ライフサイエンスコーパス: glycation

1 ase (FN3K)-a kinase that triggers protein de-glycation.

2 s peptide during GID was hindered by protein glycation.

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

4 spectrometry was used to investigate protein glycation.

5 which did not resemble the sites of advanced glycation.

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

7 on of a chemical probe for investigating MGO-glycation.

8 d structural alterations of BSA subjected to glycation.

9 hyperglycemia-induced hemoglobin and insulin glycation.

10 < 0.05) and total body methylglyoxal-protein glycation (-14%, P < 0.01).

11 ), basal uptake of glucose (>39.5%) and anti-glycation ability (92%) was found in red rice (RR), than

12 uptake, hepatic glucose homeostasis and anti-glycation ability was analyzed in vitro.

13 Increased MG glycation activates the UPR in endothelial cells and the

14 onclude that higher fractional excretions of glycation adducts are potential biomarkers for early GFR

15 cognizes and facilitates the removal of 5-AR glycation adducts in live cells, supporting the dynamic

16 Glycation affected primarily the N-terminal region of al

17 How glycation affects their functions remains to be defined.

18 can be proposed as a natural potential anti-glycation agent.

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

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

21 y than lenses subjected to thermal stress or glycation alone, and this loss was accompanied by higher

22 Protein glycation, also known as nonenzymatic glycosylation, is

23 's disease (AD) pathogenesis and is prone to glycation, an irreversible process where proteins accumu

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

25 Moreover, chemical modifications such as glycation and carbamylation serve as important biomarker

26 Flux of glucose metabolism, MG formation and glycation and changes in cytosolic protein abundances, M

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

28 l glyoxalase-1 inhibition recapitulated RyR2 glycation and defective SR-mitochondria calcium exchange

29 ate this probe's utilities to uncover ribose-glycation and deglycation events as well as track FN3K a

30 Finally, we detect intense histone glycation and DJ-1 overexpression in breast cancer tumor

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

32 Glycation and increased free radical activity underlie t

33 Furthermore, 68.3% inhibition of protein glycation and reduced formation of protein aggregates we

34 The numbers and quantities of glycation- and oxidation-related modifications were simi

35 Our findings also reveal that lysine glycation appears to be an important factor that contrib

36 supporting the dynamic regulation of ribose glycation as well as validating the probe as a new platf

37 lular antioxidant activity (CAA) and protein glycation assays, to offer an improved picture of antiox

38 in functional foods for controlling protein glycation associated diabetic complications.

39 ls of Hsp27 are important for modulating the glycation-associated cellular pathologies in synucleinop

40 We demonstrated that double-CEL glycations at Lys-16 and Lys-28 of Abeta1-42 had the mos

41 east impact on fibril formation, whereas CEL glycations at Lys-16 of Abeta1-42 delayed fibril formati

42 Single-CEL glycations at Lys-28 of Abeta1-42 had the least impact o

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

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

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

46 we report that PAD4 antagonizes histone MGO-glycation by protecting the reactive arginine sites, as

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

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

49 The level of glycation, conformational alterations and protein bindin

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

51 Therefore, inhibition of protein glycation could be a key strategy to prevent these diabe

52 N-Terminal and lysine glycation could be identified on the alpha- and beta-cha

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

54 se in turbidity ascribed to the increment of glycation degree, as well as, a decrease in the isoelect

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

56 MG formation, detoxification, and its glycation effects have paved the way for the development

57 Tissue advanced glycation end product (AGE) accumulation has been propos

58 d to the efficient synthesis of the advanced glycation end product (AGE) methylglyoxal-derived imidaz

59 x 1 (HMGB1) can engage receptor for advanced glycation end product (RAGE) to direct monocytes to a pr

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

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

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

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

64 Advanced glycation end products (AGEs) accumulate in tissues with

65 Advanced glycation end products (AGEs) accumulated during long-te

66 the formation of total fluorescent advanced glycation end products (AGEs) and Amadori adducts were d

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

68 It is hypothesized that levels of advanced glycation end products (AGEs) are higher in the gingival

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

70 sels to hyperglycemic conditions or advanced glycation end products (AGEs) ex vivo resulted in signif

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

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

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

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

75 Advanced glycation end products (AGEs) promote adverse health eff

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

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

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

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

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

81 the last two decades, many types of advanced glycation end products (AGEs), formed through the reacti

82 The three canonical RAGE ligands, Advanced Glycation End products (AGEs), HMGB1, and S100 proteins,

83 ome, prominent subpathways included advanced glycation end products (AGEs), phosphatidylcholines, sph

84 majority of RAGE ligands including advanced glycation end products (AGEs), S100 proteins, and HMGB1.

85 d Lima tomatoes on the formation of advanced glycation end products (AGEs), the activity of angiotens

86 s, MG is a predominant precursor of advanced glycation end products (AGEs), which result in protein d

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

88 g is glycation through formation of advanced glycation end products (AGEs).

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

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

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

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

93 The receptor for advanced glycation end products (RAGE) and Toll-like receptor 4 (

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

95 ave indicated that the receptor for advanced glycation end products (RAGE) is a critical molecule in

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

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

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

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

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

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

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

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

104 The receptor for advanced glycation end products (RAGE) plays a key role in mammal

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

106 The receptor for advanced glycation end products (RAGE), a cell membrane receptor,

107 mune receptor protein, Receptor for Advanced Glycation End products (RAGE), has been extensively stud

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

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

110 box 1 (HMGB1) and its receptor for advanced glycation end products (RAGE).

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

112 potential and soluble-receptor for advanced glycation end products (sRAGE) in bronchoalveolar lavage

113 nflammatory mediators (receptor for advanced glycation end products [RAGE], MPO, uteroglobin/CC-10);

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

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

116 ence for elevated levels of lipoxidation and glycation end products in the primary olfactory system,

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

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

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

120 Advanced glycation end products were assessed with a fluorometric

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

122 ds with reducing sugars and include advanced glycation end products with deleterious health effects.

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

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

125 ng the S100A8/A9-RAGE (receptor for advanced glycation end products) axis could represent a viable ap

126 ions of sRAGE (soluble receptor for advanced glycation end products) strongly associate with ARDS ris

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

128 interleukin-6, soluble receptor for advanced glycation end products, interleukin-1ra, tumor necrosis

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

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

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

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

133 Advanced glycation end-product (AGE) formation is increased in di

134 and albuminuria, and suppression of advanced glycation end-product signalling.

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

136 treated with glycolaldehyde-derived advanced glycation end-products (0, 50, 100, and 200 mug/ml) for

137 Advanced glycation end-products (AGEs) accumulate during prolonge

138 (cv. 'Weiki'), on the formation of advanced glycation end-products (AGEs) and the activity of angiot

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

140 Resulting advanced glycation end-products (AGEs) contribute to pathogenesis

141 ty against formation of fluorescent advanced glycation end-products (AGEs) in vitro of raw and roaste

142 However, heat processes generate Advanced Glycation End-products (AGEs), including N(epsilon)-carb

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

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

145 ine tuning the formation of dietary advanced glycation end-products (d-AGEs), dicarbonyls and acrylam

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

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

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

149 lation, leading to the receptor for advanced glycation end-products (RAGE) shedding into soluble and

150 olin-1, podoplanin and receptor for advanced glycation end-products (RAGE), and most cells were negat

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

152 tions of serum soluble receptor for advanced glycation end-products (sRAGE) with acute and chronic mo

153 hat tendon fibroblasts treated with advanced glycation end-products display reduced ATP production, e

154 Our findings suggest that advanced glycation end-products disrupt tendon fibroblast homeost

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

156 dy was to investigate the impact of advanced glycation end-products on tendon fibroblasts to further

157 long with a concomitant increase of advanced-glycation end-products suggesting that allysine may be i

158 We proposed that advanced glycation end-products would induce limitations to mitoc

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

160 n receptors) and RAGE (receptor for advanced glycation end-products) play a critical role in metaboli

161 gnition receptor RAGE (receptor for advanced glycation end-products) transmits proinflammatory signal

162 ric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine)

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

164 lveolar lavage soluble receptor for advanced glycation end-products, plasma interleukin-6, and monocy

165 onstrated a significant increase in advanced glycation-end product-modified proteins in the myocardiu

166 Because advanced glycation-end products accumulate throughout life, we in

167 Higher levels of advanced glycation-end products and reduced glyoxalase-1 activity

168 errin receptor and the receptor for advanced glycation-end products, cross the blood-brain-barrier an

169 Forty-five glycated, 48 advanced glycation endproduct (AGE-) modified, and 20 oxidized/ca

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

171 Advanced glycation endproducts (AGEs) and their precursors (dicar

172 Advanced glycation endproducts (AGEs) are formed in a series of n

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

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

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

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

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

178 The receptor for advanced glycation endproducts (RAGE) has been implicated as a cr

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

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

181 The receptor for advanced glycation endproducts (RAGE) is critically involved in t

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

183 es have found that the receptor for advanced glycation endproducts (RAGE) plays a significant role in

184 equently activated the receptor for advanced glycation endproducts (RAGE) receptor to promote NF-kapp

185 meric complex with the receptor for advanced glycation endproducts (RAGE).

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

187 ediated in part by the receptor for advanced glycation endproducts and Toll-like receptor proteins 2

188 Advanced glycation endproducts were measured using SDS-PAGE gels

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

190 arbonyls are reactive precursors of advanced glycation endproducts.

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

192 rosslinking mechanisms, Fenton chemistry and glycation, for their possible contribution to the preser

193 Dry heating led to protein glycation (formation of furosine, Nepsilon-(carboxymethy

194 Impaired tubular reuptake of glycation free adducts by lysine and arginine transporte

195 excretions of 6 lysine and arginine-derived glycation free adducts were higher in patients with earl

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

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

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

199 Glycation has emerged to be one of the clinically import

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

201 gulation, and consequences of NECMs, such as glycation, has been challenging due to the complex and o

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

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

204 Upon glycation, immunoreactivity was further reduced only whe

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

206 ptor (RyR2) in the SR as prominent target of glycation in aged mice, and the sites of glycation were

207 However, the levels of lysine glycation in collagen, which is not considered a cross-l

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

209 lication toward understanding protein ribose-glycation in vitro and in cellulo.

210 re we perform a detailed analysis of histone glycation in vitro and in vivo and find it has global ra

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

212 s that other proteins undergo FN3K-sensitive glycation, including translation factors, heat shock pro

213 We assessed if increased MG glycation induced proteotoxic stress, identifying relate

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

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

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

217 Glycation is a one of the post-translational modificatio

218 Glycation is a post-translational modification resulting

219 Protein glycation is an age-dependent posttranslational modifica

220 DNA glycation is associated with increased mutation frequenc

221 Glycation is referred to as the interaction of protein a

222 Glycation is the reaction of carbonyl compounds (reducin

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

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

225 nses subjected to thermal stress followed by glycation lost resilience more extensively than lenses s

226 acylation, lipidation, monoaminylation, and glycation, many of which appear to have crucial roles in

227 ce the formation of hydroxymethylfurfural, a glycation marker, at 70 and 80 degrees C.

228 tent should be interpreted with caution as a glycation marker.

229 Our studies demonstrated that glycation modification of IAPP promotes the amyloidogeni

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

231 life, we investigated whether intracellular glycation occurs in aged cardiomyocytes and its impact o

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

233 yglyoxal is commonly used for the unspecific glycation of Abeta1-42, which results in a complex mixtu

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

235 We recently showed that glycation of aSyn by methylglyoxal (MGO) potentiates its

236 our study reveals a surprising role for the glycation of cellular proteins and implicates FN3K as ta

237 se TEM to show that ribose-5-phosphate (R5P) glycation of collagen fibrils - potentially important in

238 Glycation of collagen fibrils is known to impact on cell

239 the context of cancer and in model studies, glycation of collagen molecules has been shown to affect

240 Glycation of food allergens may alter their immunologica

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

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

243 Glycation of HSA with sugars revealed 9 glyoxal- and 14

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

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

246 HbA1c is formed by the non-enzymatic glycation of terminal valine of hemoglobin.

247 Thus, glycation of the chickpea allergen attenuated the sensit

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

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

250 (AGEs), which result in protein dysfunction, glycation of vascular tissues and aging.

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

252 y, we aim to elucidate the impact of protein glycation on islet amyloid polypeptide (IAPP, also known

253 are subjected to methylglyoxal (MGO)-induced glycation on nucleophilic side chains, particularly argi

254 However, the effect of glycation on protein aggregation has not been fully inve

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

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

257 We reported levels of serum protein glycation, oxidation and nitration and related hydrolysi

258 We determined urinary protein glycation, oxidation and nitration free adducts by stabl

259 d nitration and related hydrolysis products, glycation, oxidation and nitration free adducts in patie

260 Increased protein glycation, oxidation and nitration is linked to the deve

261 ping the specific lipid content and level of glycation/oxidation, the mode of action of specific lipo

262 adation were analyzed in parallel to protein glycation patterns (exemplified with hydroimidazolone mo

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

264 Recent studies have indicated that glycation plays a role in type 2 diabetes (T2D) and neur

265 Protein glycation plays a vital role in the progression of vario

266 nd enhanced separation of a low level lysine glycation post-translational modification (+162.1 Da), p

267 Although the differences in glycation potential of monosaccharides are well characte

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

269 elationship between the antioxidant and anti-glycation properties was confirmed and green pepper and

270 ctional compounds, with antioxidant and anti-glycation properties.

271 und that in 16-week-old diabetic db/db mice, glycation reaches levels similar to those observed in 98

272 ergo a previously undocumented non-enzymatic glycation reaction.

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

274 Our findings indicate that preventing glycation reactions might reduce abdominal pain in patie

275 LAC seemed to be more susceptible to the glycation reactions than MP.

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

277 ucleotide repair system that we name guanine glycation repair.

278 e found that, similar to methylglyoxal (MGO) glycation, ribose glycation specifically accumulates on

279 including the proteins affected and specific glycation sites therein.

280 abilizing residues in close proximity to the glycation sites.

281 lar to methylglyoxal (MGO) glycation, ribose glycation specifically accumulates on histones.

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

283 Glycation strongly hindered protein breakdown, whereas c

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

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

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

287 Glycation, the hallmark of diabetes, is a prevalent NECM

288 has been implicated in this cross-linking is glycation through formation of advanced glycation end pr

289 ol for tracking, enriching, and studying MGO-glycation to aid in understanding its underlying biochem

290 inst two non-enzymatic Fenton chemistry- and glycation-treated extant chicken samples.

291 Upon glycation under physiological conditions, the chaperone-

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

293 RyR2 glycation was associated with more pronounced calcium le

294 of glycation in aged mice, and the sites of glycation were characterized by quantitative mass spectr

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

296 putational tools become necessary to predict glycation, which could help medical professionals admini

297 rix mechanics and the influence of excessive glycation, which has been linked with age-related diseas

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 re was more modified, while the influence of glycation with lactose was limited.