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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
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
22 es (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that contribute to selecti
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
29 the structural/functional requirement for a Glu side chain at this position, which is homologous to
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
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
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
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
47 residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges with key lysine residues in ER
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
56 the production of (68)Ga-labeled DOTATOC and Glu-NH-CO-NH-Lys(Ahx)-HBED-CC (PSMA-HBED-CC) intended fo
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
62 Smokers showed lower DLPFC NAA, Cr, mI and Glu concentrations and lower lenticular nuclei NAA level
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
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
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
79 ples (seven enantiomer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino
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
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
95 n asymmetric distribution of proton-carrying Glu residues, with the Glu residue of subunit c'' intera
97 mbined OCD group, within vPCC, lower pre-CBT Glu predicted greater post-CBT improvement in symptoms (
100 in the S6 segments to the negatively-charged Glu did not induce constitutive opening of Slo2.1 or Slo
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
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
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
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
120 d heteromeric assemblies with two equivalent Glu-binding sites at beta/alpha intersubunit interfaces,
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
127 trate that Cu stress impairs the pathway for Glu biosynthesis via glutamate synthase, leading to decr
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
137 t sample to date, lower Glu and elevated Gln/Glu levels were observed in adults with SZ and in older
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
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
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
152 physiological concentrations including Glx (Glu+Gln), tNAA (NAA+NAAG), mI all had coefficient of var
154 3 is positioned on a short loop (Asn-Gln-Gly-Glu-Pro) instead of an alpha-helix and forms hydrogen bo
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
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.
163 with potential catalytic function identified Glu-260 as an essential residue whose mutation abolished
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-
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
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
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
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
195 rve that salt bridges between side chains of Glu(-) and Arg(+) are most favorable for the speed of fo
197 PSMA-targeting fluorescent dye conjugates of Glu-urea-Lys-HBED-CC was synthesized, and their biologic
203 s negative feedback through the interplay of Glu and GABA transporters of adjacent astroglia can resu
205 ing the MT cytoskeleton and identify loss of Glu-MTs and RNA mislocalization as common outcomes of AL
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
214 residues, substitution of either Asp-219 or Glu-447 with any other residues resulted in robust activ
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
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
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
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
241 were examined together in relation to right Glu/NAA, only re-experiencing symptoms remained a signif
244 5 binds both thrombin exosite I with segment Glu-35-Asp-47 and the catalytic site with the region Pro
246 st that variation surrounding the C-terminal Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs as well as the number
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
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
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
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
268 90), either charged or neutral, point to the Glu(290) protonation state as a main determinant in the
270 on of proton-carrying Glu residues, with the Glu residue of subunit c'' interacting with Arg735 of su
273 ain at this position, which is homologous to Glu-148 in RPE65, a site in which substitution to Asp ha
275 in domain that mimic phosphorylation (Ser to Glu) or dephosphorylation (Ser to Ala) were mutated.
277 arboxylate residue, the mutation of which to Glu produced early Schiff base proton transfer and stron
279 ant of the protein is cross-linked to a tRNA(Glu)substrate through the terminal methylene carbon of a
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
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
292 ort a two-state model for selectins in which Glu-88 must engage ligand to trigger allostery that stab
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
299 ive site, including residues in the Glu-Xaa8-Glu (double E) loop and the Met-Gln-Trp sequence of the
301 in cells cultured in YP as well as in YNB + Glu media, whereas transcription of MDH1 and MDH2 is act
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