ライフサイエンスコーパス: glutathione

1 ent (acidic pH, reactive oxygen species, and glutathione).

2 n, salt, and reducing agents (l-cysteine and glutathione).

3 s which present high intracellular levels of glutathione.

4 in GDAP1, rendering it incapable of binding glutathione.

5 kinetics of a ternary Cu-COTI-2 complex with glutathione.

6 redox metabolites, including an increase in glutathione.

7 idized glutathione with reference to reduced glutathione.

8 nce of Ag(+), which was rescued by exogenous glutathione.

9 enous cysteine is metabolized exclusively to glutathione.

10 increased synthesis of serine, glycine, and glutathione.

11 blocked by administration of cell-permeable glutathione.

12 recursor and late-stage functionalization of glutathione.

13 are enriched with intracellular antioxidant glutathione.

14 o biliatresone-induced injury independent of glutathione.

15 otential using reduced and oxidized forms of glutathione.

16 ABCC1 substrate S-(6-(7-(11)C-methylpurinyl))glutathione ((11)C-MPG).

17 II) coordination site but can be released to glutathione (a physiological thiol) or to other complexi

18 rystal structures of human GGT1 (hGGT1) with glutathione (a substrate) and a phosphate-glutathione an

19 ing the particles to a solution of dissolved glutathione (a thiolate-based Hg chelator).

20 Levels of glutathione, a key regulator of cellular redox status, a

21 ones forming stable, nonreducible copper(II)-glutathione adducts are recognized and, in turn, effluxe

22 lic enzyme that removes S-glutathionylation, glutathione adducts of protein cysteine residues, thus m

23 In addition, mono-substituted patulin-glutathione adducts were identified as the main type of

24 xpected, as ABCC1 has strong selectivity for glutathione adducts.

25 /glutamate transport and the biosynthesis of glutathione, an antioxidant that may protect against As-

26 th glutathione (a substrate) and a phosphate-glutathione analog (an irreversible inhibitor) bound in

27 oeOXR2 plants have increased levels of total glutathione and a more oxidized cytosolic redox cellular

28 tant tumor growth by consuming intracellular glutathione and activating apoptosis.

29 PDAC cells used cysteine to synthesize glutathione and coenzyme A, which, together, down-regula

30 ps from thiol-containing metabolites such as glutathione and cysteine and reduced proteins such as in

31 the acute phase of illness leads to reduced glutathione and glutamate in the residual phase of the i

32 Glutathione and glutamate were significantly correlated

33 ducing lipid peroxidation and increasing the glutathione and GPX4 levels.

34 and had sustained mitochondrial depletion of glutathione and mitochondrial dysfunction.

35 optosis in lymph, including higher levels of glutathione and oleic acid and less free iron in lymph.

36 Thiol compounds including cysteine, glutathione and phytochelatins were significantly increa

37 Abnormalities of one carbon, glutathione and sulfide metabolisms have recently emerge

38 synthesis of the peptide phytochelatin from glutathione and the degradation of glutathione conjugate

39 (2) enters the cell via aquaporins, depletes glutathione and thus abrogates the cell's protection tow

40 es, leading to a quasi-complete depletion of glutathione and to the inactivation of different compone

41 g FGF21 levels and altered the nonenzymatic (glutathione) and enzymatic antioxidant markers (Glutathi

42 ), as well as its metabolites (ascorbate and glutathione) and uptake of nutrients (Mg, P, K, S, Ca, F

43 itochondrial matrix (NAD, NADP, thioredoxin, glutathione, and ascorbate) are in kinetic steady state

44 -porter regulating levels of the antioxidant glutathione, and it is a known target of the environment

45 alysis, we observed that glutamine, alanine, glutathione, and lactate were positively associated with

46 cosolvents or photocatalysts, is enhanced by glutathione, and operates efficiently over a wide range

47 on, and increased oxidative stress proteins, glutathione, and reactive oxygen species specific to thi

48 s, measured as reduced glutathione, oxidized glutathione, and their ratio in the blood.

49 were associated with an up-regulation of the glutathione antioxidant system and a decrease in mitocho

50 and its downstream targets (thioredoxin and glutathione antioxidant systems).

51 n the G-site which canonically interact with glutathione are altered in GDAP1, rendering it incapable

52 Biological thiols such as glutathione are of particular interest due to their func

53 , genes involved in sulfur assimilation, the glutathione-ascorbate cycle, and various antioxidant sys

54 cross Toronto, Canada (2016-2017), including glutathione/ascorbate-related oxidative potential (OP(GS

55 hniques, including the dithiothreitol assay, glutathione assay, and ascorbic acid assay, are discusse

56 cm(-2) ) in the presence of a soluble thiol (glutathione at 15 x 10(-3) m), and a photoinitiator (lit

57 ges in transmembrane helix 6 (TM6) alter the glutathione-binding site and the associated substrate-bi

58 the provision of cystine, a key precursor in glutathione biosynthesis.

59 Methylation of the ubiquitous antioxidant glutathione by dichlorvos can decrease the reducing/oxid

60 The following removal of glutathione by the formation of an intramolecular disulf

61 Herein, we report that renal clearable glutathione coated AgNPs (GS-AgNPs) can selectively accu

62 nsport and interactions of both GS-AgNPs and glutathione coated gold nanoparticles (GS-AuNPs) with th

63 a cysteine-conjugated metabolite) and M13 (a glutathione-conjugated metabolite), against macrophage c

64 12-D(3)NVP vs NVP, while glucuronidated and glutathione-conjugated metabolites increased with 12-D(3

65 egulation and modulation of the transport of glutathione conjugates in seeds of desi and kabuli chick

66 atin from glutathione and the degradation of glutathione conjugates via peptidase activity.

67 phytochelatin synthesis and deglycination of glutathione conjugates, as catalytic-site mutants of PCS

68 n of toxic alkenals, which lead to MACs upon glutathione conjugation and metabolization.

69 enous antioxidant components including total glutathione contents, and activities of catalase and sup

70 inhibited enzyme activities of the ascorbate-glutathione cycle (while transcripts of associated enzym

71 Si channel and transporter genes, ascorbate-glutathione cycle and nutrient uptake, and lowering in o

72 The glutathione cycle can compensate for decreased excitator

73 dismutase and a different regulation of the glutathione cycle compared to conspecific birds in unlog

74 its co-factor glutathione, in complex with a glutathione-cysteine adduct, and in a glutathione disulf

75 gamma-Glutamylcyclotransferase initiates glutathione degradation to component amino acids l-gluta

76 C to a common cob(II)alamin intermediate via glutathione-dependent alkyltransferase or reductive elim

77 Subsequently, glutathione-dependent dehalogenases (BbdI and BbdE) cata

78 The glutathione-dependent lipid hydroperoxidase glutathione

79 inate three iron-sulfur (Fe-S) clusters in a glutathione-dependent manner.

80 c-Myc protein mutant was sufficient to avoid glutathione depletion and rescue the proapoptotic effect

81 Here, we show that glutathione depletion is coupled to ferrous iron elevati

82 adation of the c-Myc oncoprotein that led to glutathione depletion.

83 rved with the antioxidant (ascorbic acid and glutathione) depletion (OP(AO)) assay.

84 ingobium aromaticivorans (NaAtm1) can export glutathione derivatives and confer protection against he

85 eliminates this cavity, precluding uptake of glutathione derivatives.

86 wever, neither oxidative damage nor oxidized glutathione differed between forest types.

87 ATP, Arabidopsis PLANT ELICITOR PEPTIDE, and glutathione disulfide (GSSG) treatments induced rapid sp

88 etics and equilibrium of GSSH formation from glutathione disulfide and H(2)S.

89 with a glutathione-cysteine adduct, and in a glutathione disulfide complex in order to initiate a res

90 ng, perturbed NAD-to-NADH and glutathione-to-glutathione disulfide ratios, increased NOX4 expression,

91 siological pH changes, and demonstrated that glutathione dominates sensor reduction in vivo.

92 Reduced glutathione drastically increases the warfarin sensitivi

93 6 uM) had stronger antioxidant activity than glutathione (EC(50) = 13.7 uM) and MYPGLA (EC(50) = 19.8

94 emonstrate that streptolysin O (SLO)-induced glutathione efflux from host cellular stores is a previo

95 ized gold nanorods are stable towards excess glutathione for up to six days, and under conditions wit

96 undescribed biomolecule, S-geranylgeranyl-L-glutathione (GGG), is a potent P2RY8 ligand that is dete

97 We measured glutathione, glutamate and glutamine concentrations in t

98 e schizophrenia would exhibit a reduction in glutathione, glutamate, and/or glutamine in the cerebral

99 ia had significantly lower scores on the ACC glutathione-glutamate component, an effect almost entire

100 PCA) produced three clear components: an ACC glutathione-glutamate component; an insula-visual glutat

101 thione-glutamate component; an insula-visual glutathione-glutamate component; and a glutamine compone

102 matopoiesis due to their capacity to tap the glutathione/glutaredoxin pathway for DNA biosynthesis.

103 Recent data have revealed glutathione/GPX4-independent axes for suppressing ferrop

104 ss and the antioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5 upregulated by DMF.

105 e importer Slc7a11, S47 cells show increased glutathione (GSH) accumulation compared to cells with wi

106 t with cysteine residues of proteins to form glutathione (GSH) adducts, S-glutathionylation, that are

107 brosis, levels of inflammatory mediators and glutathione (GSH) after chelation therapy.

108 low molecular weight (LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).

109 activity was successfully prepared by using glutathione (GSH) and copper (II) chloride as precursors

110 Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by l

111 converted to a PS by the mutual presence of glutathione (GSH) and hydrogen peroxide (H(2) O(2) ) wit

112 Metallothioneins (MTs) and glutathione (GSH) are abundant in the cytosol and nucleu

113 Now, ultrasound (US) and glutathione (GSH) dual responsive vesicles of Janus Au-M

114 gical yeast derivatives (YDs) with increased glutathione (GSH) enrichment.

115 Glutathione (GSH) is often upregulated in cancer, where

116 y through the replenishment of intracellular glutathione (GSH) levels.

117 Decreases in reduced glutathione (GSH) mimic the effects of biliatresone, and

118 Herein, we report glutathione (GSH) reaction rates for N-phenyl acrylamide

119 Mitigation was related to both the glutathione (GSH) redox molecule and the enzyme peroxida

120 regeneration rate of ferrocenecarboxylic by glutathione (GSH) released from cardiomyocyte, which is

121 compared with wild-type plants; besides the glutathione (GSH) steady-state levels in roots of PPSB-d

122 ition, the reactive oxygen species scavenger glutathione (GSH) was upregulated in chRCC due to decrea

123 well-known precursor of the reduced form of glutathione (GSH), but also is an scavenger of soft elec

124 (GSSG), and total glutathione (GT), reduced glutathione (GSH), catalase (CAT), peroxidase (POD), sup

125 Biothiols, such as glutathione (GSH), homocysteine (Hcy), and cysteine (Cys

126 on the chemical reaction between patulin and glutathione (GSH), in order to generate the conjugates t

127 hanges in a key marker for oxidative stress, glutathione (GSH), may associate with central neurochemi

128 diac tissue levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase

129 xification of methylglyoxal requires reduced glutathione (GSH), which accumulates to high levels in N

130 bnormal redox status due to bio-thiols, like glutathione (GSH), which constitute the most crucial def

131 ,4-dinitrobenzenesulfonate (DNBS) group as a glutathione (GSH)-activated photosensitizer, a chemo-pro

132 We developed glutathione (GSH)-responsive polyurethane nanoparticles

133 talase (CAT), superoxide dismutase (SOD) and glutathione (GSH).

134 tection from redox stress is the antioxidant glutathione (GSH).

135 ion, but dependent on ME1-produced NADPH and glutathione (GSH).

136 tributes to the maintenance of intracellular glutathione (GSH).

137 he derivative of the abundant cellular thiol glutathione (GSH).

138 d redox-system, i.e., a low reduced/oxidized glutathione (GSH-GSSG) ratio.

139 ular glutathione levels and reduced/oxidized glutathione (GSH/GSSG) ratios.

140 (cysteine: higher in AD, p < 0.001; reduced glutathione [GSH]: higher in AD, p < 0.001); (3) polyami

141 ssure, lipid panel, oxidized (GSH) & reduced glutathione (GSSG) were also evaluated for each particip

142 DA), H(2)O(2), electrolyte leakage, oxidized glutathione (GSSG), and total glutathione (GT), reduced

143 synaptic terminals and the depletion of the glutathione (GSx) stores in neural tissue.

144 kage, oxidized glutathione (GSSG), and total glutathione (GT), reduced glutathione (GSH), catalase (C

145 n autophagy, lipid, and protein metabolisms, glutathione, guanosine, and L-glutamic acid, which are i

146 demonstrated increased glycolysis, impaired glutathione homeostasis, and increased purine oxidation,

147 crease the reducing/oxidizing equilibrium of glutathione in liver extracts, which has been implicated

148 molecular weight thiols coenzyme A (CoA) and glutathione in S47 cells.

149 re of FhGST-S1 in complex with its co-factor glutathione, in complex with a glutathione-cysteine addu

150 igger lipid peroxidation under conditions of glutathione insufficiency, and a reduced capacity to rep

151 connection between copper complex chemistry, glutathione interaction, and the resistance profile of c

152 kers related to the key cellular antioxidant glutathione irrespective of the forest type.

153 While glutathione is also rapidly depleted in ggct2;1 null see

154 leted in ggct2;1 null seedlings, much higher glutathione is maintained in the primary root tip compar

155 Glutamate, glutathione, lactate, and alanine, as well as interleuki

156 stress induced by manipulating intracellular glutathione levels and reduced/oxidized glutathione (GSH

157 Higher baseline glutathione levels in female than male rats suggest that

158 ssing the iron content, malondialdehyde, and glutathione levels, ferroptosis-related protein expressi

159 bituric acid reactive substances and reduced glutathione levels, tissue markers of oxidative stress,

160 ough not through obvious modulation of total glutathione levels.

161 H/NAD(+)) ratio, and decreased intracellular glutathione levels.

162 167.0210), ascorbic acid (m/z 175.0241), and glutathione (m/z 306.0765)], were able to distinguish IB

163 increased glutamate, whereas the antioxidant glutathione may protect against inflammation-induced oxi

164 s involving glutamate receptor signaling and glutathione-mediated detoxification in both BA19 and CB;

165 oteomic and bioinformatics data by analysing glutathione metabolism and mitochondrial function.

166 in cellular detoxification, NADP metabolism, glutathione metabolism and the electron transport chain,

167 hioredoxin pathway and processes involved in glutathione metabolism compared to untreated controls.

168 tion between BA transplant-free survival and glutathione metabolism gene expression.

169 Glutathione metabolism gene mutations caused regionally

170 FZD7, Tp63, and glutathione metabolism gene sets were strongly correlate

171 rafish larvae carrying targeted mutations in glutathione metabolism genes and correlated these findin

172 Agents such as NAC that promote glutathione metabolism might be developed for treatment

173 cogenic factor Tp63, driving upregulation of glutathione metabolism pathways, including glutathione p

174 ells harboring stemness features and altered glutathione metabolism that depend on GPX4 for survival

175 Regional variation in glutathione metabolism underlies sensitivity to the bili

176 liate exposure, such as heat shock proteins, glutathione metabolism, and the reactive oxygen species

177 aled significantly altered lipid metabolism, glutathione metabolism, and urea/arginine metabolism com

178 , mutant p53, and was better associated with glutathione metabolism, providing an alternate molecular

179 r vertical migration behaviour and efficient glutathione metabolism, whereas pteropods run the risk o

180 metabolite levels and significant changes in glutathione metabolism.

181 replication/repair, signal transduction, and glutathione metabolism.

182 Cu-ATSM signal and cellular concentration of glutathione, nicotinamide adenine dinucleotide phosphate

183 Compounds that decrease glutathione normalize GAPDH-Rheb complexes and mTOR acti

184 onversely, mitochondrial dysfunction-induced glutathione oxidation and ER stress disrupted the intrac

185 kidney biochemical (malonyl-aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis fact

186 ative stress (malondialdehyde [MDA], reduced glutathione/oxidative glutathione ratio [GSH/GSSG]), and

187 xidants to antioxidants, measured as reduced glutathione, oxidized glutathione, and their ratio in th

188 g PON1 activity, upregulation of the hepatic glutathione pathway, and reduction of circulating BLM.

189 ss gene signature coupled to coagulation and glutathione-pathway genes shared between a microglia clu

190 urs are enriched for oxidation-reduction and glutathione pathways and harbor more NFE2L2/KEAP1 altera

191 Measurements of plasma glutathione peroxidase (GPx) activity and serum selenium

192 oncentration in colostrum follows the order: glutathione peroxidase (GPX) ~ selenoprotein P (SELENOP)

193 ctor erythroid 2 related factor 2 (Nrf2) and glutathione peroxidase 1 (Gpx1) mRNA in both male and fe

194 mes superoxide dismutase 2 (SOD2), catalase, glutathione peroxidase 1 (GPX1), and heme oxygenase 1 (H

195 r the optimal activity of the selenoproteins glutathione peroxidase 3 (GPx3; <86.9 ng mL(-1)) and iod

196 The expression of glutathione peroxidase 4 (GPX4) in H295R cells, however,

197 The selenium-dependent glutathione peroxidase 4 (GPX4) inhibits ferroptosis, co

198 hat cellular redox homeostasis maintained by glutathione peroxidase 4 (GPX4) is required for STING ac

199 glutathione-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4) prevents ferroptosis by

200 Glutathione peroxidase 4 (GPX4) protects against lipid p

201 Glutathione peroxidase 4 (GPX4) uses glutathione to prot

202 ibition of the ferroptosis-inhibiting enzyme glutathione peroxidase 4 (GPX4)(10).

203 e phospholipid hydroperoxide-reducing enzyme glutathione peroxidase 4 (GPX4)(3,4) and radical-trappin

204 membranes unless the lipid hydroperoxidase, glutathione peroxidase 4 (GPX4), reduces these toxic lip

205 f glutathione metabolism pathways, including glutathione peroxidase 4 (GPX4), which protected cells f

206 f intracellular antioxidant enzymes, such as glutathione peroxidase 4 (GPX4).

207 that ferroptosis is primarily controlled by glutathione peroxidase 4 (GPX4).

208 Intratumoral glutathione peroxidase 4 overexpression or acyl-CoA synt

209 Here, we provide evidence that glutathione peroxidase 8 (GPX8), a poorly characterized

210 ne-S-transferase, phospholipid hydroperoxide glutathione peroxidase and peroxidase were significantly

211 ed dual roles in EC barrier function through glutathione peroxidase and phospholipase A(2) activity.

212 Preventing H(2)O(2) reduction with the glutathione peroxidase inhibitor, mercaptosuccinate, enh

213 ays, including the antiferroptotic mediator, glutathione peroxidase type 4.

214 tathione) and enzymatic antioxidant markers (Glutathione peroxidase, and superoxide dismutase).

215 3a2 inhibition was synthetically lethal with glutathione peroxidase-4 (GPX4) inhibition; GPX4 inhibit

216 ptosis but not in that induced by inhibiting glutathione peroxidase-4 (GPX4), the most downstream com

217 essing catalase-, superoxide dismutase-, and glutathione peroxidase-mimicking enzyme properties exhib

218 olesterol, and triglyceride, while increased glutathione peroxidase.

219 e formation, acidity, and nucleophilicity of glutathione persulfide (GSSH/GSS(-)), the derivative of

220 nosa PAO1 produced sulfane sulfur, including glutathione persulfide and inorganic polysulfide, produc

221 Glutathione-pi (GST-pi) is a key enzyme that militates a

222 Reduction/oxidation (redox) changes in the glutathione pool (GSH), glutaredoxins (GRX) and thioredo

223 to confer allicin tolerance and protects the glutathione pool during allicin treatment.

224 g activators worked synergistically with the glutathione precursor N-acetylcysteine in preventing bil

225 revious data showed that palmitate (Palm) or glutathione preserved heart mitochondrial energy/redox b

226 the H(2)O(2)-induced current, while boosting glutathione production with its precursor, N-acetylcyste

227 ced GshB activity, leading to an increase in glutathione production, and promoted C. rodentium surviv

228 an increased importance of lipid synthesis, glutathione production/cycling, isoprenoids biosynthesis

229 The aggregates of glutathione-protected gold clusters (GCs) assembled thro

230 -101 solution reactive oxygen species in the glutathione protection assay was competitive and tempora

231 ldehyde [MDA], reduced glutathione/oxidative glutathione ratio [GSH/GSSG]), and matrix metalloprotein

232 as indicated by improved reduced to oxidized glutathione ratio.

233 We performed quantitative in situ hepatic glutathione redox mapping in zebrafish larvae carrying t

234 mples and experimental modeling suggest that glutathione redox metabolism and heterogeneity play a ro

235 (2+), protons (H(+)), chloride (anions), the glutathione redox potential, and H(2)O(2) Simultaneous a

236 tect pH, NAD(+), NADH, NADPH, histidine, and glutathione redox potential.

237 PP), which regenerates NADPH to preserve the glutathione redox status and survival.

238 xidase (POD), superoxide dismutase (SOD) and glutathione reductase (GR) activities, which led to a ma

239 rane domains and high sequence similarity to glutathione reductase (GR) was implicated in this proces

240 Mechanistically, AMPKalpha1 regulate the glutathione reductase (GSR) phosphorylation possibly thr

241 Thioredoxin reductase-1 (TrxR1)-, glutathione reductase (Gsr)-, and Nrf2 transcription fac

242 Active site Cys peptides of glutathione reductase 2, NADPH-thioredoxin reductase a/b

243 nistically, Klotho deficiency suppressed GR (glutathione reductase) expression and activity in the he

244 stress gene network analysis identified the glutathione-regulating compound acivicin, with potent th

245 chondrial dysfunction and ER stress impaired glutathione regulation leading to higher product aggrega

246 We demonstrate that impaired glutathione regulation underlies BisAb aggregation forma

247 Fhb7 encodes a glutathione S-transferase (GST) and confers broad resist

248 Antioxidant enzymes from the glutathione S-transferase (GST) family may protect again

249 still not clear, potential interactions with glutathione S-transferase (GST) genes due to reduced ant

250 l cytokeratin 18 (K18), caspase cleaved K18, glutathione S-transferase alpha, alpha-fetoprotein, argi

251 ection hypothesis on large gene families for glutathione S-transferase and carboxylesterase detoxific

252 stigated the association between a marker of glutathione S-transferase mediated metabolic resistance

253 Glutathione S-transferase metabolic resistance is potent

254 GSTM1 encodes glutathione S-transferase mu-1 (GSTM1), which belongs to

255 Glutathione S-transferase omega-1, an ECM-modifying enzy

256 mes could also be attenuated by silencing of glutathione S-transferase P1 (GSTP1), a mediator of meta

257 her than cysteine on target proteins such as glutathione S-transferase pi (GSTP), serum albumin, or K

258 cetyl-p-benzoquinoneimine (NAPQI) with human glutathione S-transferase pi (hGSTP), human serum albumi

259 ccumulation is TRANSPARENT TESTA19 (TT19), a glutathione S-transferase proposed to bind and stabilize

260 Here, we used site-directed mutagenesis, glutathione S-transferase pulldown experiments, immunofl

261 We used several approaches (colocalization, glutathione S-transferase pulldown, coimmunoprecipitatio

262 We found significantly higher levels of glutathione S-transferase theta 2 (GSTT2) mRNA in squamo

263 es and flavonone 3-hydroxylase and different glutathione S-transferases related with their vacuolar t

264 or NCKX4 and confirmed the interaction using glutathione-S-transferase fusion pull-down.

265 samples failed if IgG binding to the generic glutathione-S-transferase protein was observed, with 659

266 enes such as pathogenesis-related gene PR-1, glutathione-S-transferase, phospholipid hydroperoxide gl

267 ChaC glutathione-specific gamma-glutamylcyclotransferase 1 (C

268 Here we design and prepare 3.3 nm L- and D-glutathione stabilized gold nanoparticles (denoted as L3

269 ving either iron(II) or iron(III) complexes, glutathione sulfonic acid GSO(3)H appeared as the main o

270 SI-MS measurements confirmed the presence of glutathione sulfonic acid.

271 in AD, p = 0.005); (2) transsulfuration and glutathione synthesis (cysteine: higher in AD, p < 0.001

272 ysregulation carrying a permanent deficit of glutathione synthesis (gclm(-/-)), the anterior cingulat

273 , and the combination of AS15 analogues with glutathione synthesis inhibitor buthionine sulfoximine (

274 ve oxygen species (ROS) inducers such as the glutathione synthesis inhibitor, buthionine sulphoximine

275 Inhibition of glutathione synthesis using L-buthionine sulfoxamine eli

276 chizophrenia model characterized by impaired glutathione synthesis, the Gclm knockout mouse, oxidativ

277 a cycle, aspartate-glutamate metabolism, and glutathione synthesis.

278 we unexpectedly observed that the bacterial glutathione synthetase (GshB) is glycosylated by NleB on

279 /cysteine, having a dramatic effect over the glutathione system.

280 as folate cycle, nucleotides metabolism and glutathione system.

281 inal CPXC motifs of NUBP1 in the presence of glutathione that acts as a reductant.

282 se electrophilic molecules is conjugation to glutathione, then metabolization into mercapturic acid c

283 and fuels the production of the antioxidant glutathione; thus, tumors prone to redox stress may be s

284 acer that is intracellularly conjugated with glutathione to form the ABCC1 substrate S-(6-(7-(11)C-me

285 cally transferring reducing equivalents from glutathione to IDO1, representing a novel strategy of up

286 lpha1, which maintains high level of reduced glutathione to keep reduction-oxidation reaction (redox)

287 Glutathione peroxidase 4 (GPX4) uses glutathione to protect cells from ferroptosis by elimina

288 llel system, which co-operates with GPX4 and glutathione to suppress phospholipid peroxidation and fe

289 sk allele was also associated with decreased glutathione-to-glutamate ratio (-9%, P = 0.012), decreas

290 ethidium staining, perturbed NAD-to-NADH and glutathione-to-glutathione disulfide ratios, increased N

291 Here, we probed the role of glutathione transferase (GST) P1-1, an antiapoptotic pro

292 functionally necessary alpha-helix in human glutathione transferase A1-1 (hGSTA1-1).

293 Here, we show that glutathione transferase alpha4 (GSTA4), a member of the

294 aracterized in this work retains significant glutathione transport activity, suggesting that ATP hydr

295 a reactive metabolite signal in an in vitro glutathione trapping assay.

296 amma-glutamyl cyclotransferase that depletes glutathione, was increased in the R213G recruited AM.

297 cAMP and glutathione were depleted.

298 h the glutamate-cystine exchanger Sc7a11 and glutathione were increased; by contrast, the activity of

299 Baseline metabolite levels (except for glutathione) were higher in older than younger animals.

300 denced by the decrease in levels of oxidized glutathione with reference to reduced glutathione.

301 ting that GDAP1 has lost the ability to bind glutathione without a loss of substrate binding activity