ライフサイエンスコーパス: glutamic

1 nd kinetics of (S)-4-(3-[18F]fluoropropyl)-l-glutamic acid ((18)F FSPG) in healthy volunteers and to

2 cted mutagenesis of the Env7 alanine-proline-glutamic acid (APE) motif Glu269 to alanine results in a

3 However, mutation that substituted glutamic acid (E) for glutamine (Q) at amino acid positi

4 The substitution of glutamic acid (E) for lysine (K) at position 627 of the

5 C-terminal domain of connexin43 (Cx43) into glutamic acid (E) or alanine (A) residues.

6 A glutamic acid (E)-to-glycine (G) difference at position

7 e show that a single hydrogen bond between a glutamic acid (E90) and an asparagine (N258) residue suf

8 Poly-gamma-glutamic acid (gamma-PGA) is an important biochemical pr

9 e pgsBCA cluster (responsible for poly-gamma-glutamic acid (gamma-PGA) synthesis), were intentionally

10 n (CBP)/p300 interacting transactivator with glutamic acid (Glu) and aspartic acid (Asp)-tail 2 (Cite

11 ve methods for measuring glutamine (Gln) and glutamic acid (Glu) in cell cultures and other biologica

12 xidase (GmOx) microelectrode for measuring l-glutamic acid (GluA) in oxygen-depleted conditions, whic

13 l-aspartic acid (IA-Asp) and indole-3-acetyl-glutamic acid (IA-Glu) conjugates.

14 rtic acid (IAA-Asp) and indole-3-acetic acid glutamic acid (IAA-Glu) of 438- and 240-fold, respective

15 replacing this lysine with alanine (K265A), glutamic acid (K265E) or glutamine (K265Q), and the func

16 erved in NuoL (LLys(399)) but is replaced by glutamic acid (MGlu(407)) in NuoM.

17 transmitters glutamate and N-acetyl-aspartyl-glutamic acid (NAAG) and their precursor glutamine.

18 mug/mL histidine (p < 0.001), 100 mug/mL of glutamic acid (p < 0.05) and 200 mug/mL of glutamic acid

19 (EnvD) which rapidly hydrolysed poly-gamma-d-glutamic acid (PDGA), the constituent of the anti-phagoc

20 tilayers ~700nm thick fabricated from poly-l-glutamic acid (PGA) and poly-l-lysine (PLL) can be loade

21 A skin prick test for poly-gamma-glutamic acid (PGA) which is a component of jellyfish st

22 eimer's disease, covalently linked to poly-l-glutamic acid (PGA).

23 is work, we demonstrate that proline-proline-glutamic acid (PPE)17 protein of Mycobacterium tuberculo

24 atural amino acid termed a proline-templated glutamic acid (ptE) that constrained both the backbone a

25 zolin-6-yl]amino]benzoyl]-l-gamma-glutamyl-d-glutamic acid 1 (BGC 945, now known as ONX 0801), is a s

26 ive mutagenesis analysis, we identified that glutamic acid 14 (E14) of vBcl-2 is critical for KSHV ly

27 to a chemical reaction, the deprotonation of glutamic acid 148 (E148).

28 he lumen-exposed residues, threonine 162 and glutamic acid 173, form stabilizing hydrogen bonds betwe

29 interactions that include a lysine 113(K113):glutamic acid 195 (E195) salt bridge between actin subun

30 acids, L-aspartic acid 4-methyl ester and L-glutamic acid 5-methyl ester, is a convenient and sensit

31 External glutamic acid 623 (E623) is key for TMEM16A's ability to

32 ngs we propose that external protons titrate glutamic acid 623, which enables voltage activation of T

33 Previous conclusions on the involvement of glutamic acid 90 in channel opening are ruled out by dem

34 erred a small-plaque avirulent phenotype and glutamic acid a large-plaque virulent phenotype.

35 We show that protonation of the conserved glutamic acid alters the peptide insertion depth in the

36 Glutamic acid and alanine make up more than 60 per cent

37 f glutamic acid (p < 0.05) and 200 mug/mL of glutamic acid and aspartic acid (p < 0.001) without affe

38 Free glutamic acid and free aspartic acid found in the PPI hy

39 m, were conjugated quickly and directly with glutamic acid and glutamine, and further with peptides,

40 PELP1 (proline, glutamic acid and leucine rich protein 1) is a nuclear r

41 rs containing the blocks of ethylene glycol, glutamic acid and phenylalanine (PEG-PGlu-PPhe) were suc

42 TPs calculated from delta (15)N values of glutamic acid and phenylalanine, which range from 8.3-33

43 s from wet solids were significantly rich in glutamic acid and proline.

44 ng 98% of ascorbic acid and 100% of glycine, glutamic acid and uric acid.

45 as compared to adsorption of soy protein and glutamic acid as common ingredients.

46 For rat Glut5, a change of glutamine to glutamic acid at codon 166 (p.Q166E) has been reported t

47 n of the AIF-MIF interaction, or mutation of glutamic acid at position 22 in the catalytic nuclease d

48 with previous studies, we demonstrate that a glutamic acid at position 296 results in attenuation.

49 thin the C terminus of LukA, we identified a glutamic acid at position 323 that is critical for LukAB

50 In this study we found that KIR2DL2/L3 with glutamic acid at position 35 (E(35)) are functionally st

51 rily linked to HLA-DPB1 alleles possessing a glutamic acid at position 69 of the beta-chain.

52 ions not previously identified, specifically glutamic acid at positions 10 or 11 or lysine at positio

53 f-function mutation in which lysine replaced glutamic acid at residue 1021 (E1021K) in the p110delta

54 he combination of arginine at residue 11 and glutamic acid at residue 35 in KIR2DL3*005 were critical

55 associated with HLA-DP alleles possessing a glutamic acid at the 69th position of the beta-chain (be

56 71 mutant, containing lysine, glutamine, and glutamic acid at the respective residues 98, 145, and 16

57 factor and protective antigen), and a poly-d-glutamic acid capsule.

58 nd non-coding regions explained aspartic and glutamic acid consumption differences, likely due to a p

59 Glutamic acid contributed most to protein intake (21% of

60 ved DC were pulsed with preproinsulin (PPI), glutamic acid decarboxylase (65-kDa isoform; GAD65), and

61 gamma aminobutyric acid synthesizing enzyme glutamic acid decarboxylase (GAD) and choline acetyltran

62 High titers of autoantibodies to glutamic acid decarboxylase (GAD) are well documented in

63 is is controlled by enzymes derived from two glutamic acid decarboxylase (GAD) genes, GAD1 and GAD2,

64 f the rate-limiting GABA-synthesizing enzyme glutamic acid decarboxylase (GAD) is decreased in Brodma

65 of activation (Fos) of GABAergic neurons and glutamic acid decarboxylase (GAD) mRNA expression in the

66 probe for imaging the activity of the enzyme glutamic acid decarboxylase (GAD) present in neurons.

67 dinucleotide phosphate-diaphorase (NADPH-d), glutamic acid decarboxylase (GAD), cytochrome oxidase (C

68 ly detect somal immunoreactivity for GABA or glutamic acid decarboxylase (GAD), the enzyme that produ

69 e and some were parvalbumin-, calbindin-, or glutamic acid decarboxylase (GAD)-67-positive.

70 nobutyric acid (GABA) transporter (vGAT) and glutamic acid decarboxylase (GAD)65 in the GABAergic con

71 Additionally, glutamic acid decarboxylase (GAD)65-loaded tolDCs from w

72 on, with either green fluorescent protein or glutamic acid decarboxylase (GAD)65/67 immunoreactivity

73 Here, we study the distribution of glutamic acid decarboxylase (GAD)67 and GLY transporter

74 were triple-labeled for the 65 kD isoform of glutamic acid decarboxylase (GAD65), PV and the GABA(A)

75 Gad1 gene-encoded 67-kDa protein isoform of glutamic acid decarboxylase (GAD67) is a hallmark of sch

76 ntain normal levels of the 67 kDa isoform of glutamic acid decarboxylase (GAD67) protein, the enzyme

77 to lower expression of the 67-kDa isoform of glutamic acid decarboxylase (GAD67), a key enzyme for GA

78 ext, we produced conditional null alleles of Glutamic acid decarboxylase 1 (Gad1) and Resistant to di

79 nerated transgenic mouse lines that suppress glutamic acid decarboxylase 1 (GAD1) in either cholecyst

80 Levels of gamma-aminobutyric acid (GABA) and glutamic acid decarboxylase 1 (GAD1), the enzyme that sy

81 In contrast, the silencing of glutamic acid decarboxylase 2-positive interneurons, whi

82 n of T1D-related autoantigens [proinsulin or glutamic acid decarboxylase 65 (GAD)] delayed T1D onset,

83 tis Abs as well as thyroperoxidase (TPO) and glutamic acid decarboxylase 65 (GAD65) Abs.

84 Glutamic acid decarboxylase 65 (GAD65) and autoantibodie

85 r the development of insulin autoantibodies, glutamic acid decarboxylase 65 (GAD65) autoantibodies, i

86 been identified, including orexin cells and glutamic acid decarboxylase 65 (GAD65) cells, but their

87 gic knowledge on cerebellar ataxia (CA) with glutamic acid decarboxylase 65 antibodies (GAD65-Abs) is

88 id, beta-lactoglobulin, and the autoantigens glutamic acid decarboxylase 65, heat shock protein 60, a

89 globulin) and diabetes-related autoantigens (glutamic acid decarboxylase 65, insulin, heat shock prot

90 Serologic study results revealed glutamic acid decarboxylase 65-IgG in all cases (median

91 man syndrome (4 classic; 5 variant; 66% were glutamic acid decarboxylase 65-IgG positive) and 1 with

92 brane protein (PMP) antibody positivity; and glutamic acid decarboxylase 65-kDa isoform (GAD65) antib

93 atus of the second GABA-synthesizing enzyme, glutamic acid decarboxylase 65-kDa isoform (GAD65), rema

94 lation of the corresponding mRNAs, including glutamic acid decarboxylase 67 (GAD67) and reelin (RELN)

95 The expression of GABAergic marker glutamic acid decarboxylase 67 (GAD67) and the number of

96 pendent expression levels of parvalbumin and glutamic acid decarboxylase 67 (GAD67) in schizophrenia

97 dies have consistently found lower levels of glutamic acid decarboxylase 67 (GAD67) messenger RNA (mR

98 Levels of the GABA-synthesizing enzyme glutamic acid decarboxylase 67-kDa isoform (GAD67) in th

99 antibodies against the GABA synthetic enzyme glutamic acid decarboxylase and synaptophysin support th

100 Four patients also had high glutamic acid decarboxylase antibodies (>1000 U/ml), and

101 ms of pathology, many patients with SPS have glutamic acid decarboxylase antibodies (GAD-ab), but the

102 Little is known of glutamic acid decarboxylase antibodies (GAD-abs) in the

103 tions of SPS despite the persistence of anti-glutamic acid decarboxylase antibodies following auto-HS

104 Two anti-glutamic acid decarboxylase antibody-positive patients w

105 balanced for age, sex, disease duration, and glutamic acid decarboxylase autoantibody titers.

106 ain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert

107 he presence of the GABA-synthesizing enzyme, glutamic acid decarboxylase in EC were confirmed by immu

108 brillary acidic protein-immunocytochemistry, glutamic acid decarboxylase in situ hybridization, and p

109 Glutamic acid decarboxylase is the rate-limiting enzyme

110 hat specific promoter regulatory elements of glutamic acid decarboxylase isoforms (Gad1 and Gad2), wh

111 IgE responses to insulin, autoantibodies to glutamic acid decarboxylase or insulinoma-associated ant

112 gic neurons expressing different isoforms of glutamic acid decarboxylase were found to have different

113 (Hu, Yo, Ri, CV2, Tr, amphiphysin, and Ma2), glutamic acid decarboxylase, and mGluR1 antibodies.

114 Autoantibodies to insulin, glutamic acid decarboxylase, and the insulinoma-associat

115 re also immunopositive to antibodies against glutamic acid decarboxylase, suggesting that they use ga

116 ith SPS have antibodies directed against the glutamic acid decarboxylase, the rate-limiting enzyme fo

117 nel of immunocytochemical markers, including glutamic acid decarboxylase-67 (GAD67), somatostatin, an

118 lear layer and in the ganglion cell layer is glutamic acid decarboxylase-positive and shows the morph

119 etween PS and control rats, there were fewer glutamic acid decarboxylase-positive neurons in the form

120 actin-2, GlyR, D1R, D2R, AMPAR, GABA(B)R and glutamic acid decarboxylase.

121 e transporter 2; VGluT2) and GABA signaling (glutamic acid decarboxylase; GAD, and vesicular GABA tra

122 o patients with novel de novo Tpm3.12 single glutamic acid deletions at positions DeltaE218 and Delta

123 A beta-glutamic acid dendron anchor was used to attach a PEG ch

124 With a protected glutamic acid derivate as the starting material, the pro

125 toes resulted in robust GABA production from glutamic acid derived from blood protein digestion.

126 d-Alanine and d-glutamic acid derived from peptidoglycan decomposition e

127 Arginine-glutamic acid dipeptide repeats (RERE) is located in the

128 at binding did not require the gamma-carboxy glutamic acid domain.

129 w potatoes and also thermally generated from glutamic acid during frying.

130 e engaged, despite the lack of aspartic acid/glutamic acid encoded in the mouse repertoire.

131 arginine finger in conjunction with a novel glutamic acid finger, which forms a salt bridge with an

132 uvignon, the light body of Xinomavro and the glutamic acid for Malvasia.

133 line for enamine formation on one side and a glutamic acid for nitronate protonation on the other sid

134 for Ser2 and/or Ser7 and the phosphomimetic glutamic acid for Ser7.

135 Substitution of glutamic acid for tyrosine between the Syk SH2 domains (

136 /pvdN double mutant produced exclusively the glutamic acid form of pyoverdine.

137 igh-level activity in humans compared to the glutamic acid found at this position in avian isolates.

138 This mutation ('DeltaE') removes a single glutamic acid from the encoded protein, torsinA.

139 Several studies have advocated the role of glutamic acid in cancer therapy.

140 transamination of the three acids to produce glutamic acid in cancerous cells.

141 rearrangements that expressed aspartic acid/glutamic acid in CDR L2.

142 und that a single change of aspartic acid to glutamic acid in CW3 NS1/2 was sufficient for persistenc

143 he E2 envelope glycoprotein (lysine in SFV4, glutamic acid in SFV6).

144 Replacement of a glutamic acid in the central gate with a positively char

145 Importantly, determination of free glutamic acid in the daily diet could also prevent vario

146 Point mutation of either glutamic acid in the Galpha13-binding (767)EKE motif in

147 avian influenza virus isolates have carried glutamic acid in this position (PB2 627E), commonly desc

148 The oral introduction of glutamic acid increased virus acquisition by mosquitoes

149 2, one cancer-derived ECRG2 mutant harboring glutamic acid instead of valine at position 30 (V30E) fa

150 The data suggest that glutamic acid is a nitrogen acceptor while alanine, aspa

151 Furthermore, we also found that when the glutamic acid is adjacent to the alkyl tail the supramol

152 important and unexpected result is that the glutamic acid ligand to FeB is not essential for functio

153 out diabetes and was functionally related to glutamic acid metabolism, suggesting a mechanistic link.

154 A previous study documented a glycine to glutamic acid mutation (G4946E) in ryanodine receptor (R

155 ations involved replacements by glutamine or glutamic acid of E2 glycoprotein amino acids in the acid

156 form the active site, by the new N-terminal glutamic acid of mature SplB is observed.

157 sp70EEVD was restored upon substitution of a glutamic acid of the J-domain.

158 he nonhelical tailpiece or their mutation to glutamic acid or aspartic acid.

159 mutation of these residues to phosphomimetic glutamic acid or transfection with the Src kinases Lyn o

160 activation is reversed by the removal of the glutamic acid penultimate to the tyrosine.

161 nts in complex with L-aspartic acid versus L-glutamic acid provide insights into their differential s

162 cing of the ALMS1 coding region identified a glutamic acid repeat polymorphism in exon 1, which was s

163 The glutamic acid repeat polymorphism of ALMS1 identified in

164 ion (DeltaGAG), which causes a deletion of a glutamic acid residue (DeltaE) in the C-terminal region

165 acid substitutions at this highly conserved glutamic acid residue and illustrates the value of syste

166 hemically identical carboxylate group on the glutamic acid residue and on the glycine residue shows a

167 ous missense substitutions in the paralogous glutamic acid residue in TWIST2 (p.Glu75Ala, p.Glu75Gln

168 , and a strictly conserved fluorophore-bound glutamic acid residue is converted to a range of variant

169 17Val and p.Glu117Gly) at a highly conserved glutamic acid residue located in the basic DNA binding d

170 th a constitutively phosphorylated mimicking glutamic acid residue or a phosphorylation-dead mimickin

171 ing a calcium ion-binding site and chelating glutamic acid residue that mediate the formation of HC.T

172 304 was replaced with either an alanine or a glutamic acid residue was also affected.

173 enesis of any of the two conserved catalytic glutamic acid residues (Glu(200) and Glu(414)) of the ac

174 by a central tryptophan flanked by aspartic/glutamic acid residues (W-acidic).

175 ution of Ala, Gly, Cys, or Gln for these two glutamic acid residues abrogated all capacity to stimula

176 Interestingly, introduction of three glutamic acid residues alone was not sufficient to estab

177 etal ion bridge, confirm that the serine and glutamic acid residues anchor the bridge, demonstrate th

178 ned oligoarginine peptides equipped with six glutamic acid residues and an anionic pyranine at the N-

179 pecific amino acid substitutions: lysine and glutamic acid residues are replaced by arginine and aspa

180 These peptides possess aspartic and glutamic acid residues at p4 and p7, respectively, that

181 arboxylic groups of various key aspartic and glutamic acid residues by monitoring their C=O stretchin

182 Three glutamic acid residues in epsin UIM were found to intera

183 ouble dehydration and decarboxylation of two glutamic acid residues in the 30-residue precursor PaaP.

184 etween histidine 64 in CAII and a cluster of glutamic acid residues in the C terminus of the transpor

185 of different species with varying numbers of glutamic acid residues in the side chain ranging from 12

186 Second, two glutamic acid residues located on the distal side of the

187 dopted to probe solvent-exposed aspartic and glutamic acid residues on the CP43 protein.

188 lanine, arginine, glycine, aspartic acid and glutamic acid residues represented the major amino acids

189 Notably, the glutamic acid residues were not solely gamma-linked, as

190 ted by the gamma-carboxylase (GGCX) on three glutamic acid residues, a cellular process requiring red

191 s, Hec1 possessed an unusual distribution of glutamic acid residues, Glu-334, Glu-341, and Glu-348, b

192 sensitive to the protonation state of buried glutamic acid residues.

193 rod cGMP-gated cation channel and associated glutamic acid rich proteins (GARPs) are required for pho

194 y, p66 with Thr(206) and Ser(213) mutated to glutamic acid showed a gain-of-function phenotype with s

195 a photolabile dimethoxynitrobenzyl-protected glutamic acid side chain used to impede hydrolysis of th

196 Charge reversal by glutamic acid substitution at Arg-I or Arg-II has opposi

197 The simulations also show why glutamic acid substitution at either serine does not con

198 Furthermore, neither alanine nor glutamic acid substitutions had a significant effect on

199 The alanine and glutamic acid substitutions reduced actin-activated ATPa

200 Serine-to-glutamic acid substitutions that mimicked the phosphoryl

201 cation as a transformation of the N-terminal glutamic acid to a succinamide.

202 to be responsible for the conversion of the glutamic acid to alpha-ketoglutaric acid.

203 two amino acid mutations in the PB2 protein (glutamic acid to lysine at position 627 and aspartic aci

204 to alanine to prevent phosphorylation or to glutamic acid to mimic phosphorylation had no effect on

205 an internal proton transfer from a conserved glutamic acid to the proton-loading site of the pump.

206 a revealed three novel mutations including a glutamic acid to valine substitution (E1338D), a glutami

207 ediated trafficking of the aspartic acid and glutamic acid transporter Dip5 to the vacuole, but it do

208 ulting variant, which has cysteine-histidine-glutamic acid triads on each helix, hydrolyses p-nitroph

209 atural language (NL) largely untapped (e.g. 'glutamic acid was substituted by valine at residue 6').

210 ythro-beta-d-methylaspartic acid and gamma-d-glutamic acid were key for an isomerization-free synthes

211 er-tasting caffeine, and the umami-tasting l-glutamic acid were the main contributors to the taste of

212 We conjugate doxorubicin to poly(L-glutamic acid) by means of a pH-sensitive cleavable link

213 His6-OPH) and poly(ethylene glycol)-b-poly(l-glutamic acid) diblock copolymer.

214 d on both the grafting density of the poly(l-glutamic acid) on the NPs and the size of the NPs.

215 hybrid hydrogels consisting of a poly(gamma-glutamic acid) polymer network physically cross-linked v

216 D-aas such as D-Asp (aspartic acid), D-Glu (glutamic acid), combined D-[Asp/Glu] and others were eac

217 he DOTAGA (1,4,7,10-tetraazacyclododecane-1-(glutamic acid)-4,7,10-triacetic acid) conjugate PSMA I&T

218 k copolymers, poly(ethylene glycol)-b-poly(L-glutamic acid)-b-poly(L-phenylalanine), which effectivel

219 n we report self-assembly behavior of poly(l-glutamic acid)-grafted gold NPs in solution and describe

220 eptidase in which the third zinc ligand is a glutamic acid).

221 lyceraldehyde 3-phosphate dehydrogenase with glutamic acid, a malonyllysine mimic, suppressed its enz

222 feri and Burkholderia thailandensis bound to glutamic acid, a TrpRS from the eukaryotic pathogen Ence

223 Glucose, trehalose and glutamic acid, alanine were the major sugars and amino a

224 nificant effects were noticed in the case of glutamic acid, alanine, aspartic acid and proline betwee

225 and size, such as arginine, serine, lysine, glutamic acid, and cysteine.

226 l interference from ascorbic acid, cysteine, glutamic acid, and glucose was also studied, and the obt

227 Here, we identify proline, glutamic acid, and leucine-rich protein 1 (PELP1), a chr

228 thic and thin-film MIPs against Z-L-Phe, Z-L-glutamic acid, and penicillin G.

229 We examined whether the intake of glutamic acid, arginine, cysteine, lysine, or tyrosine w

230 Our data do not suggest a major role for glutamic acid, arginine, lysine, tyrosine, or cysteine i

231 d with nontumor tissues (proline, threonine, glutamic acid, arginine, N1-acetylspermidine, xanthine,

232 here is no interference from d-glucose and l-glutamic acid, ascorbic acid and o-nitrophenol.

233 roline, glycine, serine, alanine, glutamine, glutamic acid, aspargine, aspartic acid were detected.

234 ant amino acids that contributed to flavour (glutamic acid, aspartic acid and alanine) were present a

235 chemically well-defined amphoteric carriers, glutamic acid, aspartyl-histidine (Asp-His), cycloserine

236 The peptide, which contains a photocaged glutamic acid, forms a solid-like gel in a syringe and c

237 the source (phenylalanine, Phe) and trophic (glutamic acid, Glu) AAs were 4.1 (muscle) and 5.4 (red b

238 spartic acid, cystathionine, total cysteine, glutamic acid, glutamine, glycine, histidine, total homo

239 rus, cancer, human papillomavirus, dopamine, glutamic acid, IgG, IgE, uric acid, ascorbic acid, acetl

240 Cytoplasmic localization of proline, glutamic acid, leucine-rich protein 1 (PELP1) is observe

241 side chains amino acids that were aspartate, glutamic acid, lysine and tyrosine on the negative side

242 n sources (L-Asparagine, L-Aspartic Acid, L- Glutamic Acid, m- Erythritol, D-Melezitose, D-Sorbitol)

243 Glutamic acid, serine, and glycine concentrations are kn

244 appaBalpha C-terminal PEST (rich in proline, glutamic acid, serine, and threonine residues) sequence

245 ontains PEST sequences (enriched in proline, glutamic acid, serine, and threonine) and is normally su

246 amily contains an unnatural 4,4-disubstitued glutamic acid, the synthesis of which provides a key cha

247 Molecular modeling analysis reveals that the glutamic acid, which is negatively charged, interacts wi

248 Structural analysis revealed that this key glutamic acid, which is not present in Ydj1, forms a sal

249 with 3-aminophenyl boronic acid (APB) and L-glutamic acid-(2,2,2)-trichloroethyl ester (GTE).

250 ein tyrosine phosphatases from the proline-, glutamic acid-, serine- and threonine-rich (PEST) family

251 mutations causing deletions of the proline-, glutamic acid-, serine-, and threonine-rich (PEST) domai

252 nT, tyrosine-43, lysine-69, arginine-254 and glutamic acid-493, were required for activity.

253 to characterize the human aspartic acid- and glutamic acid-ADP-ribosylated proteome.

254 ous lambda variable gene segments encoding a glutamic acid-aspartic acid (ED) motif for K169 recognit

255 tin-1, QHREDGS (glutamine-histidine-arginine-glutamic acid-aspartic acid-glycine-serine), as a therap

256 ity but cleaved gamma-links in both d- and l-glutamic acid-containing polymers.

257 sporter 1 (VGLUT1) and the 65 kDa isoform of glutamic acid-decarboxylase (GAD65) as markers of, respe

258 d allylation of serine-, aspartic acid-, and glutamic acid-derived organozinc reagents, followed by c

259 lin autoregulatory MREI (methionine-arginine-glutamic acid-isoleucine) domain, highly expressed in th

260 he common C-terminal epitope of neuropeptide glutamic acid-isoleucine/alpha-melanocyte-stimulating ho

261 Here, we examined the role of non-glutamic acid-leucine-arginine CXC chemokine CXCL9 for T

262 plantation and has been shown to up-regulate glutamic acid-leucine-arginine-positive (ELR(+)) CXC che

263 hese findings demonstrated that three buried glutamic acid-lysine pairs, in concert with hydrophobic

264 dominant negative termed A-ZIP53 that has a glutamic acid-rich amphipathic peptide sequence attached

265 ARF) encodes a KSHV LANA-like glutamine- and glutamic acid-rich protein, whereas KSHV LANA1(ARF) enco

266 overy of Src homology 3 (SH3) domain-binding glutamic acid-rich-like protein (SH3BGRL), a novel c-Src

267 from glucose, guanine, and p-aminobenzoyl-l-glutamic acid.

268 of tRNAs specific for lysine, glutamine and glutamic acid.

269 tion of HMF from fructose in the presence of glutamic acid.

270 e digestion motifs flanked with aspartic and glutamic acid.

271 molecule was replaced by the side chain of a glutamic acid.

272 s associated with consumption of excess free glutamic acid.

273 r phenylalanine or to the negatively charged glutamic acid.

274 caspases can also hydrolyze substrates after glutamic acid.

275 ycine, l-proline, l-serine, l-alanine, and l-glutamic acid.

276 either the wild type (WT) or with alanine or glutamic acid/aspartic acid substitutions at the phospho

277 tudy, we examined the efficacy of poly-gamma-glutamic acid/chitosan (PC) nanogel as an adjuvant for t

278 In 09HA_mut, a lysine-to-glutamic-acid mutation leads to the loss of both salt br

279 he CREKA-peptide-modified (Cysteine-Arginine-Glutamic-acid-Lysine-Alanine) omega-3-fatty acid oil con

280 used significantly higher levels (p<0.05) of glutamic acids (343.0+/-22.09mg/100g), total FAAs (1720.

281 n the soluble structure that comprised three glutamic acids (Glu92, Glu94, and Glu97) that we hypothe

282 eins that are unusually rich in aspartic and glutamic acids [4-6], the role of these proteins in biom

283 complex with the Nix LIR peptide containing glutamic acids as phosphomimetic residues and NMR experi

284 ting sequence of approximately 4 consecutive glutamic acids followed by approximately 4 consecutive b

285 nin still can form pores, but mutating these glutamic acids to glutamines rendered the toxin pH-insen

286 served when acidic amino acids, aspartic and glutamic acids, are present near the cleavage site.

287 Glutamic acids, NGlu(133), MGlu(144), and LGlu(144), are

288 arity to predict the effect of mutating each glutamic and aspartic acid located in MTBD domain to ala

289 Glycine, glutamic and aspartic acids accounted for 40% of total a

290 in the presence of acidic amino acids (i.e. glutamic and aspartic acids).

291 cubation with another NAD-dependant enzyme L-glutamic dehydrogenase.

292 count was 60,000 cells per mm(3), and serum glutamic oxaloacetic transaminase was 234 U/l.

293 hypertension and liver expression levels of glutamic-oxaloacetic transaminase 2 (GOT2) messenger RNA

294 t the time of admission and revealed a serum glutamic-oxaloacetic transaminase level of 9 U/L [0.15 m

295 (GOT1) and mitochondrial (GOT2) isoforms of glutamic-oxaloacetic transaminase were repressed in HCU

296 ange, 5-40 U/L [0.08-0.67 mukat/L]), a serum glutamic-pyruvic transaminase level of 34 U/L [0.57 muka

297 aptotagmin 1 indicated the presence of a key glutamic residue in the polybasic cluster of synaptotagm

298 carbonylation (alpha-amino adipic and gamma-glutamic semialdehyde).

299 red, while alpha-aminoadipic (AAS) and gamma-glutamic semialdehydes (GGS) increased when cooking at 6

300 carbonylation (alpha-amino adipic and gamma-glutamic semialdehydes) and Schiff base cross-links.