ライフサイエンスコーパス: advanced glycation end product

1 8 is an agonist for TLR4 or the receptor for advanced glycation end products.

2 y by activating TLR4 and/or the receptor for advanced glycation end products.

3 ibly because of accumulation of irreversible advanced glycation end products.

4 rial DNA and involved TLR9 and receptors for advanced glycation end products.

5 substantial protein damage via formation of advanced glycation end products.

6 ) and formation of different products called advanced glycation end products.

7 eactive dicarbonyl with the capacity to form advanced glycation end products.

8 of Toll-like receptor-4 and the receptor for advanced glycation end products.

9 C and accelerated non-enzymatic formation of advanced glycation end products.

10 ed in part on expression of the receptor for advanced glycation end products.

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

12 ion of protein modifications that are called advanced glycation end products.

13 nd intra-alveolar levels of the receptor for advanced glycation end-products.

14 We investigated whether H(2)O(2) and AGE (advanced glycation end products), 2 well-known mediators

15 enase (5.7 [1.7-19.1]), soluble receptor for advanced glycation end products (3.5 [1.7-7.2]), and von

16 ed against HMGB1 or against the receptor for advanced glycation end products, a putative HMGB1 recept

17 Advanced glycation end products acting via their recepto

18 effects of multiple ligands, including AGEs (advanced glycation end products), advanced oxidation pro

19 emonstrate that the interaction of RAGE with advanced-glycation end products affects myocardial energ

20 molecule 1), increased expression of CB(1), advanced glycation end product (AGE) and angiotensin II

21 Advanced glycation end product (AGE) content of apolipop

22 We hypothesized that breaking advanced glycation end product (AGE) cross-links could i

23 hogenetic pathways include oxidative stress, advanced glycation end product (AGE) formation, protein

24 pounds are known as central intermediates in advanced glycation end product (AGE) formation.

25 vascular endothelial cells after exposure to advanced glycation end product (AGE)-BSA by enzyme-linke

26 pleckstrin is involved in RAGE signaling and advanced glycation end product (AGE)-elicited mononuclea

27 hat dendritic cells preferentially recognize advanced glycation end product (AGE)-modified proteins,

28 Advanced glycation end products (AGE) accumulate in diab

29 Advanced glycation end products (AGE) have been found in

30 In addition, to determine the effect of advanced glycation end products (AGE) in the presence an

31 burden of reactive oxygen species (ROS) and advanced glycation end products (AGE) is increased.

32 Zhu and colleagues clearly demonstrate that advanced glycation end products (AGE), generated under h

33 tion receptor, RAGE with key ligands such as advanced glycation end products (AGE), S100 proteins, am

34 peratures are major environmental sources of advanced glycation end products (AGE).

35 Advanced glycation end-product (AGE) deposition and expr

36 Advanced glycation end-products (AGE) are reactive metab

37 s are alpha-dicarbonyls and the receptor for advanced glycation end products (AGER).

38 The receptor of advanced glycation end products, AGER (previously known

39 Advanced glycation end products (AGEs) accumulate in T2D

40 eat damage, starch digestibility, release of advanced glycation end products (AGEs) and antioxidant c

41 n amino acids, peptides and proteins to form advanced glycation end products (AGEs) and cause carbony

42 y aimed to determine the association between advanced glycation end products (AGEs) and glaucoma base

43 pathways of necroptosis include formation of advanced glycation end products (AGEs) and reactive oxyg

44 n macrophages, and increased accumulation of advanced glycation end products (AGEs) and receptor for

45 re model was used to investigate the role of advanced glycation end products (AGEs) and the receptor

46 This review concentrates on the formation of advanced glycation end products (AGEs) and the role they

47 Advanced glycation end products (AGEs) and their recepto

48 Advanced glycation end products (AGEs) are a heterogeneo

49 Advanced glycation end products (AGEs) are believed to i

50 the complex reaction cascade, the so-called advanced glycation end products (AGEs) are formed, inclu

51 Advanced glycation end products (AGEs) are important med

52 ted periodontal destruction and the roles of advanced glycation end products (AGEs) are investigated.

53 Advanced glycation end products (AGEs) are involved in t

54 Advanced glycation end products (AGEs) are proteins or l

55 that hypoxia stimulates brisk generation of advanced glycation end products (AGEs) by endothelial ce

56 Advanced glycation end products (AGEs) contribute to len

57 ssive basement membrane (BM) modification by advanced glycation end products (AGEs) contributes to im

58 Although advanced glycation end products (AGEs) derived from both

59 lglyoxal (MG) is a predominant precursor for advanced glycation end products (AGEs) due to its protei

60 s unavoidably favours methylglyoxal (MG) and advanced glycation end products (AGEs) formation in canc

61 This process is partially explained by advanced glycation end products (AGEs) from ascorbic aci

62 specific interactions of platelet CD36 with advanced glycation end products (AGEs) generated under h

63 Previously, modification by oxidation and advanced glycation end products (AGEs) had been shown to

64 The consumption of advanced glycation end products (AGEs) has increased bec

65 Advanced glycation end products (AGEs) have been linked

66 Advanced glycation end products (AGEs) have been suggest

67 Experimental data suggest a role for advanced glycation end products (AGEs) in cardiovascular

68 We previously showed that the content of advanced glycation end products (AGEs) in the diet corre

69 Presence of advanced glycation end products (AGEs) in the heart indu

70 kin fluorescence (SF) noninvasively measures advanced glycation end products (AGEs) in the skin and i

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

72 ic disease can result in the accumulation of advanced glycation end products (AGEs) of proteins, lipi

73 g the effects of consumption of diets low in advanced glycation end products (AGEs) on cardiometaboli

74 Six skin collagen advanced glycation end products (AGEs) originally measur

75 Advanced glycation end products (AGEs) play a significan

76 linked to increases in the oxidative stress-advanced glycation end products (AGEs) receptor for AGEs

77 ve substances (e.g. alpha-dicarbonyls) yield advanced glycation end products (AGEs) that can alter th

78 Binding of advanced glycation end products (AGEs) to their receptor

79 ermeability of cultured cells in response to advanced glycation end products (AGEs) was significantly

80 ted by transmission electron microscopy, and advanced glycation end products (AGEs) were evaluated by

81 This process leads to the formation of advanced glycation end products (AGEs) which accumulate

82 We examined associations of advanced glycation end products (AGEs) with renal functi

83 Ligation of advanced glycation end products (AGEs) with their recept

84 Advanced glycation end products (AGEs), a heterogeneous

85 further degradation results in formation of advanced glycation end products (AGEs), also originating

86 phogenic protein-7 (BMP-7) and inhibitors of advanced glycation end products (AGEs), aminoguanidine a

87 lar chymase is associated with deposition of advanced glycation end products (AGEs), an increase in e

88 licated in diabetic complications, including advanced glycation end products (AGEs), protein kinase C

89 l roles in both the toxicity and disposal of advanced glycation end products (AGEs), substances that

90 ld-type bone marrow-derived macrophages with advanced glycation end products (AGEs), which accumulate

91 streptozotosin-induced diabetic mice and on advanced glycation end products (AGEs)-induced H9c2 card

92 ion in turn leading to altered production of advanced glycation end products (AGEs).

93 ence, were also described in SIPS induced by advanced glycation end products (AGEs).

94 r disease are linked to pro-oxidants such as advanced glycation end products (AGEs).

95 ed oxidative stress (OS) and accumulation of advanced glycation end products (AGEs).

96 It can modify DNA and proteins to form advanced glycation end products (AGEs).

97 ndothelial cells in response to diabetes and advanced glycation end products (AGEs).

98 ds, lipids, and proteins, yielding early and advanced glycation end products (AGEs).

99 anced oxidation protein products (AOPPs) and advanced glycation end products (AGEs).

100 sed SIRT1 partly due to oxidant glycotoxins [advanced glycation end products (AGEs)].

101 Advanced glycation end-products (AGEs) are also present

102 decreased circulating levels of pro-oxidant advanced glycation end-products (AGEs).

103 ged hyperglycemia activates the formation of advanced glycation end-products (AGEs).

104 F and TEF inhibited formation of fluorescent advanced glycation end-products (AGEs).

105 hanical properties due to an accumulation of advanced glycation end-products (AGEs).

106 thesis that activation of RAGE (receptor for advanced glycation end products [AGEs]) by its ligands,

107 For investigating the advanced glycation end-product-albumin (AGE-albumin) fro

108 Receptor for advanced glycation end product and immediate early respo

109 e depended on expression of the receptor for advanced glycation end products and could be reversed by

110 ns by multiple mechanisms, with formation of advanced glycation end products and increased oxidative

111 to significantly attenuate the formation of advanced glycation end products and malondialdehyde in a

112 Advanced glycation end products/receptor of advanced glycation end products and nuclear factor-kappa

113 advanced glycation end products (RAGE) binds advanced glycation end products and other inflammatory l

114 t regarding the role of soluble receptor for advanced glycation end products and receptor for advance

115 yridorin, NephroGenex) inhibits formation of advanced glycation end products and scavenges reactive o

116 Receptor for advanced glycation end products and soluble receptor for

117 kers of lung epithelial injury (receptor for advanced glycation end products and surfactant protein D

118 l injury was assessed by plasma receptor for advanced glycation end products and systemic endothelial

119 Raised tissue expression of advanced glycation end products and their receptor has b

120 relevant role in preventing the formation of advanced glycation end products and therefore potentiall

121 ndicated their engagement with receptors for advanced glycation end products and TLR9, respectively,

122 Lower receptor for advanced glycation end products and tumor necrosis facto

123 -like 3 and accumulation of the receptor for advanced glycation end-products and its ligand S100A8 in

124 ated N-glycans expressed on the receptor for advanced glycation end-products and other cell surface g

125 mical (acrylamide, hydroxymethylfurfural and advanced glycation end products) and microbiological saf

126 changes in wall content (i.e. less elastin, advanced glycation end-products) and increase in conduit

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

128 loride intracellular channel 4, receptor for advanced glycation end products, and periostin.

129 tokines and soluble form of the receptor for advanced glycation end-products, and safety.

130 s receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are not involved.

131 tics and multivariate analysis (receptor for advanced glycation end products: area under the curve, 0

132 , 0.943+/-0.05; p<.001; soluble receptor for advanced glycation end products: area under the curve, 0

133 ent of TLR4 and the multiligand receptor for advanced glycation end products as receptors during MRP8

134 ing integrin alphaIIb and RAGE (receptor for advanced glycation end products) as model type I recepto

135 We define RAGE (receptor for advanced glycation end products) as the hS100A7 receptor

136 Toll-like receptor ligands, and receptor for advanced glycation end-products, as well as CpG methylat

137 en was observed following mineralization and advanced glycation end product-associated modification.

138 istration of anti-TNF or soluble receptor of advanced glycation end products attenuated nuclear facto

139 Extracellular newly identified receptor for advanced glycation end products-binding protein levels o

140 bited in cells pretreated with soluble RAGE, advanced glycation end product-bovine serum albumin, or

141 ern recognition receptor that interacts with advanced glycation end products, but also with C3a, CpG

142 Activation of the receptor for advanced glycation end products by its ligands promotes

143 is common, secondary to effects of glucose, advanced glycation end products, C-reactive protein, uri

144 suggests that soluble forms of receptor for advanced glycation end products circulating in the plasm

145 bone are a result of reduced accumulation of advanced glycation end products compared with the strut

146 Alagebrium breaks advanced glycation end product crosslinks and improves L

147 and murine models of TLR4- and receptor for advanced glycation end products-dependent signaling.

148 of RAGE ligand HMGB1 and carboxymethyllysine-advanced glycation end product epitopes in liver and adi

149 Enhanced monocytic receptor for advanced glycation end products expression and decreased

150 Receptor for advanced glycation end products expression and soluble r

151 Monocytic receptor for advanced glycation end products expression assessed by f

152 Thus, it is hypothesized that receptor for advanced glycation end products expression might be dele

153 dose reductase inhibitor alrestatin, and the advanced glycation end product formation inhibitor amino

154 n modifications, such as O-GlcNAcylation and advanced glycation end product formation.

155 Both receptor for advanced glycation end products>103.6 mean fluorescence

156 Advanced glycation end products have been implicated in

157 of Toll-like receptors 2 and 4, receptor for advanced glycation end-products, high-mobility group box

158 nced glycation end products and receptor for advanced glycation end products in humans with cardiogen

159 f antibodies against methamphetamine-derived advanced glycation end products in rats chronically self

160 Given the known role of advanced glycation end products in the alteration of pro

161 ate types and site of PTM of glyoxal-derived advanced glycation end-products-in the neuropeptide subs

162 l pathway flux, increased formation of AGEs (advanced glycation end products), increased expression o

163 Receptor for advanced glycation end products is targeted by FBXO10 fo

164 um N(epsilon)-carboxymethyl-lysine (CML), an advanced glycation end product, is associated with proin

165 Methylglyoxal (MGO), a major precursor for advanced glycation end products, is increased in diabete

166 lly or completely repressed by inhibitors of advanced glycation end products, L-type calcium channels

167 aemia, oxidative stress, and accumulation of advanced glycation end products, leading to altered bone

168 cantly decreased plasma soluble receptor for advanced glycation end products levels (79.87+/-10.62 ar

169 on and decreased plasma soluble receptor for advanced glycation end products levels play a central ro

170 products expression and soluble receptor for advanced glycation end products levels were determined a

171 tokines and soluble form of the receptor for advanced glycation end-products levels in the sevofluran

172 phils with high glucose and the receptor for advanced glycation end products ligand S100B greatly enh

173 uorescence intensity or soluble receptor for advanced glycation end products<76.88 arbitrary units in

174 ective role of Tpi and support the idea that advanced glycation end products may also contribute to p

175 cation end products and soluble receptor for advanced glycation end products may be prognostic biomar

176 at chronic hyperglycemia causes receptor for advanced glycation end products-mediated epigenetic modi

177 be deleterious, whereas soluble receptor for advanced glycation end products might be beneficial in c

178 Therefore, we measured oxidized LDL (oxLDL), advanced glycation end products-modified LDL (AGE-LDL),

179 hase upregulation, and methylglyoxal-derived advanced glycation end product, nitrotyrosine, and nitri

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

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

182 physically interacts with AGEs/receptor for advanced glycation end products on the cell surface and

183 omide (PTB), which cleaves the crosslinks of advanced glycation end products on the extracellular mat

184 resent study, we introduced an analog of the advanced glycation end product, OP-lysine, at the 90th p

185 The potential roles of advanced glycation end products, oxidative stress, angio

186 Advanced glycation end products play major roles in diab

187 in various diseases, methamphetamine-derived advanced glycation end products provide an unrecognized

188 to prevent it from engaging the receptor for advanced glycation end product (RAGE) that may sustain i

189 Receptor for advanced glycation end product (RAGE)-dependent signalin

190 rting extracellular DNA through receptor for advanced glycation end products (RAGE) and induces produ

191 Receptor for advanced glycation end products (RAGE) and its ligands a

192 The receptor for advanced glycation end products (RAGE) and its ligands h

193 We studied the expression of receptor for advanced glycation end products (RAGE) and neuronal dens

194 activation of monocytes through receptor for advanced glycation end products (RAGE) and Toll-like rec

195 nvolved internalization of both receptor for advanced glycation end products (RAGE) and Toll-like rec

196 Receptor for advanced glycation end products (RAGE) binds advanced gl

197 Receptor of advanced glycation end products (RAGE) has been implicat

198 ed to an increased expression of receptor of advanced glycation end products (RAGE) in gingival tissu

199 onstrate that overexpression of receptor for advanced glycation end products (RAGE) in imbroglio exag

200 we investigated the role of the receptor for advanced glycation end products (RAGE) in neuroinflammat

201 we have established a role for receptor for advanced glycation end products (RAGE) in RSV infection.

202 We studied the function of the receptor for advanced glycation end products (RAGE) in the developmen

203 The receptor for advanced glycation end products (RAGE) is a highly expre

204 The receptor for advanced glycation end products (RAGE) is a member of th

205 The receptor for advanced glycation end products (RAGE) is a member of th

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

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

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

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

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

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

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

213 The receptor for advanced glycation end products (RAGE) is a pattern reco

214 The receptor for advanced glycation end products (RAGE) is a pattern reco

215 The receptor for advanced glycation end products (RAGE) is a pattern reco

216 Receptor for advanced glycation end products (RAGE) is an activation

217 The receptor for advanced glycation end products (RAGE) is an important c

218 The receptor for advanced glycation end products (RAGE) is highly express

219 The receptor for advanced glycation end products (RAGE) is highly express

220 In the kidney, the receptor for advanced glycation end products (RAGE) is principally ex

221 The receptor for advanced glycation end products (RAGE) is produced eithe

222 The receptor for advanced glycation end products (RAGE) is upregulated in

223 However, in Receptors for Advanced Glycation End Products (RAGE) knockout mice aft

224 Receptor for advanced glycation end products (RAGE) mediates Abeta-in

225 The receptor for advanced glycation end products (RAGE) mediates immune c

226 and persistent upregulation of receptor for advanced glycation end products (RAGE) messenger RNA, bu

227 9 (S100A8/A9) interact with the receptor for advanced glycation end products (RAGE) on hepatic Kupffe

228 (S100A8/A9), which binds to the receptor for advanced glycation end products (RAGE) on Kupffer cells,

229 HMGB1 required the presence of receptor for advanced glycation end products (RAGE) on neutrophils bu

230 After binding to the receptor for advanced glycation end products (RAGE) or toll-like rece

231 pharmacological blockade of the receptor for advanced glycation end products (RAGE) prevents the earl

232 by Toll-like receptor (TLR) and receptor for advanced glycation end products (RAGE) signals.

233 A-box) that signals through the receptor for advanced glycation end products (RAGE) to reverse apopto

234 mation of AGEs and suppress the receptor for advanced glycation end products (RAGE) via nuclear facto

235 nuclear receptor C2 (RORC2), and receptor of advanced glycation end products (RAGE) were evaluated by

236 port avid binding of LPA to the receptor for advanced glycation end products (RAGE), a member of the

237 recognition receptors, such as receptor for advanced glycation end products (RAGE), allows for a com

238 w the major receptor for HMGB1, receptor for advanced glycation end products (RAGE), also binds to he

239 Receptor for advanced glycation end products (RAGE), an immunoglobin

240 y mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of R

241 With its receptor for advanced glycation end products (RAGE), colocalization a

242 its cell surface receptor, the receptor for advanced glycation end products (RAGE), in aortic smooth

243 on of the receptor for S100A12, receptor for advanced glycation end products (RAGE), in murine aortic

244 GB-1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited respon

245 toll-like receptor (TLR)2, the receptor for advanced glycation end products (RAGE), myeloid differen

246 of toll-like receptor 4 (TLR4), receptor for advanced glycation end products (RAGE), p-ERK1/2, nuclea

247 ing S100/calgranulin ligands of receptor for advanced glycation end products (RAGE), promote chondroc

248 hereas B16F10 cells express the receptor for advanced glycation end products (RAGE), which is a known

249 effects in the ischemic retina, receptor for advanced glycation end products (Rage)-deficient mice (R

250 ) by articular chondrocytes via receptor for advanced glycation end products (RAGE)-mediated signalin

251 P-13) through activation of the receptor for advanced glycation end products (RAGE).

252 mers, and are secreted and bind receptor for advanced glycation end products (RAGE).

253 n response to the activation of receptor for advanced glycation end products (RAGE).

254 ular matrix and by engaging the receptor for advanced glycation end products (RAGE).

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

256 counteracted by blockade of the receptor for advanced glycation end products (RAGE)/nuclear factor-ka

257 s, AIM2-like receptors, and the receptor for advanced glycation end products (RAGE)] to promote autop

258 hisms in the human gene for the receptor for advanced glycation end-products (RAGE) are associated wi

259 rward signals downstream of the receptor for advanced glycation end-products (RAGE) can fuel chronic

260 Studies of the receptor for advanced glycation end-products (RAGE) indicate that thi

261 The receptor for advanced glycation end-products (RAGE) is a multiligand

262 The receptor for advanced glycation end-products (RAGE) is a single-trans

263 Expression of receptor for advanced glycation end-products (RAGE) is suggested to p

264 In this study, we show that the receptor for advanced glycation end-products (RAGE) promoted DNA upta

265 ental Medicine reports that the receptor for advanced glycation end-products (RAGE) promotes uptake o

266 -like receptor-4 (TLR4) and the receptor for advanced glycation end-products (RAGE) revealed the invo

267 h factor receptor CD114 and the receptor for advanced glycation end-products (RAGE), a CREB inducer a

268 s (or alarmins) by engaging the receptor for advanced glycation end-products (RAGE).

269 major alarmin that binds to the receptor for advanced glycation end-products (RAGE).

270 actants and S100A9, through the receptor for advanced glycation end-products (RAGE; ie, its receptor)

271 ngiotensin II type 1 receptors (receptor for advanced glycation end product [RAGE], angiotensin II re

272 o its second proposed receptor (receptor for advanced glycation end products [RAGE]) has no significa

273 Toll-like receptors [TLRs] and receptor for advanced glycation end products [RAGE]) present on vascu

274 g, reducible HMGB1 binds to the receptor for advanced glycation end products (RAGEs), but not to Toll

275 Advanced glycation end products/receptor of advanced gly

276 Advanced glycation end product receptors (AGERs) play di

277 s in vitro through both TLR4 and receptor of advanced glycation end product receptors.

278 ading enzyme, via activation of receptor for advanced glycation end product signaling.

279 tic collaboration with TLR2 and receptor for advanced glycation end products signaling, mediates HS-i

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

281 Circulating levels of soluble receptor for advanced glycation end products (sRAGE) likely comprise

282 ma subpopulation is the soluble receptor for advanced glycation end products (sRAGE).

283 een early postoperative soluble receptor for advanced glycation end-product (sRAGE) levels, a marker

284 vels of the soluble form of the receptor for advanced glycation end-products (sRAGE) are elevated dur

285 than carboxymethyl-lysine, one of the major advanced glycation end products, suggesting the prominen

286 nt differences were observed in receptor for advanced glycation end products, surfactant protein D, a

287 ribonucleic acid expression of receptor for advanced glycation end products, surfactant protein-B, t

288 Moreover, the receptor for advanced glycation end products that recognizes MG and G

289 eeded to maintain expression of receptor for advanced glycation end products, the ubiquitously expres

290 ulin superfamily molecule RAGE (receptor for advanced glycation end product) transduces the effects o

291 ole in preventing the increased formation of advanced glycation end products under certain pathologic

292 genase-1 (HO-1), TNF-alpha, the receptor for advanced glycation end products, vascular endothelial gr

293 ytes were identified, including receptor for advanced glycation end product, vimentin, heat-shock pro

294 ene induction by ligands of the receptor for advanced glycation end products was also attenuated in S

295 ria, proteinuria, blood creatinine, urea and advanced glycation end products was also observed.

296 Plasma receptor for advanced glycation end products was significantly lower

297 einase cleavage product soluble receptor for advanced glycation end products were significantly atten

298 llagen content, hydroxyproline, and collagen advanced glycation end products were similar in both old

299 onyl glucose metabolites, the precursors for advanced glycation end products, were significantly elev

300 ta, MIP-2, TNF-alpha, TLR4, and receptor for advanced glycation end products, whereas mRNA levels of

301 al and the consequent enhanced production of advanced glycation end products, which are ultimately re