ライフサイエンスコーパス: Glu

1 Glu and Gly levels were measured in vivo in the anterior

2 Glu and Gly levels were positively correlated in patient

3 Glu and WM rCBF decreased linearly with age while Gln an

4 Glu and WM rCBF were correlated with the UCSD Performanc

5 Glu may be involved in the pathophysiology of OCD and ma

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

7 Glu-135, which showed noticeably different calculated pK

8 Glu-143, a key residue for catalysis coordinating the ma

9 Glu-260 of PvdO is at the exact position of the active-s

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

11 Glu-311 at the tip of eL4, and various amino acids aroun

12 Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA-11

13 Glu-urea-based PSMA ligands used for both imaging and ra

14 MD simulations results indicate that: (1) Glu-25 is more frequently in the alpha helix group in th

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

16 cking all LHCSR isoforms, residues Asp(117), Glu(221), and Glu(224)were shown to be essential for LHC

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

18 Mutagenesis of Nef amino acids Arg-134, Glu-174, and Asp-175, which stabilize Nef for AP-2 alpha

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

20 largely independent of the Glu(277)-Arg(173)-Glu(282) network and accompanied by irreversible loss of

21 The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that a

22 es (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that contribute to selecti

23 3)[D-Phe(12),Nle(21,38),C(alpha)MeLeu(27,40),Glu(30),Lys(33)]-acetyl-h /r-CRF(9-41)}.

24 residues Ala-519/Asp-520 of EHD1 and Asn-519/Glu-520 of EHD3 as defining the selectivity of these two

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

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

27 Charged residues Asp-997, Glu-998, Arg-1000, and Lys-1001 in M10, participating in

28 A Glu-217-Gln amino acid substitution was found to confer

29 the structural/functional requirement for a Glu side chain at this position, which is homologous to

30 lf-channel and subsequent deprotonation of a Glu residue at a luminal half-channel.

31 sis-driven rotation causing protonation of a Glu residue at the cytoplasmic half-channel and subseque

32 results do not show evidence of accelerated Glu aging in the anterior cingulate region in SZ compare

33 nylalanine, Phe) and trophic (glutamic acid, Glu) AAs were 4.1 (muscle) and 5.4 (red blood cells), lo

34 d forming salt bridges with the Asp(127) and Glu(229) receptor residues.

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

36 talytic glutamic acid residues (Glu(200) and Glu(414)) of the active site completely abolishes the be

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

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

39 Dual substitution of Asp-219 and Glu-447 to Ala sustained pH-independent activity over a

40 ed that the ionization states of Asp-219 and Glu-447, and not His, strongly determined the pH-depende

41 R isoforms, residues Asp(117), Glu(221), and Glu(224)were shown to be essential for LHCSR3-dependent

42 and Lys-162) and the EphA3 CRD (Glu-248 and Glu-264).

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

44 alphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that contribute to selective interactio

45 s of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 r

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

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

48 rotamer pairs compared to Asp(-)/Arg(+) and Glu(-)/Lys(+).

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

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

51 ology is induced by L-enantiomers of Asp and Glu, whereas 'left-handed' (clockwise) morphology is ind

52 groups of internal (non-N-terminal) Asp and Glu; and (iii) that some isoforms of Ate1 are specific f

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

54 ncreased thalamic mI/Cr, putamen Glx/Cr, and Glu/Cr, and bilaterally decreased thalamic and putamen t

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

56 the production of (68)Ga-labeled DOTATOC and Glu-NH-CO-NH-Lys(Ahx)-HBED-CC (PSMA-HBED-CC) intended fo

57 hippocampi, and significantly higher Glu and Glu/NAA in the right hippocampus.

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

59 2-hydroxybutanoic acid, oxoproline, Gly, and Glu) were altered in UCP3 Tg mice across all training an

60 nd that proton transport between Glu(in) and Glu(ex) is possible in both the presence and absence of

61 n, and conformational changes of Glu(in) and Glu(ex).

62 Smokers showed lower DLPFC NAA, Cr, mI and Glu concentrations and lower lenticular nuclei NAA level

63 explored the use of the proteases Asp-N and Glu-C and a nonenzymatic acid induced cleavage.

64 Across the sample, higher NAA and Glu in the DLPFC and NAA concentrations in multiple loba

65 in studies of the charged variants (Orn and Glu); indeed, the Glu(B26) analog exhibited aberrant agg

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

67 e a link between Cu stress, acid stress, and Glu/Gln metabolism, establish a role for YbaS and YbaT i

68 nd between the 1-methyl heme substituent and Glu-236.

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

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

71 ermediates but is independent of the Glu-Arg-Glu network.

72 actor, bound adjacent to a conserved Glu-Arg-Glu/Asp ionic network in the enzyme's active site.

73 urbing a ctenophore-specific interdomain Arg-Glu salt bridge that is notably absent from vertebrate A

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

75 omatic polar or charged side chains (such as Glu, Ser, or ornithine (Orn)) conferred high activity, w

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

77 uscle and plasma of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced afte

78 nylated by R-transferase are N-terminal Asp, Glu, and (oxidized) Cys.

79 ples (seven enantiomer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino

80 sing cre recombinase driven by the DEAD (Asp-Glu-Ala-Asp) box protein 4 (Ddx4) gene promoter.

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

82 terminal extension containing a His- and Asp/Glu-rich hypervariable region followed by a highly conse

83 estor) ancestor that possessed the beta2-Asp/Glu motif.

84 the tip of the second beta-strand (beta2-Asp/Glu).

85 sin, this is accompanied by proton uptake at Glu(134) in the class-conserved D(E)RY motif.

86 At baseline, Glu did not differ significantly between OCD and control

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

88 We find that proton transport between Glu(in) and Glu(ex) is possible in both the presence and

89 ll trophic position were obtained using bird Glu and Phe delta(15)N values combined with beta values

90 y of the heteromeric mutant receptor to both Glu and IVM, and improved the receptor subunits' coopera

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

92 er conformational space of the salt-bridging Glu(-)/Arg(+) rotamer pairs compared to Asp(-)/Arg(+) an

93 n silico digestion with either Asp-N, Arg-C, Glu-C, Lys-C, or Lys-N.

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

95 n asymmetric distribution of proton-carrying Glu residues, with the Glu residue of subunit c'' intera

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

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

98 12 was substituted by the negatively charged Glu residue.

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

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

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

102 vates Arf6, a process reliant on a conserved Glu within the RalF Sec7 domain.

103 ) as cofactor, bound adjacent to a conserved Glu-Arg-Glu/Asp ionic network in the enzyme's active sit

104 ent of these residues with equally conserved Glu and Val counterpart residues in NusG destabilized in

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

106 A GC-A mutant containing Glu substitutions for all seven chemically identified si

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

108 ain (Arg-156 and Lys-162) and the EphA3 CRD (Glu-248 and Glu-264).

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

110 nd UDP-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala and binds to two activator muro

111 nhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala, as assessed by non-denaturing

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

113 hydro-N-acetyl-beta-d-muramyl-l-Ala-gam ma-d-Glu-meso-DAP-d-Ala-d-Ala and 1,6-anhydro-N-acetyl-beta-d

114 Furthermore, amidation of the d-Glu residue did not alter NOD2 activation.

115 NAA and anterior cingulate cortex and DLPFC Glu levels.

116 n transport between E203 (Glu(in)) and E148 (Glu(ex)), the internal and external intermediate proton

117 characterize proton transport between E203 (Glu(in)) and E148 (Glu(ex)), the internal and external i

118 vely and negatively charged residues (either Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

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

120 d heteromeric assemblies with two equivalent Glu-binding sites at beta/alpha intersubunit interfaces,

121 Addition of exogenous Glu rescues the copA mutant from Cu stress in acidic con

122 Extracellular Glu sustained cell viability under hypoglycemic conditio

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

124 strocytes evoke replacement of extracellular Glu for GABA, driving neurons away from the seizure thre

125 r residues adjacent to Asp-248 in the first (Glu-25) or fourth (Asn-127) transmembrane segments were

126 We probed the functional role of Fis1 Glu-78, whose elevated side chain pKa suggests participa

127 trate that Cu stress impairs the pathway for Glu biosynthesis via glutamate synthase, leading to decr

128 pite the substitution of a basic residue for Glu(in).

129 type and variant enzymes suggested roles for Glu-48 and His-164 in the catalytic mechanism.

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

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

132 reased specific tumor uptake, whereas (68)Ga-Glu-urea-Lys-HBED-CC-AlexaFluor488 (9.12 +/- 5.47 %ID/g)

133 ith the clinically relevant candidate (68)Ga-Glu-urea-Lys-HBED-CC-IRDye800CW reinforced a fast, speci

134 otonation of the extracellular-facing gating Glu (Ex) and Cl(-) binding to the external (Sx) and cent

135 -B8, including Glu/Asp at position 177, Gln/Glu at position 180, Gly/Arg at position 239, and Pro/Se

136 ecreased linearly with age while Gln and Gln/Glu increased linearly with age.

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

138 ignificant effects of age with Glu, Gln, Gln/Glu, and AC white matter (WM) rCBF.

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

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

141 unds (Cr), myo-inositol (mI), and glutamate (Glu) levels in the anterior cingulate cortex and right d

142 Brain glutamate (Glu) signaling may contribute to OCD pathophysiology and

143 eading to a loss of detyrosinated glutamate (Glu)-microtubules (MTs; Glu-MTs) and an inability to sup

144 (aged 8-13 years) to investigate glutamate (Glu) concentrations in two regions of the fronto-striata

145 The metabotropic glutamate (Glu) receptors (mGluRs) play key roles in modulating exc

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

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

148 Synaptic spillover and subsequent glutamate (Glu) uptake in neighboring astrocytes evoke replacement

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

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

151 uch harder N-terminus of the gamma-glutamyl (Glu) unit of GSH.

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

153 in all fractions were dominated by Ala, Gly, Glu and Ser.

154 3 is positioned on a short loop (Asn-Gln-Gly-Glu-Pro) instead of an alpha-helix and forms hydrogen bo

155 We identify a Lys-Gly-Glu (KGE) integrin-binding motif in the FVIIa protease d

156 generated from apoA-I mutants (Tyr(166) --> Glu or Asn), which showed preservation in both LCAT bind

157 ptide analogs of the urotensin II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragm

158 nd left hippocampi, and significantly higher Glu and Glu/NAA in the right hippocampus.

159 Significantly higher Glu and Gly levels were found in both the anterior cingu

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

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

162 increases in free IAA at the expense of IAA-Glu (IAA-glutamate) in the hypocotyl epidermis.

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

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

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

166 ues combined with beta values (difference in Glu and Phe delta(15)N in primary producers) for aquatic

167 e alpha3 domain of HLA-A2 and -B8, including Glu/Asp at position 177, Gln/Glu at position 180, Gly/Ar

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

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

170 ke-5 (TTLL5) glutamylates RPGR(ORF15) in its Glu-Gly-rich repetitive region containing motifs homolog

171 yzing the unfolding of LPL; and (2) that its Glu-to-Lys substitution destabilizes its N-terminal alph

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

173 ther principal differences between EFV and l-Glu in CYP46A1 activation include an apparent lack of l-

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

175 Moreover, EFV and l-Glu synergistically activated CYP46A1.

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

177 6A1 activation include an apparent lack of l-Glu binding to the P450 active site and different pathwa

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

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

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

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

182 on the substrate, and thus, a flexible loop (Glu-334-His-343) is essential in binding sucrose and bet

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

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

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

186 was reused as the PKM2 immunoblot from 1 mM Glu, fractions 1-10.

187 The PKM2 immunoblot from 5 mM Glu, fractions 1-10 was reused as the PKM2 immunoblot fr

188 rosinated glutamate (Glu)-microtubules (MTs; Glu-MTs) and an inability to support the localization of

189 ant of RPGR (RPGR(ORF15)), carrying multiple Glu-Gly tandem repeats and a C-terminal basic domain of

190 dorsal telencephalic glutamatergic neurons (Glu-CB1 -RS) or GABAergic neurons (GABA-CB1 -RS) was stu

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

192 we show that maximum transcript abundance of Glu:glyoxylate aminotransferase 1 (GGT1) is regulated by

193 f this study was to evaluate the accuracy of Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] PET compared wi

194 lasmin activity but stimulated activation of Glu and Lys forms of plasminogen by alphaFXIIa.

195 rve that salt bridges between side chains of Glu(-) and Arg(+) are most favorable for the speed of fo

196 entral region, and conformational changes of Glu(in) and Glu(ex).

197 PSMA-targeting fluorescent dye conjugates of Glu-urea-Lys-HBED-CC was synthesized, and their biologic

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

199 on to Asp-335, the catalytic essentiality of Glu-216 was revealed by site-specific mutagenesis.

200 spAla diketopiperazine and the generation of Glu as the new N-terminal residue.

201 2's localization to MTs and the induction of Glu MTs by either formin.

202 Electrostatic interaction of Glu-998 is of minor importance for the reduction of Na(+

203 s negative feedback through the interplay of Glu and GABA transporters of adjacent astroglia can resu

204 leading to decreased intracellular levels of Glu.

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

206 d NO ligands by site-directed mutagenesis of Glu-87 and His-89.

207 A dual mutation of Glu-181 to Asp in the double E loop and Gln-329 to Ala i

208 In the position of Glu-123 in channelrhodopsin-2, ACRs contain a noncarboxy

209 study was to evaluate the detection rate of Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA li

210 tes have not been described, and the role of Glu-88 in force-assisted allostery has not been examined

211 Alanine substitution of Glu(68), Tyr(92), or Asn(139), which interact with arabi

212 Herein, we investigated the use of Glu-NH-CO-NH-Lys(Ahx)-HBED-CC ((68)Ga-PSMA-HBED-CC) for

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

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

215 Substitution of Arg-72, Tyr-190, Arg-234, or Glu-282 reduced LigY activity over 100-fold.

216 ues (either Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

217 ues bearing basic (Lys, Orn) or acid (Asp or Glu) function.

218 g interface and Arg(506) functions to orient Glu(550) and to stabilize the incipient anionic transiti

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

220 a 16.2% (p=0.004) post-CBT decrease in pACC Glu.

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

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

223 d "complementary" components of the putative Glu-binding pockets.

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

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

226 e alpha-helices (SAHs), are rich in Arg (R), Glu (E) and Lys (K) residues, and stabilized by multiple

227 for CGRP/AM in part by RAMP1 Trp-84 or RAMP2 Glu-101 contacting the distinct CGRP/AM C-terminal resid

228 this was seen as well in DOPC-reconstituted Glu(134)- and Gln(134)-containing bovine opsin mutants a

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

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

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

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

233 shown that substitutions at peptide residue Glu(3) have a broad negative impact on polyclonal T-cell

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

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

236 conserved catalytic glutamic acid residues (Glu(200) and Glu(414)) of the active site completely abo

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

238 domain and substituted Cys for two residues (Glu-816 and Arg-1229) forming a salt bridge between the

239 esis of four new conformationally restricted Glu analogues, 2a-d.

240 sitively correlated with right Glu and right Glu/NAA.

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

242 ht NAA, and positively correlated with right Glu and right Glu/NAA.

243 ma load was positively correlated with right Glu/NAA in PTSD patients.

244 5 binds both thrombin exosite I with segment Glu-35-Asp-47 and the catalytic site with the region Pro

245 highly conserved residues equivalent to SOD5 Glu-110 and Asp-113.

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

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

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

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

250 ues in the active site of AmiC revealed that Glu-229 is critical for both normal cell separation and

251 cross the gp100(280-288) peptide showed that Glu(3) was critically important for TCR binding.

252 Other studies suggest that Glu(550) serves as a general base to generate the Cys(82

253 molecular dynamics simulations suggest that Glu-87 has an important role in ligand recognition, wher

254 a Further mutational analysis suggested that Glu-217 restricts the flexibility of the alpha4-beta4 su

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 n in the IVM-binding site (far away from the Glu-binding sites), which significantly increased the se

260 n the active site, including residues in the Glu-Xaa8-Glu (double E) loop and the Met-Gln-Trp sequenc

261 charged variants (Orn and Glu); indeed, the Glu(B26) analog exhibited aberrant aggregation in either

262 t process that is largely independent of the Glu(277)-Arg(173)-Glu(282) network and accompanied by ir

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

264 ergy intermediates but is independent of the Glu-Arg-Glu network.

265 beta-casein revealed favored cleavage of the Glu-X bond at subcritical water temperatures of 160 and

266 y, structural analysis demonstrated that the Glu(3) --> Ala substitution resulted in a molecular swit

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

268 90), either charged or neutral, point to the Glu(290) protonation state as a main determinant in the

269 localization, of HMA4 in planta, whereas the Glu residue is important but not essential.

270 on of proton-carrying Glu residues, with the Glu residue of subunit c'' interacting with Arg735 of su

271 PETH-2(CFTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection.

272 extracellular side, with either two or three Glu-binding site interfaces.

273 ain at this position, which is homologous to Glu-148 in RPE65, a site in which substitution to Asp ha

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

275 in domain that mimic phosphorylation (Ser to Glu) or dephosphorylation (Ser to Ala) were mutated.

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

277 arboxylate residue, the mutation of which to Glu produced early Schiff base proton transfer and stron

278 Taken together, Glu-CB1 -RS and GABA-CB1 -RS mice show the usual CB1 rec

279 ant of the protein is cross-linked to a tRNA(Glu)substrate through the terminal methylene carbon of a

280 th the observation that the geranylated tRNA(Glu) UUC recognizes GAG more efficiently than GAA.

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

282 RlmN contacts the entire length of tRNA(Glu), accessing A37 by using an induced-fit strategy tha

283 respond to P2Y14 R agonist UDP-glucose (UDP-Glu) while hCPCs with higher P2Y14 R expression showed e

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

285 ed enhanced proliferation in response to UDP-Glu stimulation.

286 Blocking modification of tRNA(UUC)(Glu) and tRNA(QUC)(Asp) increases errors, suggesting tha

287 one-third of the dentate molecular layer was Glu-CB1 -RS, 53.19% (glutamatergic terminals); 2.30% (GA

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

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

290 tations at the intersubunit interfaces where Glu (the neurotransmitter) binds.

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

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

293 ses revealed significant effects of age with Glu, Gln, Gln/Glu, and AC white matter (WM) rCBF.

294 hannel of the protein, replacing Asp217 with Glu (D217E), results in the creation of a light-driven,

295 th the most abundant peptide commencing with Glu (residue 3 in Abeta1-40/1-42) that is present as pyr

296 ced sampling trajectories of constructs with Glu(290), either charged or neutral, point to the Glu(29

297 kinase that phosphorylates the Ser in Ser-X-Glu/phospho-Ser (pSer) motifs in the small-integrin-bind

298 sphorylation of serine residues in the Ser-x-Glu/pSer motifs in several enamel matrix proteins.

299 ive site, including residues in the Glu-Xaa8-Glu (double E) loop and the Met-Gln-Trp sequence of the

300 MDH2 is activated in cells cultured in YNB + Glu but not in YP.

301 in cells cultured in YP as well as in YNB + Glu media, whereas transcription of MDH1 and MDH2 is act

302 nes in cells cultured in YP but not in YNB + Glu.