ライフサイエンスコーパス: glycation

1 ated Hb levels also had higher levels of HSA glycation.

2 xpression of IL-17-induced IL-33 via glucose glycation.

3 ferentiate between the various precursors of glycation.

4 cine collagen cross-linked by natural ribose glycation.

5 s peptide during GID was hindered by protein glycation.

6 at least partly, site-specific character of glycation.

7 spectrometry was used to investigate protein glycation.

8 which did not resemble the sites of advanced glycation.

9 < 0.05) and total body methylglyoxal-protein glycation (-14%, P < 0.01).

10 cing antioxidant power assay (FRAP) and anti-glycation activity by a bovine serum albumin (BSA)/fruct

11 n reducing antioxidant power, FRAP) and anti-glycation activity by a bovine serum albumin (BSA)/fruct

12 The anti-glycation activity ranged between 250 and 711mmol aminog

13 Glycation affected primarily the N-terminal region of al

14 estigated over 3 days of incubation with the glycation agent methylglyoxal in the absence or presence

15 ems composed of ovalbumin, glucose, and anti-glycation agents (tannic acid or calcium ion) at differe

16 ting the inhibitory activity of protein anti-glycation agents.

17 tion processes were studied as possible anti-glycation agents.

18 a manner that is only minimally sensitive to glycation, albumin concentration, or redox potential, un

19 target-based approaches, we established that glycation, an unavoidable age-associated post-translatio

20 d for 8 different oxidation and 28 different glycation and AGE modifications by mass spectrometry in

21 ycation and establishes DJ-1 as a major anti-glycation and anti-aging protein.

22 The effect of glycation and cross-linking on protein breakdown and rel

23 Parkinsonism results from excessive protein glycation and establishes DJ-1 as a major anti-glycation

24 Our goal was to determine whether fibrinogen glycation and fibrin fiber diameter have an effect on th

25 Glycation and increased free radical activity underlie t

26 up new possibilities in research on protein glycation and oxidative modification.

27 ts, whereas the second was predominantly the glycation and protein components.

28 copy has assisted us to explore in vitro DNA-glycation and provide more insights into the dynamics of

29 ucosamine was found to be more effective for glycation and provided higher protein functionality as c

30 opment of novel approaches for investigating glycation and the possibility of monitoring its modulati

31 cN) via transglutaminase (TGase), as well as glycation between fish gelatin hydrolysate and GlcN were

32 asoning solution (p<0.05) regardless of GlcN glycation (both tested at 0.3M Na(+)).

33 creased ultrasound-induced whey protein (WP) glycation by arabinose.

34 kinetic modeling of in situ rates of protein glycation by MG for confirmation of the results.

35 The present study evaluates whether collagen glycation by MGO may affect phenotypic properties and re

36 The present study shows that collagen glycation by MGO stimulates differentiation of myofibrob

37 Glycation by the Maillard reaction is a naturally occurr

38 nd characterize individual sites of advanced glycation by the methods of liquid chromatography-based

39 role as buffering, anti-oxidative, and anti-glycation capacities.

40 The best glycation conditions were 40 degrees C for 8 h at 1:3 pr

41 The level of glycation, conformational alterations and protein bindin

42 Altogether, our study demonstrates glycation constitutes a novel drug target that can be ex

43 This is attributed to the higher glycation degree and higher carbohydrate content of GCPI

44 In addition, after sonication, the glycation degree was significantly enhanced in Esperase-

45 r behaviors (storage and heating) on protein glycation degrees in bovine milk products.

46 An increase in glycation efficiency results only in slight change of WP

47 e known as central intermediates in advanced glycation end product (AGE) formation.

48 itic cells preferentially recognize advanced glycation end product (AGE)-modified proteins, upregulat

49 t it from engaging the receptor for advanced glycation end product (RAGE) that may sustain inflammati

50 Alagebrium breaks advanced glycation end product crosslinks and improves LV stiffne

51 igand HMGB1 and carboxymethyllysine-advanced glycation end product epitopes in liver and adipose tiss

52 ations, such as O-GlcNAcylation and advanced glycation end product formation.

53 yllysine (CML), a major circulating advanced glycation end product, and AMD in older adults.

54 served following mineralization and advanced glycation end product-associated modification.

55 AGEs and their receptors, including advanced glycation end product-specific receptor (RAGE), trigger

56 7 [1.7-19.1]), soluble receptor for advanced glycation end products (3.5 [1.7-7.2]), and von Willebra

57 Advanced glycation end products (AGE) accumulate in diabetic pati

58 Advanced glycation end products (AGE) have been found in inflamed

59 ddition, to determine the effect of advanced glycation end products (AGE) in the presence and absence

60 ha-dicarbonyls and the receptor for advanced glycation end products (AGER).

61 Advanced glycation end products (AGEs) accumulate in T2DM, result

62 e, starch digestibility, release of advanced glycation end products (AGEs) and antioxidant capacity o

63 of necroptosis include formation of advanced glycation end products (AGEs) and reactive oxygen specie

64 ages, and increased accumulation of advanced glycation end products (AGEs) and receptor for AGE (RAGE

65 Advanced glycation end products (AGEs) and their receptors are st

66 Advanced glycation end products (AGEs) are a heterogeneous group

67 lex reaction cascade, the so-called advanced glycation end products (AGEs) are formed, including prot

68 dontal destruction and the roles of advanced glycation end products (AGEs) are investigated.

69 Advanced glycation end products (AGEs) are involved in the inflam

70 Advanced glycation end products (AGEs) contribute to lens protein

71 (MG) is a predominant precursor for advanced glycation end products (AGEs) due to its protein glycati

72 ably favours methylglyoxal (MG) and advanced glycation end products (AGEs) formation in cancer cells.

73 usly, modification by oxidation and advanced glycation end products (AGEs) had been shown to give ris

74 The consumption of advanced glycation end products (AGEs) has increased because of m

75 xperimental data suggest a role for advanced glycation end products (AGEs) in cardiovascular disease

76 Presence of advanced glycation end products (AGEs) in the heart induces a pro

77 escence (SF) noninvasively measures advanced glycation end products (AGEs) in the skin and is a risk

78 d in roasted meat as so far unknown advanced glycation end products (AGEs) of creatinine.

79 ects of consumption of diets low in advanced glycation end products (AGEs) on cardiometabolic paramet

80 Six skin collagen advanced glycation end products (AGEs) originally measured near t

81 o increases in the oxidative stress-advanced glycation end products (AGEs) receptor for AGEs (RAGE) p

82 nces (e.g. alpha-dicarbonyls) yield advanced glycation end products (AGEs) that can alter the structu

83 Binding of advanced glycation end products (AGEs) to their receptor (RAGE) i

84 We examined associations of advanced glycation end products (AGEs) with renal function loss (

85 Advanced glycation end products (AGEs), a heterogeneous group of

86 degradation results in formation of advanced glycation end products (AGEs), also originating from alp

87 one marrow-derived macrophages with advanced glycation end products (AGEs), which accumulate in diabe

88 otosin-induced diabetic mice and on advanced glycation end products (AGEs)-induced H9c2 cardiomyocyte

89 s, and proteins, yielding early and advanced glycation end products (AGEs).

90 dation protein products (AOPPs) and advanced glycation end products (AGEs).

91 rn leading to altered production of advanced glycation end products (AGEs).

92 partly due to oxidant glycotoxins [advanced glycation end products (AGEs)].

93 racellular DNA through receptor for advanced glycation end products (RAGE) and induces production of

94 n of monocytes through receptor for advanced glycation end products (RAGE) and Toll-like receptor 2,

95 nternalization of both receptor for advanced glycation end products (RAGE) and Toll-like receptor-9 (

96 igated the role of the receptor for advanced glycation end products (RAGE) in neuroinflammation, neur

97 ed the function of the receptor for advanced glycation end products (RAGE) in the development of phen

98 The receptor for advanced glycation end products (RAGE) is a highly expressed cell

99 The receptor for advanced glycation end products (RAGE) is a multiligand transmemb

100 The receptor for advanced glycation end products (RAGE) is a pattern recognition r

101 The receptor for advanced glycation end products (RAGE) is a pattern recognition r

102 The receptor for advanced glycation end products (RAGE) is a pattern recognition r

103 The receptor for advanced glycation end products (RAGE) is highly expressed in hum

104 The receptor for advanced glycation end products (RAGE) is highly expressed in var

105 However, in Receptors for Advanced Glycation End Products (RAGE) knockout mice after postna

106 The receptor for advanced glycation end products (RAGE) mediates immune cell activ

107 istent upregulation of receptor for advanced glycation end products (RAGE) messenger RNA, but not tol

108 /A9) interact with the receptor for advanced glycation end products (RAGE) on hepatic Kupffer cells,

109 9), which binds to the receptor for advanced glycation end products (RAGE) on Kupffer cells, ultimate

110 ike receptor (TLR) and receptor for advanced glycation end products (RAGE) signals.

111 at signals through the receptor for advanced glycation end products (RAGE) to reverse apoptosis-induc

112 AGEs and suppress the receptor for advanced glycation end products (RAGE) via nuclear factor erythro

113 ion receptors, such as receptor for advanced glycation end products (RAGE), allows for a complex regu

114 d by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was a

115 e receptor (TLR)2, the receptor for advanced glycation end products (RAGE), myeloid differentiation p

116 ike receptor 4 (TLR4), receptor for advanced glycation end products (RAGE), p-ERK1/2, nuclear NF-kapp

117 y by mainly binding to receptor for advanced glycation end products (RAGE).

118 ted by blockade of the receptor for advanced glycation end products (RAGE)/nuclear factor-kappaB (NF-

119 ulation is the soluble receptor for advanced glycation end products (sRAGE).

120 ond proposed receptor (receptor for advanced glycation end products [RAGE]) has no significant effect

121 e receptors [TLRs] and receptor for advanced glycation end products [RAGE]) present on vascular and i

122 d on expression of the receptor for advanced glycation end products and could be reversed by inhibiti

123 ung epithelial injury (receptor for advanced glycation end products and surfactant protein D) and end

124 was assessed by plasma receptor for advanced glycation end products and systemic endothelial injury b

125 role in preventing the formation of advanced glycation end products and therefore potentially mitigat

126 Lower receptor for advanced glycation end products and tumor necrosis factor-alpha (

127 R4 and the multiligand receptor for advanced glycation end products as receptors during MRP8-mediated

128 a result of reduced accumulation of advanced glycation end products compared with the strut interior.

129 Advanced glycation end products have been implicated in the patho

130 Receptor for advanced glycation end products is targeted by FBXO10 for ubiquit

131 aged mice may involve the effect of advanced glycation end products on DC migration.

132 B), which cleaves the crosslinks of advanced glycation end products on the extracellular matrix.

133 Moreover, the receptor for advanced glycation end products that recognizes MG and GO adducts

134 eventing the increased formation of advanced glycation end products under certain pathological condit

135 einuria, blood creatinine, urea and advanced glycation end products was also observed.

136 Plasma receptor for advanced glycation end products was significantly lower in the si

137 eavage product soluble receptor for advanced glycation end products were significantly attenuated in

138 rylamide, hydroxymethylfurfural and advanced glycation end products) and microbiological safety and s

139 rs TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved.

140 rin alphaIIb and RAGE (receptor for advanced glycation end products) as model type I receptor systems

141 The receptor of advanced glycation end products, AGER (previously known as RAGE),

142 nition receptor that interacts with advanced glycation end products, but also with C3a, CpG DNA oligo

143 lyoxal (MGO), a major precursor for advanced glycation end products, is increased in diabetes.

144 mpletely repressed by inhibitors of advanced glycation end products, L-type calcium channels, protein

145 idative stress, and accumulation of advanced glycation end products, leading to altered bone metaboli

146 boxymethyl-lysine, one of the major advanced glycation end products, suggesting the prominent role of

147 ences were observed in receptor for advanced glycation end products, surfactant protein D, angiopoiet

148 eic acid expression of receptor for advanced glycation end products, surfactant protein-B, type III p

149 (HO-1), TNF-alpha, the receptor for advanced glycation end products, vascular endothelial growth fact

150 ose metabolites, the precursors for advanced glycation end products, were significantly elevated in p

151 , TNF-alpha, TLR4, and receptor for advanced glycation end products, whereas mRNA levels of anti-infl

152 lular newly identified receptor for advanced glycation end products-binding protein levels only showe

153 ne models of TLR4- and receptor for advanced glycation end products-dependent signaling.

154 c hyperglycemia causes receptor for advanced glycation end products-mediated epigenetic modification

155 t on expression of the receptor for advanced glycation end products.

156 (MGO) and reducing the formation of advanced glycation end products.

157 otein modifications that are called advanced glycation end products.

158 gonist for TLR4 or the receptor for advanced glycation end products.

159 vating TLR4 and/or the receptor for advanced glycation end products.

160 use of accumulation of irreversible advanced glycation end products.

161 postoperative soluble receptor for advanced glycation end-product (sRAGE) levels, a marker of type I

162 For investigating the advanced glycation end-product-albumin (AGE-albumin) from activat

163 Advanced glycation end-products (AGE) are reactive metabolites pr

164 Advanced glycation end-products (AGEs) are also present in foods.

165 inhibited formation of fluorescent advanced glycation end-products (AGEs).

166 roperties due to an accumulation of advanced glycation end-products (AGEs).

167 glycemia activates the formation of advanced glycation end-products (AGEs).

168 nuclear isoform of the Receptor for Advanced Glycation End-products (nRAGE) in DSB-repair.

169 the human gene for the receptor for advanced glycation end-products (RAGE) are associated with an inc

170 The receptor for advanced glycation end-products (RAGE) is a multiligand pattern r

171 Expression of receptor for advanced glycation end-products (RAGE) is suggested to play a cru

172 tudy, we show that the receptor for advanced glycation end-products (RAGE) promoted DNA uptake into e

173 icine reports that the receptor for advanced glycation end-products (RAGE) promotes uptake of DNA int

174 eptor-4 (TLR4) and the receptor for advanced glycation end-products (RAGE) revealed the involvement o

175 rmin that binds to the receptor for advanced glycation end-products (RAGE).

176 nd S100A9, through the receptor for advanced glycation end-products (RAGE; ie, its receptor), are inv

177 he soluble form of the receptor for advanced glycation end-products (sRAGE) are elevated during acute

178 nd accumulation of the receptor for advanced glycation end-products and its ligand S100A8 in lung sam

179 nd soluble form of the receptor for advanced glycation end-products levels in the sevoflurane group,

180 in wall content (i.e. less elastin, advanced glycation end-products) and increase in conduit artery d

181 nd soluble form of the receptor for advanced glycation end-products, and safety.

182 ike receptors 2 and 4, receptor for advanced glycation end-products, high-mobility group box 1, uric

183 alveolar levels of the receptor for advanced glycation end-products.

184 e associated with the generation of advanced glycation endproduct (AGE) modifications.

185 n D (SP-D) and soluble receptor for advanced glycation endproduct (sRAGE) were significantly associat

186 substantial gene enrichment in the advanced glycation endproduct/receptor for advanced glycation end

187 ent of brain microvascular ECs with advanced glycation endproducts (AGE), a metabolite commonly eleva

188 Advanced glycation endproducts (AGEs) accumulate in patients with

189 Advanced glycation endproducts (AGEs) are believed to play a sign

190 MS) method for the determination of advanced glycation endproducts (AGEs) in food items and to analyz

191 rmation of early (Amadori) and late advanced glycation endproducts (AGEs) together with free radicals

192 Advanced glycation endproducts (AGEs), a pathogenic factor implic

193 c changes, accelerated formation of advanced glycation endproducts (AGEs), oxidative stress, activati

194 The inactivation of NO by advanced glycation endproducts (AGEs), which accumulate on tissue

195 a=-0.250; P<0.001) and receptor for advanced glycation endproducts (beta=-0.095; P<0.007) were invers

196 Here, we show that the receptor for advanced glycation endproducts (RAGE) and one of its primary liga

197 n and mutations in the receptor for advanced glycation endproducts (RAGE) are risk factors for asthma

198 The receptor for advanced glycation endproducts (RAGE) binds diverse ligands linke

199 The receptor for advanced glycation endproducts (RAGE) is a multiligand receptor a

200 The receptor for advanced glycation endproducts (RAGE) is a scavenger receptor of

201 The receptor for advanced glycation endproducts (RAGE) is an ubiquitous, transmemb

202 d glycation endproduct/receptor for advanced glycation endproducts (RAGE) pathway and showed that RAG

203 of epithelial (soluble receptor for advanced glycation endproducts [sRAGE]) and endothelial biomarker

204 Advanced glycation endproducts were measured using SDS-PAGE gels

205 rization of macrophages after AGEs (advanced glycation endproducts) treatment, blocking the IRF8 with

206 AGE (Advanced Glycation Endproducts)-RAGE (Receptor for AGEs) interact

207 Furthermore, increased glycation enhanced HTT toxicity in human cells and neuro

208 d is capable of rapidly assessing Hb and HSA glycation from low volumes of whole blood with minimal s

209 e to many factors but can be measured as the glycation gap (GGap).

210 cing capacity and ability to inhibit protein glycation greatly increased in the fortified purees.

211 We found that fibrinogen glycation had no significant systematic effect on single

212 The ability to assess both Hb and HSA glycation has the potential to provide a more complete p

213 early indicated the existence of age-related glycation hot spots in the plant proteome.

214 Thus, the sites of glycation hot spots might be defined by protein structur

215 Upon glycation, immunoreactivity was further reduced only whe

216 We found that glycation impairs HTT clearance thereby promoting its in

217 DJ-1 prevented protein glycation in an Escherichia coli mutant deficient in the

218 ds, only a little information about advanced glycation in plants is available.

219 metry detection (CE-MS) to assess hemoglobin glycation in whole blood lysate.

220 We observed that glycation increased the aggregation of mutant HTT exon 1

221 ients with low, moderate, or high hemoglobin glycation index (HGI), a measure of glycated hemoglobin

222 To identify and characterize glycation, induced modifications of DNA are crucial towa

223 hylglyoxal in the absence or presence of the glycation inhibitor aminoguanidine (pimagedine).

224 Strikingly, using glycation inhibitors, we demonstrated that normal cleara

225 By modifying amino-groups, glycation interferes with folding of proteins, increasin

226 AGEs can be formed via degradation of early glycation intermediates (glycoxidation) and by interacti

227 amino acids and proteins by acting on early glycation intermediates and releases repaired proteins a

228 Protein glycation involves formation of early (Amadori) and late

229 Protein glycation is a complex process that plays an important r

230 Glycation is a post-translational modification resulting

231 Protein glycation is an age-dependent posttranslational modifica

232 Glycation is an inevitable nonenzymatic covalent reactio

233 DNA glycation is associated with increased mutation frequenc

234 paper, a first sensing strategy for protein glycation is proposed, based on protein electroactivity

235 Glycation is the reaction of carbonyl compounds (reducin

236 ainly methylglyoxal and glyoxal), called DNA glycation, is quantitatively as important as oxidative d

237 evident by UV-Vis spectral changes, with the glycation level determined by matrix assisted laser deso

238 rage and heating appear to influence protein glycation levels in milk at similar or even higher degre

239 blood lipids, the antioxidant capacity, and glycation markers.

240 The extent of glycation measured in terms of glycated albumin and hemo

241 deposition in nerves, extracellular protein glycation, mitochondrial dysfunction, and oxidative stre

242 Oxidation and glycation modifications correlated weakly with color in

243 Overall, our study provides evidence that glycation modulates HTT exon-1 aggregation and toxicity,

244 he healthy individuals had a mean fibrinogen glycation of 4.0 mol glucose/mol fibrinogen.

245 Faox I lowered the glycation of almost all the free amino acids resulting e

246 The aim of this study was to test glycation of beta-lactoglobulin (BLG) in Maillard reacti

247 Glycation of food allergens may alter their immunologica

248 possibly owing to racial differences in the glycation of hemoglobin.

249 lycemic control or racial differences in the glycation of hemoglobin.

250 Glycation of human serum albumin (HSA) can also be measu

251 ol, respectively; P < .01) with preferential glycation of lysines 107 and 557, sites involved in fibr

252 Parameters for glycation of muscle protein were optimised using the bid

253 kinetic data revealed that calcium inhibited glycation of ovalbumin by a mixed non-competitive mechan

254 Glycation of plasminogen in diabetes directly affects fi

255 Thus, glycation of the chickpea allergen attenuated the sensit

256 The fibrinogen glycation of the diabetic patients was reduced from 8.8

257 Further, glycation of this purified protein was carried out.

258 Glycation on alpha-Hb is also detected in the alpha-Hb m

259 estigated the effects of in vivo plasminogen glycation on fibrinolysis, plasmin generation, protein p

260 ntal lesions, the precise effect of collagen glycation on gingival connective tissue biology is not f

261 pharmacological and genetic manipulation of glycation on huntingtin (HTT), the causative protein in

262 We sought to investigate the impact of glycation on the allergenicity of a food protein.

263 oteomic methods have been utilized to assign glycation, oxidation and glycoxidation protein targets i

264 the qualitative and quantitative changes in glycation patterns in terms of the general metabolic bac

265 e more insights into the dynamics of the DNA-glycation process in an easier fashion.

266 amalgam electrode (AgSAE) for monitoring the glycation process in samples of bovine serum albumin, hu

267 The glycation process was monitored as the decrease in the e

268 sequential order of the mechanism of the DNA-glycation process, and most likely, it occurs in the fol

269 As well as AGE-OVA, a crude glycation product in thermal incubation of OVA with gluc

270 at deletion of the receptor for advanced end-glycation products (RAGE) in mice was protective in long

271 induced expression of receptor for advanced glycation products (RAGE), but not that of Toll-like rec

272 the identification of the link between these glycation products and NO inactivation, and what lessons

273 ergo a previously undocumented non-enzymatic glycation reaction.

274 Both pI and Mr. of BSA were modified upon glycation reaction.

275 us group of compounds formed by nonenzymatic glycation reactions between reducing sugars and amino ac

276 ation end products (AGEs) due to its protein glycation reactions, which are the major causes of diabe

277 Protein glycation refers to the reversible reaction between aldo

278 ucleotide repair system that we name guanine glycation repair.

279 As the glycation sites are typically distributed across the ent

280 ons were quantified by mass spectrometry and glycation sites located by peptide mapping.

281 including the proteins affected and specific glycation sites therein.

282 We found the glycation sites to be distributed across the entire anti

283 FL), to monitor the progression of the early glycation stage.

284 Glycation strongly hindered protein breakdown, whereas c

285 Here, we aimed to identify specific glycation structure(s) that could influence the T-cell i

286 are formed, including proteins with various glycation structures.

287 as specifically modified with representative glycation structures: N(epsilon)-carboxymethyl lysine (C

288 (HRGS) (0.05-0.2mM Fe(3+)+0.6mM H2O2) and a glycation system (GLY) (0.05-0.2mM Fe(3+)+0.05M glucose)

289 The Maillard reaction (also referred to as "glycation") takes place between reducing sugars and comp

290 cilitated the identification of unrecognized glycation targets of DPD in a prokaryotic system.

291 truncation, soluble protein aggregates, and glycation that all likely have a limited clinical impact

292 eriod of basic and translational research in glycation that encompassed new pathologic phenomena and

293 of MG on the cell proteome and targets of MG glycation was analysed, and confirmed by Western blottin

294 PSA glycation was confirmed by a reduction in the number of

295 Combining proteolysis and Maillard-induced glycation was investigated to reduce the immunoreactivit

296 en sulfonylurea drugs or as the level of HSA glycation was varied.

297 eveals nonspecific, non-enzymatic reactions (glycation), which are not detected under standard denatu

298 e C, lysozyme, and beta-casein formed during glycation with d-glucose were identified and monitored i

299 under optimized conditions was subjected to glycation with dextran.

300 hanges in total secondary structures through glycation with GOSs (61.2%) and galactan (36.7%) and als