ライフサイエンスコーパス: Glu

1 Glu and WM rCBF were correlated with the UCSD Performanc

2 Glu was lower in adults with SZ compared with healthy co

3 Glu-310 of this motif auto-catalytically forms an ester

4 Glu-PLGA is a branched (also known as star-shaped) polym

5 We propose that IGF-1 Glu-58 interacts with IGF-1R Arg-704 and belongs to IGF-

6 -1 action at the GLP-1R, whereas des-His(1)-[Glu(9)]glucagon antagonized glucagon action at the GluR,

7 ing Ex(9-39) in combination with des-His(1)-[Glu(9)]glucagon in INS-1 832/13 cells, we validated a du

8 Exposed glutamate residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges with key l

9 1) The central gate residue Glu(130) (Glu(90) in Chlamydomonas reinhardtii (Cr) ChR2) (i) unde

10 d glutamate residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges with key lysine re

11 In contrast, Ala substitution of Lys-57, Glu-77, and Lys-96, located in the loops adjacent to the

12 around the portal region, including Lys-57, Glu-77, and Lys-96.

13 the additional C-terminal serine-rich Asn-63-Glu-82 region (absent in orthologues from anophelines of

14 ing with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN

15 on three residues in the CT, namely Glu-719, Glu-721, and Leu-725, that are part of a novel motif, EX

16 We found that Tyr 96, Glu 201, Arg 204, and Trp 234 in the presumptive active

17 beta-binding proteins 3 and 4 (LTBP3/4) at a Glu-Val and Glu-Ala site, respectively.

18 CrmD to inhibit human LTalpha is caused by a Glu-Phe-Glu motif in its 90s loop.

19 cids, aspartic acid (Asp) and glutamic acid (Glu) can enhance the solubility of many poorly soluble d

20 located and highly conserved glutamic acid (Glu-176) within the beta3 transmembrane region and its p

21 The amino acids Glu-282 and Phe-286 near the extracellular domain on the

22 ) and extracellular alpha-glucosidase (alpha-Glu) and protease (PRO) enzymes were significantly inhib

23 titratable residues, such as DFG-Asp, alphaC-Glu, and HRD-Asp, change protonation states dependent on

24 so noted that residues Lys-101, Trp-103, and Glu-184 are crucial for proteolytic activity.

25 on coordinated by His-6, His-8, His-179, and Glu-282.

26 n the conserved acidic residues, Asp-189 and Glu-247.

27 that residues Glu-179, His-175, His-202, and Glu-276 are directly involved in the coordination of the

28 ation, our results revealed that Asp(21) and Glu(89) both play key roles in dimer dynamics and contri

29 ort signal, because substituting Asp-211 and Glu-213 with alanine induced retention of the MERS-CoV M

30 t a putative pH-sensing role for Asp-219 and Glu-447 in hENT3 and that the size, ionization state, or

31 veral BT0997 variants identified Glu-294 and Glu-361 as the catalytic acid/base and nucleophile, resp

32 chemokine XCL1 (Val(1), Gly(2), Ser(3), and Glu(4)) contribute a large fraction of the binding energ

33 cate that key glutamate residues (Glu-31 and Glu-61) in these domains may be sites of pH-sensitive in

34 its Ala variants of Leu-725 and Glu-719 and Glu-721 revealed that Leu-725 enhances PC7 localization

35 ndosomes and that, together with Glu-719 and Glu-721, it increases the endosomal activity of PC7 on h

36 n of PC7 and its Ala variants of Leu-725 and Glu-719 and Glu-721 revealed that Leu-725 enhances PC7 l

37 that autolysis occurs at Glu-729-Val-730 and Glu-732-Ala-733 in the ADAMTS7 Spacer domain, which was

38 ng pocket in mVDAC1 localized to Thr(83) and Glu(73), respectively.

39 residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges with key lysine residues in ER

40 in this binding site are Ile-92, Lys-97, and Glu-99, which are entirely or mostly specific to the TGF

41 suggest that Ile-A10, Ser-A12, Leu-A13, and Glu-A17 also belong to insulin's site 2.

42 The presence of acidic residues Asp and Glu near the peptide N-terminus is by far the most promi

43 a(2+) binding was perturbed when the Asp and Glu residues in the motif were substituted by alanine.

44 by adding chiral acidic amino acids (Asp and Glu).

45 a protonable side chain, i.e., His, Asp, and Glu, were able to mediate electron transfer at physiolog

46 cids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively silent with regard to (.) OH.

47 two non-arginyl dipeptides: Asp-Asp (DD) and Glu-Asp (ED).

48 lactate in the first step medium and EAA and Glu in the second step medium were competent to implant

49 des enhanced resolution to quantify GABA and Glu levels in the thalamus of CHR individuals.

50 novel insights implicating accumbal Gln and Glu balance on the prediction of specific computational

51 ng with higher levels of glutamate (Glu) and Glu/NAA.

52 wo Cys residues from one subunit and His and Glu residues from the other.

53 in 5-HT(2A)/mGlu(2) cells and both 5-HT- and Glu-induced responses in 5-HT(2A)/mGlu(2)/Gqo5 cells.

54 f Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

55 of a high percentage (>75%) of Arg, Lys, and Glu residues, are exceptions to this rule but have been

56 s contain a high percentage of Arg, Lys, and Glu residues.

57 h in charged residues (such as Arg, Lys, and Glu) with potential ion pairs across adjacent turns of t

58 As NAA and Glu are commonly regarded to reflect neuronal health and

59 er proteinaceous or labile DOM (Alg, PA, and Glu) revealed that DOM with higher molecular weights wou

60 rg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two non-arginyl dipeptides: Asp-Asp (D

61 tCho (glia-related metabolites) and tNAA and Glu (neuron-related metabolites) in ACC, DLPFC, hippocam

62 proteins 3 and 4 (LTBP3/4) at a Glu-Val and Glu-Ala site, respectively.

63 iments indicate a clear role for the Glu-Arg-Glu network in both catalysis and oxidative maturation.

64 is was highly dependent on an intact Glu-Arg-Glu network, as only Glu --> Asp substitutions retain ac

65 la-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two non-arginyl dipeptid

66 of enzymes complementary to trypsin, such as Glu-C, Asp-N, Lys-N, Arg-C, LysargiNase has been reporte

67 A extracted from Sandostatin LAR, as well as Glu-PLGAs obtained from three different manufacturers.

68 atic mutagenesis of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that although bo

69 Target of Egr1 (TOE1) is an Asp-Glu-Asp-Asp (DEDD) domain containing deadenylase that is

70 eptor, which recognises a C-terminal Lys-Asp-Glu-Leu (KDEL) sequence.

71 t recognition of a carboxyl-terminal Lys-Asp-Glu-Leu (KDEL) signal by the KDEL receptor.

72 reveal that a conserved diacidic motif (Asp-Glu) in these proteins is necessary for their export.

73 cumulation of the gene encoding the sole Asp-Glu-Ala-Asp (DEAD)-box RNA helicase in Synechocystis sp.

74 GEs contain a Ser-His-Asp/Glu catalytic triad, but the location of the catalytic a

75 IFICANCE STATEMENT Alterations in astrocytic Glu uptake can play a role in synaptic plasticity and ne

76 tment of WT preparations with the astrocytic Glu uptake blocker TFB-TBOA (100 nm) mimicked the TauD c

77 Thus, astrocytic Glu transport remains a promising target for therapeutic

78 odegeneration, a mismatch between astroglial Glu uptake and presynaptic Glu release could be detected

79 Gly junction and regioselective ligation at Glu junction were theoretically studied by computational

80 It also suggested that autolysis occurs at Glu-729-Val-730 and Glu-732-Ala-733 in the ADAMTS7 Space

81 e results imply distinct roles for the beta3-Glu-176 residue and the beta3-ECD in regulating the conf

82 der caused by a single point mutation (beta6 Glu -> Val) on the beta-chain of adult hemoglobin (HbA)

83 ted to promote salt-bridge formation between Glu and Lys/Arg.

84 nd capable of unambiguously identifying both Glu and isoGlu.

85 ndings demonstrate abnormally elevated brain Glu and Gly levels in patients with first-episode psycho

86 d triggers the loss of a distal salt bridge (Glu-343/Arg-378) via a large side-chain motion that comp

87 Exposed glutamate residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges wi

88 orresponds to the general base in catalysis, Glu-34.

89 mbined OCD group, within vPCC, lower pre-CBT Glu predicted greater post-CBT improvement in symptoms (

90 CAIV was mediated by the negatively charged Glu-73 and in rat CD147 by the positively charged Lys-73

91 Slo2.1 or Slo2.2 with the negatively-charged Glu did not induce constitutive channel opening.

92 in the S6 segments to the negatively-charged Glu did not induce constitutive opening of Slo2.1 or Slo

93 ntified three residues on the C-linker-CNBD (Glu(478), Gln(482), and His(559)) that form direct inter

94 itor extracellular glutamate concentration ([Glu]) at individual corticostriatal synapses, we can now

95 entiated based on a cis- or trans-configured Glu(18)-Pro(19) peptide bond.

96 The conserved Glu residue at position 5 (E5) of mature (pseudo)pilins

97 s work demonstrates that peptides containing Glu or Asp that are preorganized to adopt beta-hairpin s

98 Within controls, Glu was stable from scan-to-scan.

99 erage than that obtained with a conventional Glu-C digestion approach.

100 ate the N, S, and O side chains of His, Cys, Glu, Asp, and Lys residues.

101 n-nitrogen hydrolase domain containing a Cys-Glu-Lys catalytic triad.

102 The anti-biofilm activity of D-Asp and D-Glu was studied on Staphylococcus aureus biofilms.

103 ingly at equimolar combinations, D-Asp and D-Glu were able to significantly disperse (at 20 mM and 40

104 improved minigastrin analog (177)Lu-DOTA-(d-Glu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-PheNH(2) ((177)Lu-PP-F11

105 Methods: DOTA-D-Glu-Ala-Tyr-Gly-Trp-(N-Me)Nle-Asp-1-Nal-NH(2) (DOTA-MGS5

106 nhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP.

107 Moreover, the state-trait changes in dACC Glu and rsFC strength between the dACC and both SFG and

108 We observed reduced dACC Glu (P = 0.029) along with a significant reduction in pl

109 mination of the relevant parameters defining Glu-PLGA, such as the branching number, and the presence

110 lots were also used to distinguish different Glu-PLGAs.

111 round the Ca(2+) coordination site, enabling Glu-88 to engage Ca(2+) and fucose.

112 genetic defect in ER alpha-glucosidase I (ER Glu I) who showed resistance to viral infections, identi

113 sistance to viral infections, identifying ER Glu I as a key antiviral target.

114 The first crystal structure of mammalian ER Glu I will constitute the basis for the development of p

115 Targeting ER Glu I with UV-4B-derived compounds may alter treatment p

116 Extracellular Glu sustained cell viability under hypoglycemic conditio

117 bolism of otherwise neurotoxic extracellular Glu through a truncated tricarboxylic acid cycle under h

118 de-chain phenolates and one carboxylate from Glu.

119 dered alpha-helical structure extending from Glu-6 to Lys-63.

120 erived Gln via the blood to the PDTX to fuel Glu and glutathione synthesis while gluconeogenesis occu

121 cetic acid (HBED-CC)-based PET tracer (68)Ga-Glu-urea-Lys(Ahx)-HBED-CC ((68)Ga-PSMA-11) to allow accu

122 Aergic and glutamatergic balance (i.e., GABA/Glu), may underlie thalamic deficits linked to the risk

123 however, a lack of in vivo evidence of GABA/Glu thalamic abnormalities in the CHR state.

124 ltogether, these findings indicate that GABA/Glu abnormalities are present in the thalamus before the

125 We found that GABA/Glu was significantly reduced in the right medial anteri

126 The GABA/Glu reduction was negatively correlated with general sym

127 Signals from Gln, Glu with chemical shift around 2.4 ppm, from Cr, PCr, an

128 t sample to date, lower Glu and elevated Gln/Glu levels were observed in adults with SZ and in older

129 o measure anterior cingulate (AC) glutamate (Glu) and glutamine (Gln) and arterial spin labeling eval

130 etic resonance imaging (fMRI) and glutamate (Glu) concentration with magnetic resonance spectroscopy

131 te (Alg), polyaspartate (PA), and glutamate (Glu).

132 ), lysine (Lys), aspartate (Asp), glutamate (Glu) and cysteine (Cys) phosphorylation sites on human p

133 Changes in the balance between glutamate (Glu) release and uptake may stimulate synaptic reorganiz

134 elta9-THC significantly increased Glutamate (Glu) + Glutamine (Gln) metabolites (Glx) in the left cau

135 NAA), along with higher levels of glutamate (Glu) and Glu/NAA.

136 Lower and moderate levels of glutamate (Glu) in the right pACC significantly moderated the inter

137 and hippocampus; lower levels of glutamate (Glu) were observed in DLPFC.

138 ns and inquired whether levels of glutamate (Glu), glutamine (Gln), GABA or their ratios predict inte

139 d tolerance and contribute to the glutamate (Glu)-dependent acid resistance system in this organism.

140 his study was to quantify in vivo glutamate (Glu) and glycine (Gly) levels in patients with first-epi

141 Total protein (TP) and glutelin (Glu), albumin (Alb) and globulin (Glo) fractions were di

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

143 physiological concentrations including Glx (Glu+Gln), tNAA (NAA+NAAG), mI all had coefficient of var

144 s associated with MRS markers of hippocampus Glu excess, together with indices of compromised neuron

145 olarity and length (i.e. Ala, Arg, Cys, His, Glu, and Leu) on transporter stability and function.

146 th autosomal dominant PD) through homologous Glu-to-Lys substitutions in alphaSyn's N-terminal region

147 with potential catalytic function identified Glu-260 as an essential residue whose mutation abolished

148 zation of several BT0997 variants identified Glu-294 and Glu-361 as the catalytic acid/base and nucle

149 Mal)(2), Fe(III)(Mal)(2), glutamine: Fe(III)(Glu)(2) and nicotianamine: Fe(II)(NA); copper complexes

150 with the heme 5-methyl, and the immobilized Glu-310 contributes to substrate positioning.

151 c binding site at the functionally important Glu(73) residue.

152 abolite data also indicate a major change in Glu and GABA metabolism.

153 The peptides were rich in Glu, Asp, Lys, Gly and Leu, and also exhibited diverse b

154 ynojirimycin; MON-DNJ) capable of inhibiting Glu I in vivo is sufficient to prevent death in mice inf

155 e-specific membrane antigen (PSMA) inhibitor Glu-NH-CO-NH-Lys(Ahx) using the (68)Ga chelator HBED-CC

156 As an intact Glu-343/Arg-378 bridge is the default state in unbound E

157 catalysis was highly dependent on an intact Glu-Arg-Glu network, as only Glu --> Asp substitutions r

158 roducing a positive charge at the interface (Glu(32) to Lys) also lowered the affinity.

159 tions revealed functional contacts involving Glu(4) of XCL1 and Tyr(117) and Arg(273) of XCR1.

160 rutinoside (K-Ru), kaempferol-3-glucoside (K-Glu) and derivative of quercetin produced in the reactio

161 Key Glu residues within a Csm1 loop segment of Csm(crRNA) ad

162 EFV and l-Glu similarly increased the CYP46A1 kcat, the rate of th

163 f PGA with canonical substrates (L-Asp and L-Glu) and an opportunistic ligand, a citrate anion, were

164 xperiments revealed the LBD preference for l-Glu but also for sulfur-containing amino acids.

165 ively higher activity with IA derived from L-Glu and aromatic amino acids.

166 that CYP46A1 is activated by l-glutamate (l-Glu), l-aspartate, gamma-aminobutyric acid, and acetylch

167 the methods of Marfey and Mosher indicated l-Glu, l-Ile, l-Phe and 1S-configurations, respectively; R

168 ith cholesterol, in the presence of EFV or l-Glu, suggest that water displacement from the heme iron

169 We also found that l-Glu and other activating neurotransmitters bind to the s

170 nd in vivo studies by others, suggest that l-Glu-induced CYP46A1 activation is of physiological relev

171 aminobutyric acid, and acetylcholine, with l-Glu eliciting the highest increase (3-fold) in CYP46A1-m

172 lts suggest that gallium 68 ((68)Ga)-labeled Glu-urea-Lys (Ahx)-HBED-CC ligand targeting the prostate

173 alue of combined gallium 68 ((68)Ga)-labeled Glu-urea-Lys (Ahx)-HBED-CC ligand targeting the prostate

174 In the largest sample to date, lower Glu and elevated Gln/Glu levels were observed in adults

175 ia using supplemental oxygen in vivo lowered Glu levels as measured by (1)H magnetic resonance spectr

176 scopy, of substituting key charged Arg, Lys, Glu, and Asp residues by Gly or His.

177 beta) production, and predominantly at major Glu(11) site to generate C89, resulting in truncated Abe

178 (as an indicator of uptake) and the maximal [Glu] elevation next to the active zone (as an indicator

179 bou-2 mutant deficient in the mitochondrial Glu transporter A BOUT DE SOUFFLE (BOU) and identified 2

180 widely used 4-methoxy-7-nitro-indolinyl(MNI)-Glu probe prevented such off-target effects while not ch

181 G5-MNI-Glu was used with optofluidic delivery to stimulate dopa

182 changing the photochemical properties of MNI-Glu significantly.

183 on of Y155, or its phospho-mimetic mutation (Glu), prevents the interaction of RLC with the myosin he

184 tion of the following metabolites: Ala, NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG, and A

185 demonstrate the following metabolites: NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, NAAG, and A

186 zoom in on three residues in the CT, namely Glu-719, Glu-721, and Leu-725, that are part of a novel

187 utamatergic and forebrain GABAergic neurons (Glu/GABA-CB1-KO) resulted in an increased septa area in

188 had no effect or increased Vmax Ala but not Glu substitution for Ser-497 increased the Michaelis con

189 talysis including the catalytic nucleophile (Glu-297) and acid/base residue (Glu-160).

190 cular weight to <4 for the majority (94%) of Glu-PLGA.

191 mass spectrometry for the target analysis of Glu-1-Fibrinopeptide B spiked in a protein digest mixtur

192 nt amino acid side chains as ligands, and of Glu acting as ligand to a [2Fe-2S] cluster.

193 GPC-4D enabled characterization of Glu-PLGA in its concentration, absolute molecular weight

194 study were developed for characterization of Glu-PLGA with the lactide:glycolide (L:G) ratio of 55:45

195 res can also be used for characterization of Glu-PLGAs made of different L:G ratios.

196 elping to explain the detrimental effects of Glu-221 substitution on HABP2 activity.

197 next to the active zone (as an indicator of Glu release).

198 ing the MT cytoskeleton and identify loss of Glu-MTs and RNA mislocalization as common outcomes of AL

199 Intriguingly, mutation of Glu-51, a single residue within this region, permits for

200 in subunit e (eArg-8) with Ala or Glu or of Glu-83 in subunit g (gGlu-83) with Ala or Lys destabiliz

201 Se accumulated in the order of Glu > Alb > Glo.

202 sed to determine the branching parameters of Glu-PLGA extracted from Sandostatin LAR, as well as Glu-

203 and characterize the branching parameters of Glu-PLGA.

204 cies could be traced to the participation of Glu-818 in an intricate hydrogen-bonding/salt-bridge net

205 cleaved substrates on the C-terminal side of Glu irrespective of neighboring residues, as shown using

206 In contrast, substitution of Glu-106, which might be part of a dimerization interface

207 ealed that single or double substitutions of Glu-47 and Lys-50 do not restore GlcNAc glycoconjugates.

208 DP-GlcNAc uptake; and (iii) substitutions of Glu-47 and Lys-50 dramatically alter kinetic parameters,

209 rogated pH sensitivity, and substitutions of Glu-67 and Phe-269 altered the pH and voltage modulation

210 tiator, was tracked through the synthesis of Glu-PLGA by both (13)C NMR and enzymatic analysis.

211 A processing, thus preventing translation of Glu codons.

212 on methods indicate that the branch units of Glu-PLGAs extracted from Sandostatin LAR range from 2 (i

213 nt on an intact Glu-Arg-Glu network, as only Glu --> Asp substitutions retain activity.

214 al telencephalic glutamatergic neurons only (Glu-CB1-KO) or in both glutamatergic and forebrain GABAe

215 residues, substitution of either Asp-219 or Glu-447 with any other residues resulted in robust activ

216 n of Arg-8 in subunit e (eArg-8) with Ala or Glu or of Glu-83 in subunit g (gGlu-83) with Ala or Lys

217 , a cyclization product of N-terminal Gln or Glu residues, is a widespread post-translational modific

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

219 en bond donor to Tyr191(*) (via Leu232His or Glu) substantially alters activity by increasing the ET

220 ction (p=0.034) was observed, driven by pACC Glu dropping 19.5% from scan-to-scan for patients random

221 the decay time constant of the perisynaptic Glu concentration (TauD), as an indicator of uptake, and

222 quantify the time constant of perisynaptic [Glu] decay (as an indicator of uptake) and the maximal [

223 inhibit human LTalpha is caused by a Glu-Phe-Glu motif in its 90s loop.

224 hts led to the identification of H-d-Pro-Pip-Glu-NH2 as a highly reactive and stereoselective amine-b

225 etermination of glucose within glucose-PLGA (Glu-PLGA) branched polymers.

226 Glucose-initiated PLGA (Glu-PLGA) has been used in Sandostatin(R) LAR Depot (oct

227 ell division, DNA methylation, pluripotency, Glu metabolism, neurogenesis, and cardiogenesis.

228 etween astroglial Glu uptake and presynaptic Glu release could be detected if both parameters were as

229 s) in the negative regulatory region and Pro-Glu-Ser-Thr-rich domains, the same two hotspots seen in

230 amilies of proteins, named for conserved Pro-Glu and Pro-Pro-Glu motifs in their N termini.

231 ins, named for conserved Pro-Glu and Pro-Pro-Glu motifs in their N termini.

232 We found that at least five PPE (Pro-Pro-Glu) proteins are targets for T-cell recognition in Mtb.

233 n quercetin-glucoside and p-coumaric acid (Q-Glu-p-CouA).

234 -rutinoside (Q-Ru), quercetin-3-glucoside (Q-Glu), kaempferol-3-rutinoside (K-Ru), kaempferol-3-gluco

235 electins and to E88D selectins that replaced Glu-88 with Asp.

236 er degree of frequency potentiation/residual Glu accumulation and were selected for our first iGlu (u

237 f the CntA trimer via the "bridging" residue Glu-205.

238 he interaction of the CD38 catalytic residue Glu-226 with the "northern" ribose.

239 1) The central gate residue Glu(130) (Glu(90) in Chlamydomonas reinhardtii (Cr) ChR2

240 region around the conserved glutamyl residue Glu(49) of TatB from Escherichia coli Functional analyse

241 ic interaction with post-relay helix residue Glu-469, which affects the mechanics of the myosin power

242 residue of NT[8-13] with an acidic residue (Glu(179)) located in the ECL2 of hNTS2 or with a basic r

243 nucleophile (Glu-297) and acid/base residue (Glu-160).

244 three conserved negatively charged residues Glu-179, Asp-180, and Asp-181 that could contribute to n

245 We also found that residues Glu-179, His-175, His-202, and Glu-276 are directly invo

246 ctures indicate that key glutamate residues (Glu-31 and Glu-61) in these domains may be sites of pH-s

247 were examined together in relation to right Glu/NAA, only re-experiencing symptoms remained a signif

248 We substituted Glu-176 with lysine (E176K) in the WT beta3-subunit and

249 st that variation surrounding the C-terminal Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs as well as the number

250 mer conformations, and are more dynamic than Glu-Lys.

251 r hsp70-mediated regulation of SOD2 and that Glu(446) and Arg(447) cooperate with other amino acid re

252 s a rational explanation, demonstrating that Glu and Arg form salt bridges more commonly, utilize a w

253 bers, and a 3D-homology model predicted that Glu-47 and Lys-50 are facing the central cavity of the p

254 The Glu(49) region of TatB was found also to contact distinc

255 rotein-folding conformation triggered by the Glu-145 replacement of Asp.

256 ic experiments indicate a clear role for the Glu-Arg-Glu network in both catalysis and oxidative matu

257 beta-cleavage site of BACE1 in APP from the Glu(11) site to the Asp(1) site both in male and female

258 ion shifted the BACE1 cleavage site from the Glu(11) to the Asp(1) site, resulting in much higher C99

259 ios between Gln and the other members of the Glu family as traits.

260 ms tested despite strict conservation of the Glu(45) residue among these organisms.

261 respective of the presence or absence of the Glu-176 residue.

262 Homology modeling suggested that the Glu-221 side chain could sterically hinder insertion of

263 Our findings suggest that the Glu-rich long C-terminal extension of insect TnT functio

264 risons of nuclease enzymes suggest that this Glu(Asp)-mediated mechanism for third ion recruitment an

265 , which directs PARP-1 catalytic activity to Glu and Asp residues.

266 and straight-chain fatty acids esterified to Glu or Suc.

267 Substitution of the Lys residues to Glu markedly reduced integrin binding of E128K IL-1beta,

268 Ala, SA) or phosphomimetic residues (Ser to Glu, SE) reduced Brg1 phosphorylation by CK2.

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

270 results indicate that higher accumbal Gln-to-Glu ratio predicts better overall performance and reduce

271 based analysis revealed that accumbal Gln-to-Glu ratio specifically relates to stamina; i.e., the cap

272 cco (Nicotiana tabacum) plants to alter tRNA(Glu) expression levels and introduced a point mutation i

273 of GluTR activity through inhibition by tRNA(Glu) precursors causes tetrapyrrole synthesis to become

274 the transfer of glutamate from charged tRNA(Glu) to the peptide substrate, or how they carry out the

275 t analogs that mimic substrate glutamyl-tRNA(Glu) and the glutamylated peptide intermediate, and dete

276 of glutamyl-tRNA reductase by immature tRNA(Glu) We further demonstrate that whereas overexpression

277 ly cleaves a subset of tRNAs, including tRNA(Glu), tRNA(Gly), tRNA(Lys), tRNA(Val), tRNA(His), tRNA(A

278 s(2) modification at U34 of tRNA(Lys), tRNA(Glu), and tRNA(Gln) causes ribosome pausing at the respe

279 dings provide insight into the roles of tRNA(Glu) at the intersection of protein biosynthesis and tet

280 onstrate that whereas overexpression of tRNA(Glu) does not affect tetrapyrrole biosynthesis, reductio

281 How the tRNA(Glu) pool is distributed between the two pathways and wh

282 The chloroplast glutamyl-tRNA (tRNA(Glu)) is unique in that it has two entirely different fu

283 ed between the two pathways and whether tRNA(Glu) allocation limits tetrapyrrole biosynthesis and/or

284 indered amino acid junctions (Gly, Ala, Trp, Glu).

285 e interaction between a highly conserved Trp/Glu residue pair in the lower pore is detrimental to gat

286 Mechanistically, UDP-Glu stimulation enhanced the activation of canonical gro

287 assay with the genetically encoded ultrafast Glu sensor iGlu (u) We report findings from individual c

288 Ultrafiltrated Glu hydrolysate of four days germinated chickpeas treate

289 atients (mean age, 64.2 y old) who underwent Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA11)

290 e aggregation of the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segment

291 tive excitatory and inhibitory synapses were Glu-CB1 -RS, 21.89% (glutamatergic terminals); 2.38% (GA

292 When Glu(73) was mutated to a glutamine, KK174 no longer phot

293 walls of the ion-selectivity filter, whereas Glu and Lys are in positions to accept and release Na(+)

294 We assessed whether Glu measured with magnetic resonance spectroscopy (MRS)

295 ort a two-state model for selectins in which Glu-88 must engage ligand to trigger allostery that stab

296 ii) simultaneous substitution of eArg-8 with Glu and of gGlu-83 with Lys rescued digitonin-stable F-A

297 emarkably, double replacement of eArg-8 with Glu and of gGlu-83 with Lys restored high-conductance ch

298 by replacing Gly in a CCK-8 derivative with Glu.

299 d g, most likely through an interaction with Glu-83 of subunit g.

300 n to early endosomes and that, together with Glu-719 and Glu-721, it increases the endosomal activity