primarily attributed to glutamine deamidation by microbial transglutaminase in t

100 Mechanistically, we demonstrate that glutamine deficiency regulates EMT through the up-regula

101 Glutamine-deficient pancreatic cancer cells up-regulate

102 However, glutamine dependence can be highly variable between in v

103 Glutamine dependence drove CAF migration toward this ami

104 This pathway is glutamine dependent and triggered by binding of beta1-in

105 ommunication mechanism for the regulation of glutamine-dependent activity and NH(3) transport.

106 Therefore, glutamine depletion or mTORC1 inhibition stimulates rele

107 -135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activat

108 Here, we show that nutrient stress caused by glutamine deprivation leads to the induction of epitheli

109 Our results demonstrate that glutamine deprivation promotes CAF migration and invasio

110 Furthermore, glutamine deprivation, as well as the antimetabolic drug

111 find that Slug is required in PDAC cells for glutamine deprivation-induced EMT, cell motility, and nu

112 vironments and complex adaptive responses to glutamine deprivation.

113 is an amino acid analog of l-glutamate and l-glutamine derived from various plant sources, including

114 Glucose and/or glutamine-derived alpha-KG maintained low H3K27me3 in H3

115 Glutamine did not increase the NMDAR potentials in slice

116 Accordingly, glutamine directed invasion of xenografted tumors in imm

117 Stimulation of glutamine-driven epithelial tumor invasion by fibroblast

118 ts support a role for PGC1alpha in mediating glutamine-driven oxidative phosphorylation to facilitate

119 omic analysis reveals that dietary uptake of glutamine effectively increases the concentration of glu

120 Higher glutamine export from astrocytes would increase extracel

121 ), Fe(III)(Cit)(2)(Mal)(2), Fe(III)(Mal)(2), glutamine: Fe(III)(Glu)(2) and nicotianamine: Fe(II)(NA)

122 We find that carbons from (13)C-glutamine feed into amastigote sterols and into metaboli

123 tigational PET radiotracer for imaging tumor glutamine flux and metabolism.

124 Metabolite tracing with 13C-glucose and 13C-glutamine following MCT1 inhibitor treatment revealed in

125 ve a notable addiction to anaplerotic use of glutamine for macromolecular synthesis.

126 with an increased expression and activity of glutamine fructose 6-phosphate amidotransferase (GFAT),

127 The rate-limiting enzyme of the pathway, glutamine-fructose amidotransferase 1 (GFAT1), uses glut

128 ynthetic pathway, which is controlled by the glutamine:fructose-6-phosphate amidotransfera-se (GFAT).

129 Overexpression of Gfat1 (glutamine:fructose-6-phosphate amidotransferase 1), the

130 Hyperoxia induces glutamine-fueled anaplerosis that reverses basal Muller

131 We used the method to monitor glutamate, glutamine, gamma-aminobutyric acid and lactate in the br

132 circuitry mediated by the neurotransmitters glutamine, gamma-aminobutyric acid, and dopamine.

133 Glutamine (Gln) is converted to excitatory (glutamate, a

134 HC significantly increased Glutamate (Glu) + Glutamine (Gln) metabolites (Glx) in the left caudate he

135 inquired whether levels of glutamate (Glu), glutamine (Gln), GABA or their ratios predict interindiv

136 Glutamine, glucose, and other metabolites drive the hexo

137 Interestingly, interference with glutamine-glutamate conversion preferentially blocked pr

138 o In addition to their classical role in the glutamine-glutamate cycle, system A transporters regulat

139 gulating D-serine synaptic turnover, and the glutamine-glutamate cycle.

140 spectroscopy to measure glutamate, glutamate+glutamine (Glx), and GABA levels in dorsal anterior cing

141 Plasma levels of glutamic acid (GLU), glutamine, glycine, proline (PRO), tryptophan (TRP), tyr

142 Based on multivariate analysis, glutamine had no significant effect on the severity of o

143 ported across the plasma membrane by SLC1A5, glutamine has emerged as a metabolic fuel that is catabo

144 of glutamine, which results in unproductive glutamine hydrolysis.

145 We have determined the structure of the glutamine-II riboswitch ligand binding domain using X-ra

146 by Yoo et al., identifying the mitochondrial glutamine importer as a variant of SLC1A5.

147 formation of protein crosslinks, deamidating glutamine in a side-reaction.

148 eta induced the biosynthesis of proline from glutamine in a Smad4-dependent fashion.

149 Rewired metabolism of glutamine in cancer has been well documented, but less i

150 t residue 226, which is glutamate in elk and glutamine in deer, the effect of this difference on CWD

151 Notably, targeting a glutamine in NEMO for cleavage has been observed only wi

152 reduction in glutathione, glutamate, and/or glutamine in the cerebral cortex, consistent with a post

153 These features include hydroxy-glutamine in the peptide core instead of a serine or thr

154 e effectively increases the concentration of glutamine in tumours and its downstream metabolite, alph

155 These transporters are not saturated with glutamine in vivo and provide an unexpected link between

156 at these transporters are not saturated with glutamine in vivo and regulate the extracellular levels

157 Glutamine increased the NMDAR-dependent long-term potent

158 nt of one of them with acetylation-mimicking glutamine increases the sensitivity of mutant EGFR to er

159 s of Me(10)Tu[3](2+) and an interaction of L-glutamine indicate a potential for binding anionic molec

160 Incorporation of (13)C-glutamine into endogenously synthesized sterols is incre

161 pha-ketoglutarate, suggesting that exogenous glutamine is an essential carbon source for the TCA cycl

162 d of D-serine, indicating that the effect of glutamine is caused by outcompeting D-serine for a dual

163 We find that up to 30% of the glutamine is metabolized in the cytosol, primarily for n

164 at in MDV infection, as in many tumor cells, glutamine is used for generation of energetic and biosyn

165 e, an amino acid analog of l-glutamate and l-glutamine, is capable of preventing long-term THC side e

166 d decreased concentrations of phenylalanine, glutamine, isoleucine, leucine and glycerophosphocholine

167 minal domain lysine residues were mutated to glutamines (K to Q mutations at K367, K369, K370, K378,

168 gher expression of key transporter proteins (glutamine: LAT1, LAT2, SNAT5, glutamate: EAAT1) versus A

169 blotting, using strains expressing different glutamine leader constructs fused to GFP.

170 Intracellular glutamine levels are decreased in the absence of HUWE1 a

171 levels of glutamate, and cerebrospinal fluid glutamine levels were increased.

172 feration of N-Myc overexpressing cells, when glutamine levels were reduced.

173 melanoma, tumour cells often experience low glutamine levels, which promote cell dedifferentiation.

174 2 knockdown decreased cell proliferation and glutamine-linked metabolic phenotypes.

175 acetylcarnitine, creatinine, L-asparagine, L-glutamine, linoleic acid, pyruvic acid, palmitoleic acid

176 Our findings support the hypothesis that glutamine may be a key marker for glioma progression and

177 Levels of enzymes in the glucose and glutamine metabolic pathways are elevated in Tregs and B

178 Surprisingly, blocking glutamine metabolism also inhibited IDO expression of bo

179 and transcriptional processes that regulate glutamine metabolism and fibrotic development in a TGF-b

180 n part, through a metabolic maladaptation in glutamine metabolism and how the inhibition of glutamina

181 s pilot study was to characterize changes in glutamine metabolism and inflammation in human glioma sa

182 (2020) find that the dual targeting of glutamine metabolism and the PD-L1 checkpoint inhibitor

183 We reveal glutamine metabolism as critical for sarcomagenesis, wit

184 a mechanistic understanding of the role that glutamine metabolism has on the survival of glioblastoma

185 g link between cytoplasmic and mitochondrial glutamine metabolism is now provided by Yoo et al., iden

186 Targeting tumor glutamine metabolism led to a decrease in CSF3 and hence

187 sults effectively demonstrate that targeting glutamine metabolism may be an effective approach for tr

188 Alternatively, inhibiting glutamine metabolism of the MDSCs themselves led to acti

189 Indeed, targeting glutamine metabolism rendered checkpoint blockade-resist

190 In addition, manipulating glutamine metabolism restrained the assembly of stress g

191 d unbiased metabolomics, we demonstrate that glutamine metabolism supports sarcomagenesis.

192 d with BPTES treatment, an inhibitor of host glutamine metabolism that sensitizes amastigotes to azol

193 tamine pool size and is inversely related to glutamine metabolism through the glutaminase enzyme.

194 ancers have a well-established dependence on glutamine metabolism to support survival and growth, a p

195 In this study, we found that glutamine metabolism was upregulated after EGFR activati

196 amine pool size, a key indicator of cellular glutamine metabolism, by both a 1-compartment model and

197 By employing a small-molecule inhibitor of glutamine metabolism, not only were we able to inhibit t

198 on support the ability to assess response to glutamine metabolism-targeted therapy.

199 excrete glutamate, the first intermediate in glutamine metabolism.

200 ly rewired and elevated pathways involved in glutamine metabolism.

201 e transcription of GDH1, which then promoted glutamine metabolism.

202 t inflammation is associated with changes in glutamine metabolism.

203 glutamine transport and can be used to infer glutamine metabolism.

204 ng new insight into oncogenic alterations of glutamine metabolism.

205 Here we use lysine-to-glutamine mutations as acetylmimetics to map the relevan

206 ions (N-acetylaspartate, choline, glutamate, glutamine, myo-inositol, and total creatine).

207 the observed (1)H MRS increase in glutamate/glutamine occurred prior to tumor shrinkage.

208 We used (13)C-labeled glucose, glutamine or a long-chain fatty acid mixture added to ce

209 sis and the pentose shunt, but no changes in glutamine or fatty acid uptake or utilization.

210 n defined medium supplemented with ammonium, glutamine or glutamate, we revealed that ammonium and gl

211 ing amino-acid-deprived cells with exogenous glutamine or glutaminase inhibitors restores tRNA(Gln) c

212 Moreover, introduction of lysine, glutamine or proline at residue A578 also elicited capsa

213 ase (hsNadE) lacks substrate specificity for glutamine over ammonia and displays a modest activation

214 the block in the TCA cycle at SDH, the high glutamine oxidation activity is only maintained through

215 ic hairpin stabilized through interdigitated glutamine packing.

216 As a result, glutamine pathways are an emerging pharmacologic target.

217 nded to enrichment of glutamate receptor and glutamine pathways in ATM deficient background compared

218 ed by functional analyses, we identified the glutamine permease, GNP1 as a specific transporter for t

219 Hence, glutamine plus glutamate (Glx) and other metabolites wer

220 ase (HD) is caused by an expansion of a poly glutamine (polyQ) stretch in the huntingtin protein (HTT

221 at (18)F-Gln uptake correlates directly with glutamine pool size and is inversely related to glutamin

222 targeted therapies that impact intracellular glutamine pool size and tumor glutaminolysis rates.

223 ated the ability to measure V(D) to estimate glutamine pool size, a key indicator of cellular glutami

224 a and simulations suggests that estimates of glutamine pool size, specifically the distribution volum

225 We found that limiting exogenous glutamine protects actively dividing amastigotes from er

226 In addition to their classical role as the glutamine providers, the system A transporters regulate

227 pendent on the presence of a lysine (K) or a glutamine (Q) at amino acid position 223 in the carbohyd

228 tive disease caused by abnormal expansion of glutamine (Q) encoding CAG repeats in the gene Ataxin-1

229 rpesvirus (KSHV)-transformed cells depend on glutamine rather than glucose for energy production and

230 tryptophan and GABA-to-glutamate and GABA-to-glutamine ratio (FDR-p < 0.05).

231 ional network deficits and reduced glutamate/glutamine ratio in the striatum of HD mice.

232 tration and glutamate turnover (glutamate-to-glutamine ratio) in the putamen in patients with CUD, wh

233 der stems from the abnormal lengthening of a glutamine repeat in a different protein.

234 degenerative disease caused by CAG (encoding glutamine) repeat expansion in the Ataxin-3 (ATXN3) gene

235 copy-derived hippocampal levels of glutamate/glutamine, represents early hippocampal dysfunction in C

236 In the presence of minimum glutamine requirements based on optimal cell viability,

237 osphorylate Ser/Thr-containing motifs with a glutamine residue at position +1 and a hydrophobic resid

238 as amine nucleophile, substantial amounts of glutamine residues were converted in theanine residues.

239 zide handles onto the side chain of internal glutamine residues.

240 r of the two main carbon sources, glucose or glutamine, resulted in distinct shifts in steady-state m

241 esponding rTRPV1 residue E570 with lysine or glutamine retained capsaicin sensitivity.

242 le (TCA) intermediates from both glucose and glutamine revealing this previously unknown role for mit

243 -binding protein and splicing factor proline/glutamine-rich.

244 The mutation causes an arginine-to-glutamine (RQ) substitution within the first cGMP-bindin

245 We report that D-serine and glutamine share the same neuronal transport system, cons

246 hree metabolites (spermidine, putrescine and glutamine) significantly differed between groups (P < 0.

247 Here, we show that glutamine-specific tRNAs selectively become uncharged wh

248 - and C-terminal regions at Serine/Threonine-Glutamine (SQ) motifs.

249 aminase (GLS) levels are highly sensitive to glutamine starvation.

250 Mutant forms of ataxin-1 containing expanded glutamine stretches cause the movement disorder spinocer

251 Glutamine supplementation abolishes the latter abnormali

252 herefore, our findings provide evidence that glutamine supplementation can serve as a potential dieta

253 Here, we show that dietary glutamine supplementation significantly inhibits melanom

254 Mechanistically, we find that glutamine supplementation uniformly alters the transcrip

255 xal level, which was completely prevented by glutamine supplementation.

256 xpression of the adjacent gene GLUL encoding glutamine synthase, converting glutamic acid to glutamin

257 d ammonia transport into these cells impairs glutamine synthesis.

258 A single peptide from the glutamine synthetase (GlnA1) enzyme was identified in 61

259 by conversion of pericentral vein-juxtaposed glutamine synthetase (GS)(-) hepatocytes into GS(+) hepa

260 Exaiptasia glutamine synthetase and glutamate synthase transcripts

261 nal enhancers, the hyperosmotic induction of glutamine synthetase by intron 1 is position dependent.

262 ired for precise enhancement of hyperosmotic glutamine synthetase expression.

263 sed levels of glutamate decarboxylase-65 and glutamine synthetase in PFC; reduced fractional anisotro

264 e O. mossambicus OmB cell line revealed that glutamine synthetase is transcriptionally regulated by h

265 study we show that hyperosmotic induction of glutamine synthetase represents a prominent part of this

266 hanism by which intron 1 positively mediates glutamine synthetase transcription.

267 the 5' regulatory sequence of O. mossambicus glutamine synthetase was investigated.

268 the preferential localization of the enzyme, glutamine synthetase, in pericentral hepatocytes, where

269 her and express markers, including Glast and glutamine synthetase.

270 resulting purported light-adapted state, the glutamine tautomer forms a hydrogen bond with the flavin

271 the light-adapted state with the imidic acid glutamine tautomer reproduces the experimentally observe

272 nd other mesenchymal cells rely much more on glutamine than epithelial tumor cells; consequently, the

273 s labeled with [1-(13)C]glucose and [3-(13)C]glutamine, the principal sources of cellular glutamate,

274 Here we report using our QTY (glutamine, threonine, tyrosine) code to systematically r

275 goes RNA editing in GluA2 subunits replacing glutamine to arginine, with the percent inhibition being

276 Tumor cells rely on glutamine to fulfill their metabolic demands and sustain

277 atalyzes the first step in the conversion of glutamine to glutamate.

278 Tumour cells frequently utilize glutamine to meet bioenergetic and biosynthetic demands

279 ivates anaplerotic substrate from glucose to glutamine to provide energy and macromolecules required

280 Cancer cells can metabolize glutamine to replenish TCA cycle intermediates, leading

281 2S,4R)4-fluoroglutamine ((18)F-Gln) reflects glutamine transport and can be used to infer glutamine m

282 dynamic PET is a sensitive tool for studying glutamine transport and metabolism in human malignancies

283 oted the plasma membrane localization of the glutamine transporter ASCT2, enhancing glutamine uptake

284 6)A-seq and mRNA-seq analysis identified the glutamine transporter SLC1A5 as an FTO target that promo

285 SLC38A8 is a putative glutamine transporter with strong expression within the

286 AlsT was identified as an efficient glutamine transporter, indicating that preventing glutam

287 y genetic and small molecule inhibitors that glutamine transporters are essential for the H4K16Ac-neg

288 Diapause furthermore activates expression of glutamine transporters SLC38A1/2.

289 f the glutamine transporter ASCT2, enhancing glutamine uptake in PDAC cells.

290 mine transporter, indicating that preventing glutamine uptake in rich medium rescues the growth of th

291 In addition, our results demonstrate that glutamine uptake is elevated by MDV-infected cells in vi

292 In the current manuscript, we targeted this glutamine-utilizing enzyme by a small molecule glutamine

293 Ammonium and uptake of glutamine via AlsT and hence likely a higher intracellul

294 rmation from crotonaldehyde, creatinine, and glutamine was 72.2 +/- 0.4 kJ.mol(-1).

295 artate (NAA) were reduced after LPS, whereas glutamine was increased.

296 se via the tricarboxylic acid cycle and from glutamine were increased following temozolomide treatmen

297 e inhibitor weakened the affinity of GAC for glutamine, whereas activating anions such as P(i) increa

298 ing or depleting the key metabolic substrate glutamine, which diverts membrane flux through recycling

299 even in the presence of equimolar amounts of glutamine, which results in unproductive glutamine hydro

300 Deprivation of glutamine by glutamine-withdrawal, GLS knockdown, or exposure to the