ライフサイエンスコーパス: Gln

1 Gln is a key player in plant metabolism.

2 Gln is also protective but this relies on the activities

3 Gln- and Asp-150-substituted versions of ACO further con

4 Gln-2 was highly expressed in shoots but only at a very

5 Gln-282 contributed to sugar binding in all GLUT1 confor

6 Gln-free incubation or treatment with the glutaminolytic

7 ize or charge conservative mutations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred that a cry

8 and -B8, including Glu/Asp at position 177, Gln/Glu at position 180, Gly/Arg at position 239, and Pr

9 A Glu-217-Gln amino acid substitution was found to confer high Rca

10 t residues (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that contribute to

11 ree residues on the C-linker-CNBD (Glu(478), Gln(482), and His(559)) that form direct interactions wi

12 ino acid sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).

13 onstrating that amino acid sequence Leu(480)-Gln(481): 1) is crucial for proper recognition of the fV

14 -thrombin with amino acids Ser(478)/Leu(480)/Gln(481) deleted).

15 t necessary step toward validating [(18)F]4F-Gln PET as a PD marker for GLS-targeting drugs.

16 ctivity ratios (T/B) obtained from [(18)F]4F-Gln PET images matched the distinct glutamine pool sizes

17 In conclusion, [(18)F]4F-Gln PET tracked cellular glutamine pool size in breast c

18 f [(18)F](2S,4R)4-fluoroglutamine ([(18)F]4F-Gln) PET to measure tumor cellular glutamine pool size,

19 substitution of the conserved central Gly(6)-Gln(7) residues or by random sequence scrambling demonst

20 e helix 1 (Phe-40), helix 3 (Leu-63, Arg-68, Gln-69, Ile-72, Tyr-76), and C-terminal segment (Leu-81,

21 restingly, a short sequence of FtsN (Leu(75)-Gln(93), known as (E)FtsN) was shown to be essential and

22 to RORgammat, the length of helix 11' and a Gln-487 residue, are crucial for the formation of the al

23 of a Thr side chain to the alpha-carbon of a Gln residue.

24 Collectively, these results reveal a Gln synthetase-dependent increase and resilience of FOXP

25 molecule stabilized by hydrogen bonding to a Gln side chain in the active site, offering a structural

26 onformation spectroscopy is used to study Ac-Gln-Gln-NHBn in order to probe the interplay between sid

27 Our results indicate that higher accumbal Gln-to-Glu ratio predicts better overall performance and

28 provide novel insights implicating accumbal Gln and Glu balance on the prediction of specific comput

29 model-based analysis revealed that accumbal Gln-to-Glu ratio specifically relates to stamina; i.e.,

30 at are dependent upon essential amino acids, Gln, and finally, a checkpoint mediated by mammalian tar

31 ell as associations between rACC activation, Gln/Glu, Glu, Gln, behavioral, and clinical measures wer

32 amino-acid insertion (Leu583-Ala586DelInsSer/Gln/Pro) within the JH2 domain of JAK2.

33 l additional cases of Leu583-Ala586DelInsSer/Gln/Pro, allowing for complete characterization of this

34 whether genetic inactivation of Hace1 alters Gln metabolism.

35 ic functions of the two isogenes Gln-1;1 and Gln-1;2 in shoots for ammonium detoxification, single an

36 In cone Pgamma, Asn-13 and Gln-14 significantly enhanced Gt(alpha)*-GTPgammaS activ

37 s (such as at residues Gly(12), Gly(13), and Gln(61)) have the same impact on RAS signaling and funct

38 as well in DOPC-reconstituted Glu(134)- and Gln(134)-containing bovine opsin mutants and demonstrate

39 pond to ammonium treatment while Gln-1;4 and Gln-1;5 isogenes in all cases were expressed at a very l

40 lso suggested the involvement of Tyr(45) and Gln(200) (potency) and Tyr(116) and Glu(288) (affinity).

41 lowed for the identification of Leu(480) and Gln(481) as the two essential amino acids responsible fo

42 nformational flexibility of Arg-4, Lys-5 and Gln-6 of BCL11B.

43 o CRS2 in CXCR4 (positions Ser-103(2.63) and Gln-301(7.39)) increased CXCL11 binding, but reduced CXC

44 Bank voles have a high number of Asn and Gln residues and a high Asn:Gln ratio.

45 ndings suggest that a high number of Asn and Gln residues at specific positions may stabilize beta-sh

46 For two of the four positions, Asn and Gln residues were not interchangeable, revealing a stric

47 atic (Phe, Trp, Tyr, and His)/amide (Asn and Gln)/Guanidine (Arg)) side-chains and charged hydrophili

48 nism of AMSDH, we created Ala, Ser, Asp, and Gln mutants and studied them using biochemical, kinetic,

49 iation between reduced rACC deactivation and Gln/Glu, Glu, or Gln in the OCD group.

50 BF decreased linearly with age while Gln and Gln/Glu increased linearly with age.

51 However, Gln/Glu, Glu, and Gln in the rACC did not differ between groups nor was th

52 lutamine/glutamate ratio (Gln/Glu), Glu, and Gln levels, as well as associations between rACC activat

53 n of Glu-181 to Asp in the double E loop and Gln-329 to Ala in the canonical THW loop enables the enz

54 er, Gln metabolism also generates NADPH, and Gln-derived glutamate is used for synthesis of glutathio

55 ese proteins prevented Akt2 polarization and Gln-driven CAF invasion.

56 of Gln-39 >> Gln-298 > Gln-345 approximately Gln-65 >> Gln-144.

57 e found that S. suis is auxotrophic for Arg, Gln/Glu, His, Leu, and Trp in chemically defined medium.

58 Thus, the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific substrates of the mammal

59 de variants containing amino acids Ala, Asn, Gln, His, Ile, and Lys at positions equivalent to 782 an

60 mposition of labile amino acids such as Asn, Gln, Trp, Cit, and theanine.

61 e Asn-473 is positioned on a short loop (Asn-Gln-Gly-Glu-Pro) instead of an alpha-helix and forms hyd

62 that multiple PrP(C) segments containing Asn/Gln residues may act in concert along a replicative inte

63 from side chain amides forming extended Asn/Gln ladders.

64 umber of Asn and Gln residues and a high Asn:Gln ratio.

65 bioactive peptides, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and different bile salts i

66 deamidase activity that targets ubiquitin at Gln(40).

67 Besides Gln, H. suis can also convert glutathione (GSH) to gluta

68 that the motifs YRYRQ and RYESK are the best Gln and Lys substrates of KalbTG, respectively.

69 Finally, comparisons are made between Gln deamidation, which is relatively poorly understood,

70 ity panel using all potential ratios between Gln and the other members of the Glu family as traits.

71 This gain was abolished by blocking Gln synthetase, an enzyme that responds to Gln and purin

72 This finding indicates that both Gln and GLS play key roles in shaping the seed metabolic

73 ation of ammonium into amino acids, via both Gln synthesis and Orn-urea pathway.

74 replacing Phe(604), Ile(608), or Ile(612) by Gln.

75 he induction of superoxide and cell death by Gln starvation.

76 of TM4SF20, as it cannot be replaced even by Gln.

77 action, with additional influence exerted by Gln-38.

78 l pore radius of approximately 3 A formed by Gln-4933, rather than Ile-4937 in the closed-channel str

79 ns, differing by a substitution of Glu373 by Gln, which correlated with the ability to induce camalex

80 Of the 5 Glu and Asp residues replaced by Gln or Asn in our experiments, none of the mutant pigmen

81 ecretion, and metabolic labeling using (13)C-Gln revealed that Hace1 loss increases incorporation of

82 chF does not possess the canonical catalytic Gln required for nucleotide hydrolysis.

83 mutating the corresponding residue in CFTR, Gln-1291, selectively disrupts adenylate kinase-dependen

84 ogen-bonded arrays of glutamine side chains (Gln ladders) in amyloid-forming peptides.

85 n-glycan profiling revealed that a conserved Gln residue in the GnTI TMD is essential for its cis/med

86 Mutation of the highly conserved Gln-758, which chelates a nucleotide-associated Mg(2+) i

87 In contrast, Gln-316 has an autoinhibitory role, and its mutation to

88 Glutaminolysis converts Gln into alpha-ketoglutarate (alpha-KG), a critical inte

89 taminase (GLS) isoform, GLS1, which converts Gln into glutamate, at both the mRNA and protein levels.

90 Increased right thalamic Glx/Cr, Glu/Cr, Gln/Cr, Asc/Cr, and decreased GPC/Cr and decreased left

91 Substitution of the crucial Gln residue with other amino acids resulted in mislocali

92 a pilus tip-end adhesin equipped with a Cys-Gln thioester bond.

93 adhesins have revealed an intramolecular Cys-Gln thioester bond that can react with surface-associate

94 e X-ray crystallographic structure of N-Me-d-Gln(4),d-aza-Thr(8),Arg(10)-teixobactin reveals an amphi

95 This decreases Gln uptake, levels of TCA cycle components, mTOR signali

96 show that the liver supplies glucose-derived Gln via the blood to the PDTX to fuel Glu and glutathion

97 TA-p-aminomethylaniline-diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tum

98 In addition, the C=O group of each Gln sidechain participates in a seven-membered ring hydr

99 rgest sample to date, lower Glu and elevated Gln/Glu levels were observed in adults with SZ and in ol

100 ly oligomer requiring a pathogenic, expanded Gln length and N17 alpha-helix formation.

101 The removal of extracellular Gln postmyofibroblast differentiation decreased the expr

102 Depletion of extracellular Gln prevented TGF-beta1-induced myofibroblast differenti

103 n, MM cells strictly depend on extracellular Gln and show features of Gln addiction.

104 the dependence of MM cells on extracellular Gln, a gene expression profile analysis, on both proprie

105 cative of largely reversible uptake of (18)F-Gln in tumors.

106 nograft studies have demonstrated that (18)F-Gln uptake correlates directly with glutamine pool size

107 sis of (18)F-Gln-PET, we have examined (18)F-Gln uptake kinetics in mouse models of breast cancer at

108 tracer (18)F-(2S,4R)4-fluoroglutamine ((18)F-Gln) reflects glutamine transport and can be used to inf

109 lly the distribution volume (V(D)) for (18)F-Gln, were more reliable using the 1-compartment reversib

110 onclusion: Kinetic analysis of dynamic (18)F-Gln-PET images demonstrated the ability to measure V(D)

111 rovide a framework for the analysis of (18)F-Gln-PET, we have examined (18)F-Gln uptake kinetics in m

112 t the time of intravenous injection of (18)F-Gln.

113 Finally, Gln starvation increases superoxide levels in Hace1(-/-)

114 at the relative free energies of the flipped Gln conformation and the flipping barrier are significan

115 edback that matches translational demand for Gln-tRNAGln to aaRS recharging capacity.

116 synthetases to synthesize Asn and GatCAB for Gln-tRNA(Gln) synthesis, their AspRS enzymes were though

117 ficantly enhanced analytical sensitivity for Gln, thus enabling down-sized brain tissue sample volume

118 GatCAB can be similarly used for Gln-tRNA(Gln) formation.

119 erence of -17 Da or -18 Da, when formed from Gln or Glu, respectively, is not unique.

120 Signals from Gln, Glu with chemical shift around 2.4 ppm, from Cr, PC

121 nducible RING-domain protein termed RING-GAF-Gln-containing protein (RGQ1), which was shown to act as

122 ify three hot spot residues (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) t

123 ed significant effects of age with Glu, Gln, Gln/Glu, and AC white matter (WM) rCBF.

124 data rich in Asx (Asp + Asn) and Glx (Glu + Gln) typical of invertebrate skeletal proteins.

125 siological concentrations including Glx (Glu+Gln), tNAA (NAA+NAAG), mI all had coefficient of variati

126 mutagenesis of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that although both th

127 tions between rACC activation, Gln/Glu, Glu, Gln, behavioral, and clinical measures were examined usi

128 nstrate the following metabolites: NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG, and Asp.

129 of the following metabolites: Ala, NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG, and Asp.

130 evealed significant effects of age with Glu, Gln, Gln/Glu, and AC white matter (WM) rCBF.

131 inc in Csd4 is coordinated by a rare His-Glu-Gln configuration that is conserved among most Csd4 homo

132 link between Cu stress, acid stress, and Glu/Gln metabolism, establish a role for YbaS and YbaT in Cu

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

134 ingulate (AC) glutamate (Glu) and glutamine (Gln) and arterial spin labeling evaluation for rCBF.

135 tations including a non-canonical glutamine (Gln) metabolic pathway and that inhibition of downstream

136 enes, ybaS and ybaT, which confer glutamine (Gln)-dependent acid tolerance and contribute to the glut

137 de polymorphism substitution from glutamine (Gln, Q) to arginine (Arg, R) at codon 460 of the puriner

138 antly increased Glutamate (Glu) + Glutamine (Gln) metabolites (Glx) in the left caudate head (P = 0.0

139 hether levels of glutamate (Glu), glutamine (Gln), GABA or their ratios predict interindividual diffe

140 shown by a complete depletion of glutamine (Gln) in the medium during H. suis culture.

141 The importance of glutamine (Gln) metabolism in multiple myeloma (MM) cells and its p

142 Deamidation of glutamine (Gln) residues is a spontaneous or enzymatic process with

143 an disease include deamidation of glutamine (Gln) residues, amine incorporation into Gln residues, an

144 We show that the glutamine (Gln) deamidation and cysteine (Cys) oxidation branches a

145 ising a formamidinylated, N-hydroxylated Gly-Gln dipeptide conjugated to 6'-amino-pseudouridine.

146 Cytosolic GS1 (Gln synthetase) is central for ammonium assimilation in

147 utamines in the order of Gln-39 >> Gln-298 > Gln-345 approximately Gln-65 >> Gln-144.

148 > hydroxyproline > alpha-aminobutyric acid > Gln, Thr, Ser > Glu, Ala, Gly, Asn, Asp.

149 >> Gln-298 > Gln-345 approximately Gln-65 >> Gln-144.

150 he DAIP glutamines in the order of Gln-39 >> Gln-298 > Gln-345 approximately Gln-65 >> Gln-144.

151 However, Gln and Trp substitution at Arg-1150 significantly decre

152 However, Gln metabolism also generates NADPH, and Gln-derived glu

153 However, Gln natural variation and its regulation and interaction

154 However, Gln/Glu, Glu, and Gln in the rACC did not differ between

155 hat are adjacent to the initially identified Gln(596) and Ile(597) residues.

156 triction, and they demonstrate that impaired Gln-dependent nucleotide synthesis promotes FOXP3(hi) ce

157 ibition in HMCLs caused a marked decrease in Gln uptake and a significant fall in cell growth.

158 es of WCR-attacked roots show an increase in Gln turnover, which strongly correlates with the inducti

159 inase (GLS), which mediates an early step in Gln metabolism, represent a viable therapeutic strategy.

160 residues through Michael addition, including Gln, Arg, and Asn, which are inaccessible to existing ch

161 Hace1(-/-) MEFs exhibit increased Gln uptake and ammonia secretion, and metabolic labeling

162 led a novel amyloid formed by interdigitated Gln and His residue side chains belonging to the prion-l

163 ine (Gln) residues, amine incorporation into Gln residues, and protein crosslinking.

164 ydrogen bonding interactions of an invariant Gln residue that has been proposed to flip its amide sid

165 on of the high-affinity low-capacity isoform Gln-1;1 was reduced.

166 t enhanced the expression of the GS1 isogene Gln-1;2 encoding a low-affinity high-capacity GS1 protei

167 e the specific functions of the two isogenes Gln-1;1 and Gln-1;2 in shoots for ammonium detoxificatio

168 at the same mechanism applies to L-Asn and L-Gln, we postulate that it is common for all these struct

169 s, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and different bile salts in the submicellar

170 on assays revealing that the p7 residue (Leu/Gln) is critical for specific epitope recognition by bot

171 NA knockdown of the respective rate-limiting Gln-consuming enzymes CAD and PPAT.

172 rmance from task onset, particularly for low Gln-to-Glu individuals.

173 the Glu-Xaa8-Glu (double E) loop and the Met-Gln-Trp sequence of the canonical Thr-His-Trp (THW) loop

174 relative to people expressing wild-type Met-Gln-Rgs2 (MQ-Rgs2).

175 bond impairing modifications (alpha)N-methyl Gln or l-Pro at key positions within betaHP.

176 The murine HEMK2 enzyme methylates Gln(185) of the eukaryotic translation termination facto

177 ng a 1.7 gamma/alpha-glutamyl ratio for most Gln deamidation products.

178 Mutating Gln-282 to alanine (Q282A) doubled the Km(app) for 2-deo

179 rferometry assays, we show that PII and NadE(Gln) physically interact in vitro, that this complex rel

180 amine as a nitrogen donor and are named NadE(Gln) Previous gene neighborhood analysis has indicated t

181 as a dissociable regulatory subunit of NadE(Gln), thereby enabling the control of NAD(+) biosynthesi

182 -OG) inhibited the formation of the PII-NadE(Gln) complex within a physiological range.

183 ct in vitro, that this complex relieves NadE(Gln) negative feedback inhibition by NAD(+) This mechani

184 derived from endogenous readthrough, namely Gln, Lys, or Tyr at UAA or UAG PTCs and Trp, Arg, or Cys

185 replacement of the charged Lys-5 by neutral Gln to resemble Fyn (Src-S3C/S6C/K5Q) restored Fyn-like

186 e human Nt-Asn-specific Nt-amidase NTAN1, Nt-Gln-specific Nt-amidase NTAQ1, arginyltransferase ATE1,

187 to the roots, including the accumulation of Gln.

188 xperiments confirmed that the side chains of Gln-623 and Arg-661 play important roles in mediating PI

189 y modeling indicates that the side chains of Gln-875 and the gating charge Arg-214 of the domain I vo

190 that inhibition of downstream components of Gln metabolism leads to a decrease in tumour growth.

191 l-asparaginase depleted the cell contents of Gln, glutamate, and the anaplerotic substrate 2-oxogluta

192 Thus, RNF5 control of Gln uptake underlies BCa response to chemotherapies.

193 as been hypothesized that the degradation of Gln and GSH may lead to a deficiency for the host, possi

194 rted to a large extent by mutual exchange of Gln/Glu at position 180 or by Gly/Arg at position 239.

195 The expression of Gln-1;3 did not respond to ammonium treatment while Gln-

196 nd on extracellular Gln and show features of Gln addiction.

197 lutaminases (MTGs) catalyze the formation of Gln-Lys isopeptide bonds and are widely used for the cro

198 to our knowledge, a novel shoot function of Gln-1;2 in Arabidopsis shoots.

199 d that Hace1 loss increases incorporation of Gln carbons into the TCA cycle intermediates.

200 Therefore, the inhibition of Gln uptake is a new attractive therapeutic strategy for

201 riction was recapitulated with inhibitors of Gln-dependent pyrimidine and purine syntheses that toget

202 We identified the insertion of Gln, Tyr, and Lys at UAA and UAG, whereas Trp, Arg, and

203 lic genome-wide association study (mGWAS) of Gln-related traits measured from the dry seeds of the Ar

204 MTG for the DAIP glutamines in the order of Gln-39 >> Gln-298 > Gln-345 approximately Gln-65 >> Gln-

205 HsIPMK activities rely on a preponderance of Gln residues, in contrast to the larger Lys and Arg resi

206 The presence of Gln(180) and Gly(239), as in HLA-A2, led to higher cell

207 ncing of GLS1 expression, in the presence of Gln, abrogated TGF-beta1-induced expression of profibrot

208 large amounts of ammonium in the presence of Gln.

209 idly characterizing the isomeric products of Gln deamidation using diagnostic fragments that are abun

210 ra of hydrogen bonds involving sidechains of Gln, Asn, Ser, and Tyr residues, both along and transver

211 the ammonium content increased while that of Gln decreased, showing that Gln-1;2 was essential for am

212 showed an extensive seed-specific impact on Gln levels and composition that manifested early in seed

213 moieties due to cross-linking between Asn or Gln and Lys side chains.

214 ng a strict requirement for either an Asn or Gln residue.

215 duced rACC deactivation and Gln/Glu, Glu, or Gln in the OCD group.

216 e GLP-1 and CCK mimetics exendin-4 and (pGlu-Gln)-CCK-8, respectively.

217 Administration of the peptides, except (pGlu-Gln)-CCK-8 alone, in combination with glucose significan

218 vel (pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination wit

219 ons and therapeutic utility of a novel (pGlu-Gln)-CCK-8/exendin-4 hybrid peptide compared with the st

220 wice-daily administration of the novel (pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or

221 n-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination with exendin-4 for 21 days to

222 HbA1c was reduced in the (pGlu-Gln)-CCK-8/exendin-4 hybrid and combined parent peptide

223 OTA-4-amino-1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a sy

224 OTA-4-amino-1-carboxymethyl-piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a sy

225 MM patients have lower BM plasma Gln with higher ammonium and glutamate than patients wit

226 oration of specific binding peptide (His Pro Gln: HPQ) gives M13 bacteriophage high selectivity for t

227 rd IR-A, particularly the analogs with a Pro-Gln insertion in the C-domain.

228 GF-1R due to a synergistic effect of the Pro-Gln insertion and S29N point mutation.

229 r glucose but prevails when serine in a QSP (Gln-Ser-Pro) motif is replaced by glutamate [RS1-Reg(S20

230 CC activation and glutamine/glutamate ratio (Gln/Glu), Glu, and Gln levels, as well as associations b

231 We found that a DNA-contacting residue (Gln-336) specifically recognizes low-affinity DNA and tr

232 acids into the alpha5 helix between residues Gln(333) and Phe(334) (Ins4A).

233 ly, when substituting the conserved residues Gln(758) (Q motif) or Lys(785) (I motif) of both motifs,

234 -amino acid-long amphipathic helix (residues Gln-62-Leu-73) that together confer cholesterol responsi

235 ps to identify a 12-residue region (residues Gln-62-Leu-73), required for SM cholesterol-mediated tur

236 To assess this model, five residues (Gln(45)-TMD1, Asn(90)-TMD2, Leu(290)-TMD7, Ser(407)-TMD1

237 Our lab previously identified two residues (Gln(596) and Ile(597)) in the helical domain of the cata

238 sisting of three highly conserved residues - Gln(232/585)-Asp(262)/Asn(623)-Tyr(322/666) (the constri

239 IC-MS/MS was able to simultaneously separate Gln and asparagine (Asn) deamidation products even for t

240 activity was partially compromised, a single Gln to Lys substitution (2) restored activity equivalent

241 closed- and open-channel constriction sites (Gln-4933 and Ile-4937).

242 er metabolism is adaptive and that targeting Gln metabolism in combination with these adaptive respon

243 (pGlu), a cyclization product of N-terminal Gln or Glu residues, is a widespread post-translational

244 In Arabidopsis thaliana Gln-specific amino-terminal (Nt)-amidase (NTAQ1) control

245 We conclude that Gln-1;2 is the main isozyme contributing to shoot GS1 ac

246 We found that Gln restriction during human T cell activation favored C

247 This indicates that Gln and GSH supplementation may help reducing tissue dam

248 ed while that of Gln decreased, showing that Gln-1;2 was essential for ammonium assimilation and amin

249 The Gln-1291 mutations did not alter the potency of ATP at s

250 This checkpoint is located after the Gln checkpoint and before the mTOR-mediated cell cycle c

251 n the aliphatic glucosinolates (GLS) and the Gln-related traits.

252 al analysis of the relationships between the Gln-related traits and the presence of specific GLS in s

253 Akt2 distribution that was modulated by the Gln-dependent activity of TRAF6 and p62 in the migrating

254 asets, showed an increased expression of the Gln transporters SNAT1, ASCT2, and LAT1 by CD138(+) cell

255 complexes, arising from reorientation of the Gln-63 carboxamide by Arg85' to preclude direct hydrogen

256 ur homeostasis, which conceivably led to the Gln response.

257 (Q motif), displayed defects similar to the Gln(758) variant(s), arguing for a comparable loss of fu

258 (Ala-Glu-Glu-Arg-Tyr-Pro and Asp-Glu-Asp-Thr-Gln-Ala-Met-Pro) showed the highest ORAC values.

259 s in HeV G by conservative mutations (Asn to Gln) and found that six out of eight sites were actually

260 demonstrate that Rb and mTORC1 contribute to Gln-addiction upon the dysregulation of the Fbxo4-cyclin

261 recombinant GatAB converts Glu-tRNA(Gln) to Gln-tRNA(Gln) in vitro.

262 amidotransferase to convert Glu-tRNA(Gln) to Gln-tRNA(Gln).

263 ed ROS production due to Hace1 loss leads to Gln addiction as a mechanism to cope with increased ROS-

264 9Q receptor, with the substitution of Leu to Gln at position 129 (3.43).

265 modulin (CaM), using peroxide and the Met to Gln oximimetic mutations.

266 Second, mutagenesis to Gln of putative H(+)-binding residues, Glu-427 in Sul1 o

267 sitivity at room temperature than the Pro to Gln substitution in the extracellular segment of S6.

268 g Gln synthetase, an enzyme that responds to Gln and purine/pyrimidine deficiencies.

269 a cell lines (HMCLs) are highly sensitive to Gln depletion.

270 CAFs moving toward Gln presented a polarized Akt2 distribution that was mod

271 ion at U34 of tRNA(Lys), tRNA(Glu), and tRNA(Gln) causes ribosome pausing at the respective codons in

272 m(1)G9-containing tRNAs codons read by tRNA(Gln(TTG)), tRNA(Arg(CCG)), and tRNA(Thr(CGT)) These find

273 (CCA)) are substrates for Cm formation, tRNA(Gln(UUG)), tRNA(Pro(UGG)), tRNA(Pro(CGG)) and tRNA(His(G

274 GatCAB can be similarly used for Gln-tRNA(Gln) formation.

275 ant GatAB converts Glu-tRNA(Gln) to Gln-tRNA(Gln) in vitro.

276 es to synthesize Asn and GatCAB for Gln-tRNA(Gln) synthesis, their AspRS enzymes were thought to be s

277 sferase to convert Glu-tRNA(Gln) to Gln-tRNA(Gln).

278 tamyl-tRNA synthetase to synthesize Glu-tRNA(Gln) and a glutaminyl-tRNA amidotransferase to convert G

279 ted that recombinant GatAB converts Glu-tRNA(Gln) to Gln-tRNA(Gln) in vitro.

280 yl-tRNA amidotransferase to convert Glu-tRNA(Gln) to Gln-tRNA(Gln).

281 I, the viral core protein E11, and host tRNA(Gln).

282 rget for Am in tRNA(Pro(GGG)) and Um in tRNA(Gln(UUG)) by mass spectrometric analysis.

283 al translation, the reduced charging of tRNA(Gln) in amino-acid-deprived cells also leads to specific

284 mine or glutaminase inhibitors restores tRNA(Gln) charging and the levels of polyglutamine-containing

285 ng the residues lining the SBS-A1 site, two (Gln(700) and Tyr(717)) promoted alternan elongation.

286 The shift toward FOXP3(hi)CD4 T cells under Gln restriction was recapitulated with inhibitors of Gln

287 ease and resilience of FOXP3(hi) cells under Gln restriction, and they demonstrate that impaired Gln-

288 residue in the small subunit with Ser, Val, Gln, Gly, or Asp, and we analyzed the effects of these m

289 lted in the discovery of compound 42 (Ac-Val-Gln-(pI)DPhe-DTic-NH(2)), a full MC3R agonist that is 10

290 biquitin to Lys(92) and Lys(94) of UBE2N via Gln(40).

291 zole ring of His136, which is disrupted when Gln is present at position 136.

292 nd WM rCBF decreased linearly with age while Gln and Gln/Glu increased linearly with age.

293 did not respond to ammonium treatment while Gln-1;4 and Gln-1;5 isogenes in all cases were expressed

294 To that end, we replaced Lys-300 with Gln, either alone or together with the simultaneous subs

295 Substitution of these amino acids with Gln, Phe, and Phe, respectively, leads to complete loss

296 an alpha-helix and forms hydrogen bonds with Gln-281.

297 brane helix is mediated by a LQ7 motif, with Gln(187) being of special importance.

298 Asn-110 replacement with Gln completely abrogated rhDAO secretion and caused rete

299 in vivo effect of oral supplementation with Gln and GSH was assessed.

300 Oral supplementation with Gln was shown to temper H. suis induced gastritis and ep