ライフサイエンスコーパス: Gln

1 Gln is also protective but this relies on the activities

2 Gln starvation markedly increases ROS levels in Hace1(-/

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 ing the C terminus of thioesterase domain 2 (Gln(304)-Gly(326)), designated RegLoop2.

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

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

12 tant for AdoMet binding (Phe(443), Asp(444), Gln(445), and Asp(538)) and for AdoMet-driven inter-doma

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

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

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

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

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

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

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

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

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

22 e Yersinia pestis HasA (HasA(yp)) presents a Gln at position 32, we determined the structures of apo-

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

24 Substituting a Gln residue into the P2 of the activation site of MASP-3

25 bundling protein that oligomerizes through a Gln/Glu-rich stretch within a coiled-coil region.

26 h these findings, an R62A mutation abrogates Gln feedback inhibition but does not affect catalysis.

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

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

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

30 lar ways, exhibiting large changes per added Gln at low repeat lengths and small changes per added Gl

31 w repeat lengths and small changes per added Gln at relatively long repeat lengths.

32 whether genetic inactivation of Hace1 alters Gln metabolism.

33 orin-namely, Asn-Trp (NW), and its analogue, Gln-Trp (QW)-were synthesised to compare their antioxida

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

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

36 ons involving Propeller residues Lys-203 and Gln-145, with the latter accounting for primate specific

37 -ball domain (residues Arg-190, Asp-258, and Gln-259).

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

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

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

41 Crystal structures show that Arg-61 and Gln-38 are located near the active site and may play imp

42 te for the missing side chains of Arg-61 and Gln-38 in the Q38A/R61A mutant.

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 containing a small side chain (Ala, Asn, and Gln), but not with a bulky side chain.

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

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

51 Glu(31), Asp(32), and Trp(59) in FKBP12 and Gln(31), Asn(32), and Phe(59) in FKBP12.6.

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

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

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

55 including amino acids, lipids, glucose, and Gln.

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

57 Engineered Cys, Lys, and Gln substitutions at these positions shifted apparent pr

58 death compared with wild-type (wt) MEFs, and Gln depletion or chemical inhibition of Gln uptake block

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

60 an unprecedented ester bond joining Thr and Gln side chains.

61 As both NADPH and GSH are antioxidants, Gln may also contribute to redox balance in transformed

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

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

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

65 le-His-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compounds belonging to rele

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

67 uted one of four amino acids (Asp, His, Asn, Gln) at each of the 12 ligating positions because these

68 ariants, mutation of the Asp residue to Asn, Gln, or Glu dramatically impairs enzyme activity.

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

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

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

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

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

74 the utility of native chemical ligation at -Gln/Glu-Cys- [Glx-Cys] and -Asn/Asp-Cys- [Asx-Cys] sites

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

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

77 (Ser(144) and Ser(148)), and "beta2-beta3" (Gln(94) and Glu(101)) increased function of malpha6mbeta

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

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

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

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

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

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

84 substrate binding, since replacing Glu25 by Gln caused a >/=25-fold increase in Km.

85 cterized, are uniquely feedback-inhibited by Gln.

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Phe-Thr-Ser-Cys]-OH), PanSB1 (DOTA-PEG2-dTyr-Gln-Trp-Ala-Val-betaAla-His-Phe-Nle-NH2), and DOTA-MG11

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

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

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

103 The removal of extracellular Gln postmyofibroblast differentiation decreased the expr

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

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

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

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

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

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

110 ts of an indirect aminoacylation pathway for Gln-tRNA(Gln) biosynthesis in Plasmodium that we hypothe

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

112 metry (MS) analysis, but cyclization of free Gln and Glu to free pGlu during LC-MS analysis has not b

113 arate Gln, Glu, and pGlu, we found that free Gln and Glu cyclize to pGlu in the electrospray ionizati

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

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

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

117 ond formation with Cdk5, are changed to Gln, Gln, and Pro in p39.

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

119 (Asn, Asp, Ser, Thr, Gly), followed by Glu, Gln, or Asp in position N3 to complete a capping box.

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

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

122 were constructed by replacing Asp with Glu, Gln, or Cys and R175 with Gln, Asn, or Cys.

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

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

125 All fractions were rich in Lys, Glu/Gln, Gly, Pro, Ala, Asp/Asn, and Arg.

126 retention on C18 columns) of Asp/Asn (or Glu/Gln) peptide analogues among all naturally occurring ami

127 mation is associated with altered glutamine (Gln) metabolism.

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

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

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

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

132 altered metabolism and increased glutamine (Gln) dependence.

133 y sensitive methods for measuring glutamine (Gln) and glutamic acid (Glu) in cell cultures and other

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

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

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

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

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

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

140 We have shown that His-389 --> Gln disrupts the binding of NCF2 to the ZF domain of VAV

141 associations of rs17849502 (NCF2 His-389 --> Gln) and rs13306575 (NCF2 Arg-395 --> Trp) with systemic

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

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

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

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

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

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

148 he scaffold proteins beta-arrestin 2 and Ile Gln motif containing GTPase Activating Protein 1, a regu

149 rget of rapamycin signaling and decrease Ile Gln motif containing GTPase Activating Protein 1 phospho

150 entapeptides Cys-Ile-His-Asn-Pro and Cys-Ile-Gln-Pro-Val while low response was achieved for the dipe

151 e, glutathione, Cys-Ile-His-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compou

152 sein-derived synthetic peptides (Ile-Pro-Ile-Gln-Tyr, Leu-Pro-Leu-Pro-Leu, Tyr-Pro-Tyr-Tyr, Leu-Pro-T

153 Ile-Pro-Ile-Gln-Tyr, Tyr-Pro-Tyr-Tyr and Leu-Pro-Tyr-Pro-Tyr were su

154 The most potent inhibitory peptides were Ile-Gln-Ala (beta-CN f187-189) and Val-Glu-Pro (beta-CN f116

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

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

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

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

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

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

161 of damage recognition, which likely involves Gln(41) and Leu(81) as DNA lesion sensors.

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

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

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

165 Insertion of (one at a time) Glu, Leu, Gln, or Cys at positions R295, R141, and R363, or Lys at

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

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

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

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

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

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

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

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

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

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

176 minimum of 33% and maximum of almost 100% of Gln was converted to pGlu in the ionization source, with

177 to the roots, including the accumulation of Gln.

178 onclude that the sensitivity and accuracy of Gln, Glu, and pGlu quantitation by electrospray ionizati

179 Analysis of Gln standards over a concentration range from 0.39 to 20

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

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

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

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

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

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

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

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

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

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

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

191 and Gln depletion or chemical inhibition of Gln uptake blocks soft agar colony formation by Hace1(-/

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

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

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

195 ptide substrate binding, whereas mutation of Gln-768 doubled ATPase activity, suggesting that it may

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

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

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

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

200 large amounts of ammonium in the presence of Gln.

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

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

203 24D, and a hydrophilic residue (Lys, Asn, or Gln) recruits SEC24C.

204 Substitution of Ala, Gly, Cys, or Gln for these two glutamic acid residues abrogated all c

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

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

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

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

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

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

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

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

213 DOTA-4-amino-1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-OCH3 (ARBA05, 3) analogues a

214 DOTA-4-amino-1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leupsi(CHOH- CH2)-(CH2)2-CH3 (RM

215 The potent GRPr antagonist MJ9, Pip-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH(2) (Pip, 4-amino-1-ca

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

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

218 DOTA-4-amino-1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 (RM2, 1; DOTA:1,4,7,

219 The GRPR antagonist JMV594 (H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2) was conjugated to N

220 2], JMV4168 is DOTA-betaAla-betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], and NODA-MPAA is 2

221 MV5132 is NODA-MPAA-betaAla-betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], JMV4168 is DOTA-be

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

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

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

225 o WT for the Lys39Ala, Lys37-Lys38-Lys39/Pro-Gln-Glu, Arg67Ala, and Arg74Ala variants.

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

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

228 ntermediate oxaloacetate efficiently rescues Gln starvation-induced ROS elevation and cell death in H

229 interaction interface where a polar residue (Gln 16) plays a critical role through the formation of a

230 showed that deletion of amino acid residues Gln(489) to Trp(503) resulted in a loss of depolarizatio

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

232 on containing critical charge clamp residues Gln-272, and Phe-264 on the AF-2 surface of PXR.

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

234 ntified a unique set of amino acid residues (Gln(218), Val(277), and Ala(286)) at the putative PpORS

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

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

237 MS/MS protocol that we developed to separate Gln, Glu, and pGlu, we found that free Gln and Glu cycli

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

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

240 myl)lysine isopeptide bonds between specific Gln and Lys residues.

241 ere, we show by generation of liver-specific Gln synthetase (GS)-deficient mice that GS in the liver

242 We found that substituting Gln-1291 with bulky side-chain amino acids abolished the

243 that can enhance their ability to synthesize Gln.

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

245 In mycobacteria, the C-terminal Gln of Pup (prokaryotic ubiquitin-like protein) is deami

246 N-terminal Gln and Glu residues in proteins or peptides have been r

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

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

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

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

251 (R665P-Y667P) substitutions, suggesting that Gln(664) marks the position of the intracellular gate in

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

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

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

257 tution that changed the codon for His-187 to Gln (p.His187Gln).

258 entified a 20-amino acid peptide (Ser-415 to Gln-434) (NaKtide) from the nucleotide binding domain of

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

260 gen bond formation with Cdk5, are changed to Gln, Gln, and Pro in p39.

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

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

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

267 from Hace1(-/-) mice are highly sensitive to Gln withdrawal, leading to enhanced cell death compared

268 ession of sleB(FL) or cwlJ(FL) with a Glu-to-Gln mutation in a predicted active-site residue failed t

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

270 thetase (GluRS) that aminoacylates both tRNA(Gln) and tRNA(Glu) with glutamate.

271 the SUP70 gene encodes the CAG-decoding tRNA(Gln)(CUG).

272 Eukaryotic tRNA(Gln) and tRNA(Glu) recognition determinants are found in

273 so separately differentiated to exclude tRNA(Gln) as a substrate, and the resulting discriminating Gl

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

275 indirect aminoacylation pathway for Gln-tRNA(Gln) biosynthesis in Plasmodium that we hypothesized wou

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

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

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

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

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

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

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

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

284 nRS) enzyme, which pairs glutamine with tRNA(Gln) for protein synthesis, evolved by gene duplication

285 ork of amino acid interactions involving Tyr-Gln-Phe in both SNF and U1A RRM1, but whereas mutations

286 d U1A RRM1, but whereas mutations of the Tyr-Gln-Phe triad result in small local responses in U1A, th

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

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

289 Tumor cells utilize Gln in the tricarboxylic acid (TCA) cycle to maintain su

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

291 acyl carrier protein (65-74) fragment (H-Val-Gln-Ala-Ala-Ile-Asp-Tyr-Ile-Asn-Gly-OH), following the s

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 says showed that substitution of His-50 with Gln, Asp, or Ala promotes alphaSyn aggregation, whereas

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 cing Asp with Glu, Gln, or Cys and R175 with Gln, Asn, or Cys.

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