ライフサイエンスコーパス: glutamyl

1 or drug activity was optimized in advance of glutamyl adduct prodrug design.

2 against spontaneous NO release by linkage to glutamyl adducts that could be cleaved by gamma-glutamyl

3 mbinant GGCT2;1 converted both GSH and gamma-glutamyl Ala to 5-OP in vitro.

4 a 40-kDa/20-kDa heterodimer with full gamma-glutamyl amide bond hydrolase activity.

5 The activated enzyme hydrolyzed the gamma-glutamyl amide bond of several substrates with comparabl

6 lutathione reclamation by cleaving the gamma-glutamyl amide bond of the tripeptide.

7 icted to specify activities related to gamma-glutamyl amide linkages and/or unusual peptide bonds.

8 Notably, levels of gamma-glutamyl amino acid, linked with glutathione metabolism

9 id, food component or plant, benzoate, gamma-glutamyl amino acid, methionine, and tryptophan).

10 bial, tryptophan, plant component, and gamma-glutamyl amino acid-related metabolites.

11 hione, with no activity against either gamma-glutamyl amino acids or oxidized glutathione.

12 In contrast, nitrogen-rich and gamma-glutamyl amino acids, citrulline, and nucleotide catabol

13 ty acids and energy production, and 4) gamma-glutamyl amino acids, which represent an altered gamma-g

14 ster of differentiation 90)], and 6C3 [ENPEP glutamyl aminopeptidase (aminopeptidase A)].

15 A counter screen against glutamyl aminopeptidase (ENPEP), an enzyme with substrat

16 Homology modeling revealed glutamyl and aspartyl residues in close proximity (less

17 h contains beta-cyanoalanine (BCA) and gamma-glutamyl beta-cyanoalanine (gammaGBCA) is used for adult

18 uncertainties of beta-cyanoalanine and gamma-glutamyl-beta-cyanoalanine were obtained as 4.6% and 5.8

19 at acivicin is accommodated within the gamma-glutamyl binding pocket of the enzyme.

20 Residues that comprise the gamma-glutamyl binding site are primarily located in the 20 kD

21 hat compete with the substrate for the gamma-glutamyl binding site.

22 ation of a loop region that covers the gamma-glutamyl binding site.

23 ic breakdown of GSH by cleavage of the gamma-glutamyl bond and release of cysteinylglycine.

24 he enzyme responsible for breaking the gamma-glutamyl bond between Glu and Cys in glutathione (GSH).

25 , HpGT catalyzes the hydrolysis of the gamma-glutamyl bond in glutathione and its conjugates.

26 hile hydrolase family that cleaves the gamma-glutamyl bond of glutathione and other gamma-glutamyl co

27 acid (Gla) by the vitamin K-dependent gamma-glutamyl carboxylase (gamma-carboxylase) is an essential

28 er mainly associated with mutations in gamma-glutamyl carboxylase (GGCX) that often has fatal outcome

29 gamma-Glutamyl carboxylase (GGCX), an approximately 94 kDa tra

30 based system for studying mutations in gamma-glutamyl carboxylase (GGCX), the enzyme responsible for

31 which were shown to result in reduced gamma-glutamyl carboxylase activity and in undercarboxylation

32 Thus, reduced gamma-glutamyl carboxylase activity in individuals either comp

33 cDNAs encode the apparent orthologs of gamma-glutamyl carboxylase and vitamin K epoxide reductase.

34 Vitamin K-dependent gamma-glutamyl carboxylase catalyzes the conversion of glutamy

35 The gamma-glutamyl carboxylase converts Glu to carboxylated Glu (G

36 As a result, activation of MGP by gamma-glutamyl carboxylase is diminished, allowing slow yet pr

37 GGCX encodes a gamma-glutamyl carboxylase necessary for activation of both co

38 The gamma-glutamyl carboxylase utilizes four substrates to catalyz

39 es 346-758) of the vitamin K-dependent gamma-glutamyl carboxylase, a glycoprotein located in the endo

40 latively constant expression (Ci-Gla1, gamma-glutamyl carboxylase, and vitamin K epoxide reductase) o

41 opeptide for its binding site on human gamma glutamyl carboxylase.

42 he majority of PRGP2 is present in the gamma-glutamyl carboxylated, propeptide-cleaved (mature) form.

43 Cellular gamma-glutamyl carboxylation also exhibited differential VKOR

44 that enables quantitative analysis of gamma-glutamyl carboxylation and its antagonism in live cells.

45 ctivity relationship for inhibition of gamma-glutamyl carboxylation by warfarin metabolites, observin

46 s, we demonstrate that PRGP2 undergoes gamma-glutamyl carboxylation in a manner that is both dependen

47 Maximal gamma-glutamyl carboxylation of F9CH required vitamin K supple

48 quinone, an essential cofactor for the gamma-glutamyl carboxylation of many clotting factors.

49 Ci-Gla1 undergoes gamma-glutamyl carboxylation when expressed in CHO cells and i

50 MGP requires to be activated by gamma-glutamyl carboxylation, a vitamin K-dependent reaction,

51 freeze-trapped acetylglutamyl anhydride and glutamyl-CoA thioester adducts.

52 We evaluated a series of gamma-glutamyl compounds as substrates for human GGT1 and huma

53 o cell surface enzymes that metabolize gamma-glutamyl compounds have been identified: gamma-glutamyl

54 Gamma-glutamyl compounds include antioxidants, inflammatory mo

55 glutamyl bond of glutathione and other gamma-glutamyl compounds.

56 olism, and other pathways that involve gamma-glutamyl compounds.

57 ase that cleaves glutathione and other gamma-glutamyl compounds.

58 of methotrexate and the corresponding gamma-glutamyl conjugate were also synthesized using the same

59 of methotrexate and the corresponding gamma-glutamyl conjugate were equipotent with the parent compo

60 of extracellular glutathione and other gamma-glutamyl-containing compounds.

61 creased ratio between plasma levels of gamma-glutamyl cycle intermediates pyroglutamic and glutamic a

62 mino acids, which represent an altered gamma-glutamyl cycle of glutathione metabolism.

63 lack homologs of this enzyme (and the gamma-glutamyl cycle) but are predicted to have some way to di

64 zymatic intermediate in the eukaryotic gamma-glutamyl cycle, but it is also an unavoidable damage pro

65 We identified the gamma-glutamyl cycle, the production of glutathione, and the r

66 predominantly metabolized through the gamma-glutamyl cycle, where GSH is degraded by the sequential

67 GSH homeostasis is maintained by the gamma-glutamyl cycle, which involves GSH synthesis and degrada

68 nk between TDA/acid resistance and the gamma-glutamyl cycle.

69 The enzyme gamma-glutamyl cyclotransferase (GGCT) is involved in Glu recy

70 then to Glu by the combined action of gamma-glutamyl cyclotransferase and 5-oxoprolinase in the cyto

71 Kinetics analysis suggests that gamma-glutamyl cyclotransferase is the major source of GSH deg

72 f gamma-glutamyl transpeptidase (GGT), gamma-glutamyl cyclotransferase, and 5-oxoprolinase to yield g

73 r referred to as GGCT2;1, functions as gamma-glutamyl cyclotransferase.

74 stable-isotope labeled compound [GSX, gamma-glutamyl-cystein-glycin-(13)C2-(15)N] was used to trap r

75 ations, a mixture of glutathione [GSH, gamma-glutamyl-cystein-glycin] and the stable-isotope labeled

76 Gamma glutamyl cysteine ligase (GCL) is the rate-limiting enzy

77 nic mouse lines in which expression of gamma-glutamyl cysteine ligase, the rate-limiting enzyme in de

78 etween N-alpha-trimethyl histidine and gamma-glutamyl cysteine, which is the key step in the biosynth

79 , including arsenate reductase (HAC1), gamma-glutamyl-cysteine synthetase (gamma-ECS), phytochelatin

80 Gamma-glutamyl-cysteine synthetase (gamma-GCS) mRNA levels dec

81 as well as the tripeptide glutathione (gamma-glutamyl-cysteinyl-Gly) were found to be strong agonists

82 Glutathione (gamma-glutamyl-cysteinyl-glycine, GSH) is a major thiol-contai

83 n and characterization of glutathione (gamma-glutamyl-cysteinylglycine, GSH)-trapped reactive metabol

84 ta [g]quinazolin-6-yl]amino]benzoyl]-l-gamma-glutamyl-d-glutamic acid 1 (BGC 945, now known as ONX 08

85 m/z 272, corresponding to deprotonated gamma-glutamyl-dehydroalanyl-glycine originating from the glut

86 th hallmarks of hepatotoxicity such as gamma-glutamyl dipeptides, acylcarnitines, and proline derivat

87 2-hydroxybutyrate-related metabolites, gamma-glutamyl dipeptides, and lysophosphatidylcholines, which

88 ipid pathways and with lower levels of gamma-glutamyl dipeptides.

89 thway and positively associated with 5 gamma-glutamyl dipeptides.

90 Glutamyl endopeptidase (GE) from Alcalase 2.4 L was puri

91 uncompetitive inhibitors, binding the gamma-glutamyl enzyme complex.

92 II (FXIIIa) catalyzes the formation of gamma-glutamyl-epsilon-lysyl cross-links within the fibrin blo

93 tor XIIIa (FXIIIa) introduces covalent gamma-glutamyl-epsilon-lysyl crosslinks into the blood clot ne

94 nation monitored by tritium release from the glutamyl gamma-carbon was dependent upon CO(2), and a pr

95 minantly the desired E-olefin isosteres of L-glutamyl-gamma-D-glutamate and L-glutamyl-gamma-L-glutam

96 ternally quenched fluorogenic derivatives of glutamyl-gamma-glutamate and (4,4-difluoro)glutamyl-gamm

97 f glutamyl-gamma-glutamate and (4,4-difluoro)glutamyl-gamma-glutamate to examine the effect of fluori

98 ontaining peptidomimetics of the isopeptide, glutamyl-gamma-glutamate, have been synthesized via a ro

99 steres of L-glutamyl-gamma-D-glutamate and L-glutamyl-gamma-L-glutamate, following which peracid-medi

100 e that was reacted with a suitably protected glutamyl-gamma-semialdehyde in a Julia-Kocienski olefina

101 k at the much harder N-terminus of the gamma-glutamyl (Glu) unit of GSH.

102 mma-glutamate, aspartyl-glutamate, and gamma-glutamyl-glutamate, refined at 1.50, 1.60, and 1.67 A re

103 competitive AMPA receptor-antagonist gamma-d-glutamyl-glycine (gamma-DGG), analysis of the coefficien

104 types associated with toxicity were in gamma-glutamyl hydrolase (-401CC), 5-aminoimidazole-4-carboxam

105 Gamma-glutamyl hydrolase (GGH) catalyzes degradation of the ac

106 Using this method, we identified gamma-glutamyl hydrolase (GGH), emmprin, survivin, and diazepa

107 folate polyglutamate synthase (FPGS), gamma-glutamyl hydrolase (GGH), methylene tetrahydrofolate red

108 ened or removed by the vacuolar enzyme gamma-glutamyl hydrolase (GGH).

109 The tail can be removed by gamma-glutamyl hydrolase (GGH; EC 3.4.19.9), a vacuolar enzyme

110 folylpolyglutamate synthase [FPGS] and gamma-glutamyl hydrolase [GGH]) evaluated in germline DNA (blo

111 amyltranspeptidase (HpGT) is a general gamma-glutamyl hydrolase and a demonstrated virulence factor.

112 Gamma-glutamyl hydrolase, a cysteine peptidase, catalyzes the

113 gamma-Glutamyl hydrolases (gammaGH) catalyze the hydrolysis of

114 rate recognition of zgammaGH and other gamma-glutamyl hydrolases.

115 We previously developed gamma-glutamyl hydroxymethyl rhodamine green (gGlu-HMRG) as a

116 lidated a new fluorescent method using gamma-glutamyl hydroxymethyl rhodamine green to diagnose metas

117 ification of transglutaminase-mediated gamma-glutamyl isomers as intermediate products of transamidat

118 distinguished for the first time gamma/alpha-glutamyl isomers of deamidation, encountering a 1.7 gamm

119 S-4-mercapto-4-methylpentan-2-one-N-(l-gamma-glutamyl)-l-cysteine (gammaGluCys-4MMP) but at too low c

120 or, carbobenzoxy-L-isoleucyl-gamma-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents.

121 ATP-dependent synthesis of GSH from L-gamma-glutamyl-L-cysteine and glycine.

122 both the ATP-dependent synthesis of L-gamma-glutamyl-L-cysteine from L-glutamate and L-cysteine and

123 G) and a C-terminal NlpC/P60 domain (gamma-d-glutamyl-l-diamino acid endopeptidase) and is expected t

124 anine amidase, whereas Lc-Lys-2 is a gamma-D-glutamyl-L-lysyl endopeptidase.

125 denosine, and guanosine) and kokumi (gamma-l-glutamyl-l-valine) taste-related molecules was ascertain

126 ro-steroid monosulfate 2, uridine, and gamma-glutamyl-leucine, showed independent associations with a

127 mma-glutamyl transpeptidase (GGT1) and gamma-glutamyl leukotrienase (GGT5).

128 crystal structure of the apo-F(420)-0:gamma-glutamyl ligase (CofE-AF) from Archaeoglobus fulgidus an

129 s homologous to CofE with an annotated gamma-glutamyl ligase activity, whereas the C-terminal domain

130 n the two domains is critical for full gamma-glutamyl ligase activity.

131 vertebrates, balanced activities of tubulin glutamyl ligase and cytoplasmic carboxypeptidase degluta

132 A gamma-glutamyl ligase catalyzes the final steps of the F420bio

133 CofE, a F(420)-0:gamma-glutamyl ligase, is responsible for the last two enzymat

134 llular localization or expression of tubulin glutamyl ligases (ttlls) and nonenzymatic proteins, incl

135 of TGM2, fibronectin (FN) and epsilon-(gamma-glutamyl) lysine (GGEL) proteins.

136 oscopy suggested formation of epsilon-(gamma-glutamyl) lysine cross-linkages by transglutaminase and

137 This enzyme forms an epsilon-(gamma-glutamyl) lysine isopeptide bond between a lysine donor

138 sponsible for the formation of epsilon(gamma-glutamyl)lysine crosslinks (transamidation).

139 a) catalyzes the formation of epsilon-(gamma-glutamyl)lysine isopeptide bonds between specific Gln an

140 Factor XIIIa-catalyzed epsilon-(gamma-glutamyl)-lysyl bonds between glutamine and lysine resid

141 ethylselenocysteine (MeSeCys; 53%) and gamma-glutamyl-MeSeCys (47%).

142 Using N-acetylmuramyl-L-alanyl-gamma-D-glutamyl-meso-2,6-diaminopimelyl-D-alanyl-D-alan ine as

143 ore of Nod1 stimulatory molecules is gamma-D-glutamyl-meso-diaminopimelic acid (iE-DAP), but the iden

144 on of Nod1 by its agonist, bacterial gamma-D-glutamyl-meso-diaminopimelic acid (iE-DAP), in term trop

145 ognition of the bacterial components gamma-d-glutamyl-meso-diaminopimelic acid and muramyl dipeptide,

146 beta, and the NOD1 and NOD2 ligands (gamma-d-glutamyl-meso-diaminopimelic acid and muramyl dipeptide,

147 s induced by the bacterial dipeptide gamma-d-glutamyl-meso-diaminopimelic acid was intact in MyD88 de

148 dance of intestinal bacteria bearing gamma-d-glutamyl-meso-diaminopimelic acid, a ligand for the intr

149 nserved structural motif but also hydrolyzes glutamyl-methyl-esters at select regulatory positions.

150 fied in these SIP experiments used the gamma-glutamyl-methylamide pathway, found in both methylotroph

151 riched onion meals ( approximately 66% gamma-glutamyl-methylselenocysteine, providing the equivalent

152 The C-terminal glutamyl mimic was accessed by the stereospecific synthe

153 nd hard reactive metabolites contain a gamma-glutamyl moiety and, thus, undergo a neutral loss of 129

154 ck of specific coordination beyond the gamma-glutamyl moiety may account for the substrate binding pe

155 stal structures identifies a Mg(2+) near the glutamyl moiety of the folate cofactor, providing the fi

156 In the standard GGT assay with gamma-glutamyl p-nitroanilide as substrate, GGT1 accounted for

157 er GSH degradation or the diversion of gamma-glutamyl peptides to produce 5-oxoproline (5-OP).

158 ated lipid peroxidation products, MDA, gamma-glutamyl peptides, GGT, leukotriene B4 and 5-HETE.

159 were used to assess chymotrypsin-like, post-glutamyl peptidyl-hydrolyzing, and trypsin-like protease

160 ds are available to identify the gamma/alpha-glutamyl products of deamidation, none of these methods

161 Specificity is dictated by glutamyl-prolyl tRNA synthetase (EPRS) binding to a 3'UT

162 Glutamyl-prolyl tRNA synthetase (EPRS) is a component of

163 Importantly, the EN1-iPeps bound the glutamyl-prolyl tRNA synthetase (EPRS) target, which has

164 to the identification of a truncated form of glutamyl-prolyl tRNA synthetase (EPRS), a GAIT constitue

165 osphorylate Ser(886) in the linker domain of glutamyl-prolyl tRNA synthetase (EPRS), the initial even

166 and beta-actin) or in protein biosynthesis (glutamyl-prolyl-transfer RNA synthetase, glutaminyl-tran

167 Here we identify glutamyl-prolyl-tRNA synthetase (EPRS) as an mTORC1-S6K1

168 Here we found that the MSC component glutamyl-prolyl-tRNA synthetase (EPRS) switched its func

169 oid cells is heterotetrameric, consisting of glutamyl-prolyl-tRNA synthetase (EPRS), NS1-associated p

170 Translation of the glutamyl-prolyl-tRNA synthetase gene EPRS is enhanced in

171 leucyl-tRNA synthetase and the bifunctional glutamyl-/prolyl-tRNA synthetase at the base of this asy

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

173 uses the oxygenation of vitamin K to convert glutamyl residues (Glus) to carboxylated Glus (Glas) in

174 t of a cofactor for the VKD carboxylation of glutamyl residues (Glus) to carboxylated Glus in VKD pro

175 Specific glutamyl residues are methylated and demethylated in rea

176 o affected by reversible methylation of four glutamyl residues in the cytoplasmic domain of the recep

177 ation is mediated by methylation at specific glutamyl residues in the cytoplasmic domain.

178 dehyde intermediates, and converts the gamma-glutamyl residues of GSSG to 5-hydroxybutyrolactam.

179 amyl carboxylase catalyzes the conversion of glutamyl residues to gamma-carboxyglutamate.

180 ommon vetch: ss-cyanoalanine (BCA) and gamma-glutamyl-ss-cyanoalanine (GCA).

181 the acceptor site while binding to the gamma-glutamyl substrate complex.

182 The interaction of Mg(2+) with the glutamyl tail of the folate cofactor and nonconserved re

183 (AST), alkaline phosphatase (ALP), and gamma-glutamyl transaminase (GGT) were measured.

184 The purified enzyme exhibited gamma-glutamyl transfer activity as well as iron reduction act

185 d and correlate with an increased content of glutamyl-transfer RNA reductase.

186 n 2-week-old ntrc seedlings, the contents of glutamyl-transfer RNA reductase1 (GluTR1) and CHLM are r

187 ase (0.02 [0.01, 0.03]; P = 0.002) and gamma-glutamyl transferase (0.02 [0.01, 0.03]; P = 0.001).

188 artate aminotransferase (1251.76 U/L), gamma-glutamyl transferase (360.53 U/L), and alkaline phosphat

189 The patient's gamma-glutamyl transferase (77 U/L [1.28 mukat/L]; normal leve

190 (beta = 3.70; 95% CI: 1.78, 5.62), and gamma-glutamyl transferase (beta = 3.70; 95% CI: 0.80, 6.60) a

191 Increased gamma-glutamyl transferase (GGT) activity is associated with l

192 However, serum gamma-glutamyl transferase (GGT) concentrations were mildly el

193 docosahexaenoic acid) was catalyzed by gamma-glutamyl transferase (GGT) in human macrophages.

194 chromosome 22), one locus influencing gamma-glutamyl transferase (GGT) levels (HNF1A on chromosome 1

195 Elevated gamma-glutamyl transferase (GGT) levels are associated with hi

196 gamma-Glutamyl transferase (GGT) regulates glutathione metabol

197 ood for liver enzyme levels, including gamma-glutamyl transferase (GGT), alanine aminotransferase (AL

198 erum alanine aminotransferase (ALT) or gamma-glutamyl transferase (GGT), two markers of hepatic necro

199 - 13 versus 27 +/- 10 IU/L (P = 0.81), gamma-glutamyl transferase 54 +/- 138 versus 49 +/- 35 IU/L (P

200 Optimal conditions for gamma-glutamyl transferase activity were found to be 35 degree

201 tasis-like phenotype with normal serum gamma-glutamyl transferase activity without intestinal disease

202 dent coagulopathy, low-to-normal serum gamma-glutamyl transferase activity, elevated serum alpha-feto

203 tasis-like phenotype with normal serum gamma-glutamyl transferase activity.

204 tion, serum levels of the liver enzyme gamma-glutamyl transferase and fecal virus shedding were signi

205 sis substantially through blocking the gamma-glutamyl transferase catalysis of the first breakdown st

206 Cholestasis with normal gamma glutamyl transferase characterizes functional deficienci

207 mpared with the vemurafenib group were gamma-glutamyl transferase increase (36 [15%] in the cobimetin

208 se, CD4(+) T-cell count, HCV genotype, gamma-glutamyl transferase level, and baseline APRI.

209 using the kidney-specific podocin and gamma-glutamyl transferase promoters, but found expression pri

210 aminotransferase, total bilirubin, and gamma glutamyl transferase were higher in DSA-positive patient

211 d nausea and asymptomatic increases in gamma-glutamyl transferase were observed in some patients rece

212 yrosine phosphatase 1b, AST/ALT ratio, gamma-glutamyl transferase, and carbohydrate-deficient transfe

213 oved: compared with placebo, levels of gamma-glutamyl transferase, aspartate transaminase, and solubl

214 nalysis, younger age, higher levels of gamma-glutamyl transferase, lower pretherapeutic hemoglobin, a

215 vation of alanine aminotransferase and gamma-glutamyl transferase, two markers of fatty liver disease

216 rase IV and overexpression of CD38 and gamma-glutamyl transferase.

217 cell damage (P=0.02), higher values of gamma-glutamyl-transferase (gGT) resembling tubulus injury (P=

218 with fasting alanine aminotransferase, gamma-glutamyl-transferase, LDL cholesterol, A1C, and systolic

219 for measurements of triglycerides and gamma-glutamyl-transferase.

220 is, alanine aminotransferase, AST, and gamma-glutamyl transpeptase) and fructose or sucrose intake ap

221 39.9 +/- 28.6U/L vs 23.8 +/- 14.1U/L), gamma-glutamyl transpeptidase (34.3 +/- 16.6 vs 24.5 +/- 16.8U

222 tamyl adducts that could be cleaved by gamma-glutamyl transpeptidase (gamma-GT), found predominantly

223 ate markers of NAFLD, such as elevated gamma glutamyl transpeptidase (GGT) and alanine aminotransfera

224 Plasma levels of gamma-glutamyl transpeptidase (GGT) are associated with risk f

225 her CagA, VacA, lipopolysaccharide, or gamma-glutamyl transpeptidase (GGT) implicated the latter in H

226 Expression of gamma-glutamyl transpeptidase (GGT) in tumors contributes to r

227 gamma-Glutamyl transpeptidase (GGT) is a heterodimeric membran

228 gamma-Glutamyl transpeptidase (GGT) is the enzyme responsible

229 gamma-Glutamyl transpeptidase (GGT) is the only enzyme known t

230 Both the presence of gamma-glutamyl transpeptidase (GGT) on the apical brush-border

231 The cell surface glycoprotein gamma-glutamyl transpeptidase (GGT) was isolated from healthy

232 and H. pylori These include flagellin, gamma-glutamyl transpeptidase (ggt), collagenase, the secreted

233 degraded by the sequential reaction of gamma-glutamyl transpeptidase (GGT), gamma-glutamyl cyclotrans

234 ase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), or total bilirubin.

235 utamyl compounds have been identified: gamma-glutamyl transpeptidase (GGT1) and gamma-glutamyl leukot

236 dverse events were increased levels of gamma-glutamyl transpeptidase (two [4%]), a reduction in the n

237 gamma-Glutamyl transpeptidase 1 (GGT1) is a cell surface, N-te

238 LT], aspartate aminotransferase [AST], gamma-glutamyl transpeptidase [GGT], alkaline phosphatase [ALP

239 1.87; 95% CI, 1.10; 3.18; P = 0.021); gamma-glutamyl transpeptidase above the upper limit of normal

240 erum bile acid (BA) levels, and normal gamma-glutamyl transpeptidase activity.

241 ss than 30 kg/m(2), genotype 2, normal gamma-glutamyl transpeptidase and increased alanine aminotrans

242 wer concentrations of the liver enzyme gamma-glutamyl transpeptidase and lower scores on a measure of

243 Among secondary end points, levels of gamma-glutamyl transpeptidase decreased 48%-63%, on average, a

244 (BSEP) disease, and 4 others with low gamma-glutamyl transpeptidase disease (levels <100 U/L), were

245 5 days liver histology was normal, but gamma-glutamyl transpeptidase expression was observed, with al

246 H. pylori virulence determinants, the gamma-glutamyl transpeptidase GGT and the vacuolating cytotoxi

247 The function of gamma-glutamyl transpeptidase is to cleave glutathione and S-n

248 g induces greater phosphorylation, and gamma-glutamyl transpeptidase levels are reduced compared with

249 kaline phosphatase of 75.6%; P<0.0001; gamma-glutamyl transpeptidase of 117.9%, P<0.0001; bilirubin o

250 ses the need for GSNO bioactivation by gamma-glutamyl transpeptidase to increase CFTR maturation; 4)

251 Level of gamma-glutamyl transpeptidase was significantly higher in the

252 , significantly reduced levels of ALP, gamma-glutamyl transpeptidase, and alanine aminotransferase, c

253 ntrations of alanine aminotransferase, gamma-glutamyl transpeptidase, and alkaline phosphatase.

254 the GSH usage (glutathione peroxidase, gamma-glutamyl transpeptidase, and glutathione S-transferase).

255 inotransferases, alkaline phosphatase, gamma glutamyl transpeptidase, and homeostasis model assessmen

256 oncentrations of alkaline phosphatase, gamma-glutamyl transpeptidase, cystatin C, neutrophil gelatina

257 rgery, urinary protein and creatinine, gamma-glutamyl transpeptidase, lactate dehydrogenase, histolog

258 higher body mass index, triglycerides, gamma-glutamyl transpeptidase, maximum alanine aminotransferas

259 or ferritin) and fibrosis (P<.0001 for gamma-glutamyl transpeptidase, P=.01 for alkaline phosphatase,

260 resence of excess CapD, a B. anthracis gamma-glutamyl transpeptidase, the protective capsule is degra

261 wed that pretreatment body mass index, gamma-glutamyl transpeptidase, triglyceride, IL-28B TT genotyp

262 ught about by the action of the enzyme gamma-glutamyl transpeptidase.

263 We found that inhibition of gamma-glutamyl-transpeptidase (gamma-GT) protects human acute

264 rthermore, serial sections stained for gamma-glutamyl-transpeptidase (GGT, a marker of fetal hepatobl

265 ansfer, alkaline phosphatase activity, gamma-glutamyl-transpeptidase activity and physiological respo

266 . pylori persistence determinants, the gamma-glutamyl-transpeptidase GGT and the vacuolating cytotoxi

267 s Dug1, Dug2, and Dug3) but not by the gamma-glutamyl-transpeptidase, raising the question of the rol

268 gamma-Glutamyl transpeptidases (GGTs) are essential for hydrol

269 persister protein A) kinase, which inhibits glutamyl tRNA synthetase (GltX).

270 apicomplexans possess a unique heterodimeric glutamyl-tRNA amidotransferase consisting of GatA and Ga

271 tetrapyrrole biosynthesis and is formed from glutamyl-tRNA by two enzymatic steps.

272 Glutamyl-tRNA reductase (GluTR) as the first enzyme of A

273 of CHLH and HEMA1 encoding Mg chelatase and glutamyl-tRNA reductase were increased in rfd1 and the A

274 eflected in an enhanced level of the encoded glutamyl-tRNA reductase, which catalyzes one of the rate

275 F, which can interact with the Clp substrate glutamyl-tRNA reductase.

276 ic screen reveals that the overexpression of glutamyl-tRNA synthetase (GltX) suppresses the toxicity

277 (Gln) is produced via an indirect pathway: a glutamyl-tRNA synthetase (GluRS) first attaches glutamat

278 To date, only glutamyl-tRNA synthetase (GluRS) has been found to conta

279 in early eukaryotes from a nondiscriminating glutamyl-tRNA synthetase (GluRS) that aminoacylates both

280 nsplanting a conserved arginine residue from glutamyl-tRNA synthetase (GluRS) to glutaminyl-tRNA synt

281 ved from the archaeal-type nondiscriminating glutamyl-tRNA synthetase (GluRS), an enzyme with relaxed

282 oshii class I LysRS (LysRS1) and homology to glutamyl-tRNA synthetase (GluRS), residues implicated in

283 first enzyme in this pathway, the apicoplast glutamyl-tRNA synthetase (GluRS).

284 ntaining the anchoring protein Arc1p and the glutamyl-tRNA synthetase (GluRS).

285 ced with the corresponding residues of human glutamyl-tRNA synthetase (GluRS).

286 ompare the signaling pathways in a bacterial glutamyl-tRNA synthetase (GluRS):tRNA(Glu) and an archae

287 ng protein that forms a ternary complex with glutamyl-tRNA synthetase (GluRSc) and methionyl-tRNA syn

288 in a two-step process; a non-discriminating glutamyl-tRNA synthetase (ND-GluRS) forms Glu-tRNA(Gln),

289 First, glutamyl-tRNA synthetase activates glutamate by ligating

290 and asparaginyl-tRNA synthetase evolved from glutamyl-tRNA synthetase and aspartyl-tRNA synthetase, r

291 t-transfer states with charged tRNA bound to glutamyl-tRNA synthetase from Thermus thermophilus (Glu-

292 lation pathway utilizes a non-discriminating glutamyl-tRNA synthetase to synthesize Glu-tRNA(Gln) and

293 glutamate is ligated to its cognate tRNA by glutamyl-tRNA synthetase.

294 RNA synthetase (GlnRS) but has two divergent glutamyl-tRNA synthetases: GluRS1 and GluRS2.

295 LUCA by amidation of the mischarged species, glutamyl-tRNA(Gln) and aspartyl-tRNA(Asn), by tRNA-depen

296 nt amidation of the mischarged tRNA species, glutamyl-tRNA(Gln) or aspartyl-tRNA(Asn).

297 when it was incubated with Escherichia coli glutamyl-tRNA(Glu) and purified recombinant Chlamydomona

298 Here we show that this process involves glutamyl-tRNA(Glu) to activate Ser/Thr residues.

299 hat both wild-type and mutant GSAT stimulate glutamyl-tRNA-dependent NADPH oxidation by GTR.

300 ive mutant GSAT inhibited ALA formation from glutamyl-tRNA.