ライフサイエンスコーパス: rage

1 eceptor for advanced glycation end-products (RAGE).

2 eceptor for advanced glycation end products (RAGE).

3 mmunohistochemistry of the receptor for AGE (RAGE).

4 of recombinase-assisted genome engineering (RAGE).

5 were reduced in diabetic macrophages through RAGE.

6 ended to other PS receptors, such as Axl and RAGE.

7 was ameliorated by functional suppression of RAGE.

8 through HMGB1-mediated engagement of T cell RAGE.

9 kinase Czeta (PKCzeta), which phosphorylates RAGE.

10 32 mug/L (median = 0.31 mug/L; interquartile rage = 0.10-0.89 mug/L).

11 may reflect pathogenic interactions between RAGE, a cell surface receptor expressed on malignant cel

12 ateral septum (LS) is known to cause "septal rage," a phenotype characterized by a dramatic increase

13 is questionable, and models only containing RAGE account for the observed diffraction data just as w

14 Summer fires frequently rage across Mediterranean Europe, often intensified by h

15 ing the inflammatory response and of soluble RAGE acting as a decoy were associated with up-regulatio

16 degeneration and demonstrate that microglial RAGE activation in presence of Abeta-enriched environmen

17 n endproducts (RAGE) pathway and showed that RAGE activation induced cholangiocyte proliferation.

18 as mainly focused on the correlation between RAGE activity and pathological conditions, such as cance

19 Blockade of RAGE ameliorates elastase-induced emphysema development

20 exes successfully silenced the expression of RAGE and attenuated the inflammation and apoptosis in th

21 us of exogenous small-molecule inhibitors of RAGE and concludes by identifying key strategies for fut

22 fic danger-associated molecular patterns (EN-RAGE and heat shock protein 70) were substantially highe

23 RAGE and HMGB1 coordinately enhanced tumor cell mitochon

24 A causal link between hyperactivation of RAGE and inflammation in CF has been observed, such that

25 FBXO10 depletion in cells stabilizes RAGE and is required for ODN2006-mediated degradation.

26 s pathway is mediated through a complex with RAGE and LAIR-1 and depends on relative levels of C1q an

27 of the tick Haemaphysalis longicornis binds RAGE and modulates the host immune response.

28 ls specifically through interaction with the RAGE and P2Y1 receptors, thereby eliciting intracellular

29 smitted via a receptor-mediated process with RAGE and suggest that oral OT supplementation may be adv

30 ion, we found that HMGB1 induced EMT through RAGE and the PI3K/AKT/GSK3beta/beta-catenin signaling pa

31 In the brain, levels of RAGE and Toll-like receptor 4, glial fibrillary acidic p

32 eceptor for advanced glycation end products (RAGE) and induces production of type I interferons (IFNs

33 receptor for advanced glycation endproducts (RAGE) and one of its primary ligands, high-mobility grou

34 eceptor for advanced glycation end products (RAGE) and Toll-like receptor 2, leading to local deliver

35 eceptor for advanced glycation end products (RAGE) and Toll-like receptor-9 (TLR9).

36 ohistochemistry of the AGE and AGE receptor (RAGE), and gene expression of tumor necrosis factor-alph

37 myeloperoxidase activity, gene expression of RAGE, and markers associated with tissue repair and home

38 ellular domains of the receptors TLR2, TLR4, RAGE, and P2Y1 as competitive inhibitors, we demonstrate

39 ld suggest that a synergistic combination of RAGE antagonism and antioxidants may offer the greatest

40 We injected elastase intratracheally and the RAGE antagonist FPS-ZM1 in mice, and the infiltrated inf

41 Our results suggest that longistatin is a RAGE antagonist that suppresses tick bite-associated inf

42 Of note, intracerebral injection of RAGE antibody into the hippocampus at days 15, 17, and 1

43 highlights that HMGB1 and its main receptor, RAGE, appear to be crucial factors in the pathogenesis o

44 eceptor for advanced glycation end-products (RAGE) are associated with an increased incidence of asth

45 receptor for advanced glycation endproducts (RAGE) are risk factors for asthma development.

46 Overall, our results highlight RAGE as a candidate biomarker for TNBCs, and they reveal

47 eceptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammati

48 T cells from B6-MRL Fas lpr/j mice expressed RAGE at their surface.

49 dies on the pathophysiologic implications of RAGE axis in the mechanisms leading to edema resolution.

50 The involvement of the HMGB1-RAGE axis in the pathogenesis of inflammatory cardiomyop

51 therapeutic strategies that focus on the AGE-RAGE axis to prevent vascular complications in patients

52 ion was related to the inhibition of the AGE-RAGE axis to resume cell-matrix interactions and maintai

53 ng cellular viability and inhibiting the AGE-RAGE axis.

54 RAGE binds and mediates the cellular response to a range

55 receptor for advanced glycation endproducts (RAGE) binds diverse ligands linked to chronic inflammati

56 CaCl2-induced model revealed that HMGB1 and RAGE, both localized mainly to macrophages, were persist

57 Mechanistic investigations revealed that RAGE bound to the proinflammatory ligand S100A7 and medi

58 deposition, and expressions of TNF-alpha and RAGE but elevated the periostin level in all three phase

59 ibited S100B-induced NF-kappaB activation in RAGE(-/-), but not in WT cells.

60 of receptor for advanced glycation products (RAGE), but not that of Toll-like receptor (TLR) 2 or TLR

61 Here we tested the role of targeting RAGE by multiple approaches in the tumor and tumor micro

62 RAGE can also act as an innate immune sensor of microbia

63 y, and that the increasing incidence of "air rage" can be understood through the lens of inequality.

64 Accordingly, loss of RAGE causatively linked to perpetual DSBs signaling, cel

65 d inflammatory function were elevated in the RAGE(+) CD8(+) cells of T1D patients and at-risk relativ

66 t serve as unique molecular inputs directing RAGE cellular concentrations and downstream responses, w

67 ed emphysema development and progression via RAGE-DAMP signaling.

68 RAGE deficiency had no effect on genetic forms of obesit

69 Here, we show that RAGE deficiency impairs anti-viral immunity during an ea

70 ions of RAGE in breast cancer, we found that RAGE-deficient mice displayed a reduced propensity for b

71 methylated CpG DNA, promotes rapid lysosomal RAGE degradation through activation of protein kinase Cz

72 PKCzeta overexpression enhances RAGE degradation, while PKCzeta knockdown stabilizes RAG

73 However, RAGE deletion did not completely prevent inflammation or

74 e RAGE or inhibitors of MAPK or PI3K blocked RAGE-dependent cell migration but did not affect RAGE sp

75 ore emerge as a novel therapeutic target for RAGE-dependent disease states.

76 These findings demonstrate the role for RAGE-dependent IL-10 suppression as a key modulator of m

77 sRAGE levels could be a useful biomarker for RAGE-dependent inflammation in patients with CF.

78 dult mice, plasma OT was also increased in a RAGE-dependent manner after oral delivery or direct admi

79 peripheral inflammation and weight gain in a RAGE-dependent manner, providing a foothold in the pathw

80 ls of HDL were reduced in diabetic mice in a RAGE-dependent manner.

81 h exhibit in vitro and in vivo inhibition of RAGE-dependent molecular processes, present attractive m

82 results demonstrate a prominent role for the RAGE-dependent neuroinflammatory pathway in the synaptic

83 ic plaques of Ldlr(-/-) mice devoid of Ager (RAGE) displayed higher levels of Abca1, Abcg1, and Pparg

84 bserved diffraction data just as well as the RAGE-DNA complexes presented by the authors.

85 In contrast to the lung, the absence of RAGE does not affect IL-33-induced ILC2 influx in the sp

86 ol efflux and probed the mechanisms by which RAGE downregulates ABCA1 and ABCG1.

87 These data demonstrate that RAGE drives tumor progression and metastasis through dis

88 RAGE ectopic overexpression in breast cancer cells incre

89 monary fibrosis (RAGE-/-), reconstitution of RAGE efficiently restored DSB-repair and reversed pathol

90 Here we show that RAGE exhibits an extended life span in lung epithelia (t

91 ophil extracellular traps (NETs) mediated by RAGE, exposing additional HMGB1 on their extracellular D

92 These findings imply that RAGE expression enhances the inflammatory function of T

93 previously found constitutive intracellular RAGE expression in lymphocytes from patients with T1D.

94 his article, we show that there is increased RAGE expression in T cells from at-risk euglycemic relat

95 In this study, we report that RAGE expression is upregulated widely in aggressive trip

96 vide evidence of persistent microglial HMGB1-RAGE expression that increases vulnerability to depressi

97 At 48 h after stroke, S100B and RAGE expression was increased in stroke-affected cortex

98 cortical emotional networks (labeled SEEING, RAGE, FEAR, LUST, CARE, PANIC, and PLAY systems) that ev

99 We finally demonstrated that RAGE function is dependent on secretase activity as ADAM

100 During infection, RAGE functions to either exacerbate disease severity or

101 ulmonary parenchymal, but not hematopoietic, RAGE has a central role in promoting AAI.

102 e receptor for advanced glycan end products (RAGE) has been identified as a susceptibility gene for c

103 eceptor for advanced glycation end-products (RAGE; ie, its receptor), are involved in fibrocyte traff

104 performed on oblique coronal T2W and T1W MP-RAGE images respectively.

105 We first tested how RAGE impacts tumor cell-intrinsic mechanisms using eithe

106 nd animal models has revealed that targeting RAGE impairs inflammation and progression of diabetic va

107 Absence of RAGE impedes pulmonary accumulation of ILC2s in models o

108 We conclude that the deletion of RAGE in B6-MRL Fas lpr/j mice promotes the accumulation

109 also significantly increases the odds of air rage in both economy and first class.

110 To test the combined inhibition of RAGE in both tumor cell-intrinsic and non-tumor cells of

111 n evaluating the functional contributions of RAGE in breast cancer, we found that RAGE-deficient mice

112 The upregulated expression of S100A9 and RAGE in fibrocytes of patients in the Asthma AE group an

113 Expression of CCR7, CXCR4, S100A9, and RAGE in fibrocytes was measured by using flow cytometry.

114 The clinical relevance of RAGE in inflammatory disease is being demonstrated in em

115 The expression of membrane RAGE in initiating the inflammatory response and of solu

116 These studies suggest that expression of RAGE in T cells of subjects progressing to disease preda

117 We generated mice invalidated for RAGE in the lupus-prone B6-MRL Fas lpr/j background to d

118 as lpr/j background to determine the role of RAGE in the pathogenesis of systemic lupus erythematosus

119 eceptor for advanced glycation end products (RAGE) in neuroinflammation, neurodegeneration-associated

120 eceptor for advanced glycation end products (RAGE) in the development of phenotypes associated with h

121 s cabin-is associated with more frequent air rage incidents in economy class.

122 We use a complete set of all onboard air rage incidents over several years from a large, internat

123 th and injected hBD-MSCs in PIRI-CLI through RAGE increase.

124 tion studies of the extracellular domains of RAGE indicate that RAGE ligands bind by distinct charge-

125 linically relevant models of necrosis, HMGB1/RAGE-induced neutrophil recruitment mediated subsequent

126 o determine the molecular mechanism by which RAGE influences COPD in experimental COPD models, we inv

127 s, our data indicate for the first time that RAGE inhibition has an essential protective role in COPD

128 Our observation of RAGE inhibition provided novel insight into its potentia

129 ging clinical trials of novel small-molecule RAGE inhibitors.

130 igand binding at the extracellular domain of RAGE initiates a complex intracellular signaling cascade

131 tion end products, AGER (previously known as RAGE), interfered with polarization of macrophages to a

132 er-202)) levels; and RAGE, RAGE ligands, and RAGE intracellular signaling.

133 RAGE is a multifunctional receptor implicated in diverse

134 These results indicate that brain RAGE is an essential factor in the pathogenesis of neuro

135 Here we observed that ectodomain shedding of RAGE is critical for its role in regulating signaling an

136 gether, our data suggest that proteolysis of RAGE is critical to mediate signaling and cell function

137 The cytoplasmic tail (ct) of RAGE is essential for RAGE ligand-mediated signal transd

138 RAGE is expressed at low levels under normal physiology,

139 RAGE is highly expressed in the lung and has been report

140 RAGE is highly expressed on immune cells, including macr

141 However, less is known about how RAGE is involved in the pathogenesis of COPD.

142 RAGE is mainly involved in tissue damage and chronic inf

143 sought to test the hypothesis that pulmonary RAGE is necessary for allergen-induced ILC2 accumulation

144 RAGE is phosphorylated at Serine376 and Serine389 by the

145 We found that RAGE is present in the mitochondria of cultured tumor ce

146 We identify that RAGE is targeted by the ubiquitin E3 ligase subunit F-bo

147 eceptor for advanced glycation end products (RAGE) is a highly expressed cell membrane receptor servi

148 eceptor for advanced glycation end-products (RAGE) is a multiligand pattern recognition receptor impl

149 eceptor for advanced glycation end products (RAGE) is a multiligand transmembrane receptor that can u

150 eceptor for advanced glycation end products (RAGE) is a pattern recognition receptor capable of recog

151 eceptor for advanced glycation end products (RAGE) is a pattern recognition receptor that interacts w

152 receptor for advanced glycation endproducts (RAGE) is a scavenger receptor of the Ig family that bind

153 receptor for advanced glycation endproducts (RAGE) is an ubiquitous, transmembrane, immunoglobulin-li

154 eceptor for advanced glycation end products (RAGE) is highly expressed in human and murine diabetic a

155 eceptor for advanced glycation end products (RAGE) is highly expressed in various cancers and is corr

156 eceptor for advanced glycation end-products (RAGE) is suggested to play a crucial role in mediating c

157 r apoptosis with concomitant upregulation of RAGE itself.

158 RAGE knockdown with multiple independent shRNAs in breas

159 Furthermore, RAGE knockout (RAGE-ko) mice immunized with TnI showed n

160 AAI was induced in wild-type and RAGE knockout mice by using IL-33, house dust mite extra

161 ause anhedonic behavior and by evidence that RAGE knockout mice were resilient to stress-induced anhe

162 ceptors for Advanced Glycation End Products (RAGE) knockout mice after postnatal day 3, an identical

163 njected breast cancer cells in wild-type and RAGE-knockout C57BL6 mice.

164 RAGE-knockout mice displayed striking impairment of tumo

165 ed inflammation in the hearts of both wt and RAGE-ko mice.

166 Furthermore, RAGE knockout (RAGE-ko) mice immunized with TnI showed no structural or

167 ntroduction of the dominant-negative form of RAGE lacking RAGE signalling targeted to microglia (DNMS

168 d increased tissue oxidative stress and AGEs-RAGE levels in pulmonary and renal endothelial cells.

169 tissue oxidative stress levels, and AGEs and RAGE levels in pulmonary and renal endothelial cells.

170 ive stress levels, endothelial cell AGEs and RAGE levels, pulmonary and renal cell apoptosis, and the

171 inked to increased endothelial cell AGEs and RAGE levels.

172 resistant to ectodomain shedding, inhibited RAGE ligand dependent cell signaling, actin cytoskeleton

173 Detectable levels of the RAGE ligand high mobility group box 1 were present in se

174 that high-fat feeding induced expression of RAGE ligand HMGB1 and carboxymethyllysine-advanced glyca

175 The RAGE ligand ODN2006, a synthetic oligodeoxynucleotide re

176 We found that blockade of RAGE ligand signaling with soluble RAGE or inhibitors of

177 DAM10 and gamma-secretase inhibitors blocked RAGE ligand-mediated cell migration.

178 toplasmic tail (ct) of RAGE is essential for RAGE ligand-mediated signal transduction and consequent

179 , concomitant with a progressive increase in RAGE ligands (S100B, N-[carboxymethyl]lysine, HSP70, and

180 naling receptor, sRAGE acts as a "decoy" for RAGE ligands and prevents their interaction with the rec

181 extracellular domains of RAGE indicate that RAGE ligands bind by distinct charge- and hydrophobicity

182 Importantly, tick bite upregulated RAGE ligands in skin, and endogenous longistatin attenua

183 In vitro, RAGE ligands suppressed ABCG1 and ABCA1 promoter lucifer

184 c acetate) and endogenous stimuli (serum and RAGE ligands).

185 lated Tau (p-Tau(Ser-202)) levels; and RAGE, RAGE ligands, and RAGE intracellular signaling.

186 Similar to other RAGE ligands, longistatin specifically bound the RAGE V

187 disorder associated with the accumulation of RAGE ligands.

188 ation because of the accumulation of various RAGE ligands.

189 This review describes the role of endogenous RAGE ligands/effectors in normo- and pathophysiological

190 prepared rapid acquisition gradient-echo (MP-RAGE) magnetic resonance imaging volumes were analyzed i

191 Antagonism of RAGE may fill an important therapeutic gap in the treatm

192 for the development of therapeutics against RAGE-mediated diseases, such as those linked to diabetic

193 skin, and endogenous longistatin attenuated RAGE-mediated inflammation during tick feeding.

194 Recombinant longistatin inhibited RAGE-mediated migration of mouse peritoneal resident cel

195 This study introduces the HMGB1-RAGE-mediated pathway as a key mechanism explaining the

196 eceptor for advanced glycation end products (RAGE) mediates immune cell activation at inflammatory si

197 tudy demonstrates that a parenchymal factor, RAGE, mediates lung-specific accumulation of ILC2s.

198 e that results from a persistent increase in RAGE messenger RNA expression.

199 eceptor for advanced glycation end products (RAGE) messenger RNA, but not toll-like receptor 4 in hip

200 significantly increased in B6-MRL Fas lpr/j RAGE(-/-) mice compared with B6-MRL Fas lpr/j mice (resp

201 ve T cells in the spleen of B6-MRL Fas lpr/j-RAGE(-/-) mice exhibited a delay in apoptosis and expres

202 The increased survival of RAGE(-/-) mice is associated with increased circulating

203 Neutralization of IL-10 in RAGE(-/-) mice results in decreased survival during syst

204 In contrast, RAGE(-/-) mice systemically infected with A. baumannii e

205 s involved in ubiquitin-mediated disposal of RAGE might serve as unique molecular inputs directing RA

206 eceptor for advanced glycation end products (RAGE), myeloid differentiation primary response gene-88,

207 astasis, systemic blockade by injection of a RAGE neutralizing antibody inhibited metastasis developm

208 (mS100a7a15 mice), administration of either RAGE neutralizing antibody or soluble RAGE was sufficien

209 ces in detection of cancer cells with linear rage of 1x10(1) to 1x10(6) cellsmL(-1) exhibiting low de

210 perimental metastasis, ectopic expression of RAGE on human prostate cancer cells was sufficient to pr

211 PR3 bound to RAGE on the surface of prostate cancer cells in vitro, i

212 eceptor for advanced glycation end products (RAGE) on hepatic Kupffer cells, resulting in increased p

213 eceptor for advanced glycation end products (RAGE) on Kupffer cells, ultimately leading to increased

214 ect of HMGB1 is not necessarily dependent on RAGE only.

215 Lack of RAGE or inhibition of HMGB1 release diminished ATP produ

216 ockade of RAGE ligand signaling with soluble RAGE or inhibitors of MAPK or PI3K blocked RAGE-dependen

217 inding was dramatically inhibited by soluble RAGE or RAGE siRNA.

218 Hematopoietic deficiency of RAGE or treatment with soluble RAGE partially protected

219 armacological blockade of S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induced fibroblast activ

220 Debates have raged over many years with regard to whether to correct

221 tumor cell-intrinsic mechanisms using either RAGE overexpression or knockdown with short hairpin RNAs

222 significantly downregulated TLR2 (P <0.05), RAGE (P <0.01), and TNF-alpha (P <0.05) relative to the

223 educed (P <0.05), with significantly reduced RAGE (P <0.05) and significantly elevated fibronectin an

224 eceptor for advanced glycation end products (RAGE), p-ERK1/2, nuclear NF-kappaB p65, and proinflammat

225 deficiency of RAGE or treatment with soluble RAGE partially protected against peripheral HFD-induced

226 al injury by reducing activation of the AGEs-RAGE pathway in endothelial cells in both organs.

227 ould be abrogated by inhibition of the HMGB1-RAGE pathway or direct cytokine neutralization.

228 findings link, for the first time, the HMGB1-RAGE pathway with changes in bioenergetics.

229 receptor for advanced glycation endproducts (RAGE) pathway and showed that RAGE activation induced ch

230 ation end products (AGEs) receptor for AGEs (RAGE) pathway, and (3) enalapril (which has antioxidant

231 of tumor necrosis factor-alpha (TNF-alpha), RAGE, periostin, fibronectin, and type I collagen.

232 Because RAGE plays a role in many pathological disorders, it has

233 In this study, we establish that RAGE-PR3 interaction mediates homing of prostate cancer

234 Our findings demonstrate how RAGE-PR3 interactions between human prostate cancer cell

235 eceptor for advanced glycation end products [RAGE]) present on vascular and innate immune cells.

236 Genetic deficiency of RAGE prevented the effects of HFD on energy expenditure,

237 eceptor for advanced glycation end-products (RAGE) promotes uptake of DNA into endosomes and lowers t

238 radation, while PKCzeta knockdown stabilizes RAGE protein levels and prevents ODN2006-mediated degrad

239 CUS also increased surface expression of RAGE protein on hippocampal microglia as determined by f

240 olid density gold foils was modeled with the RAGE radiation-hydrodynamics code, and the average surfa

241 Ectopic expression of the splice variant of RAGE (RAGE splice variant 4), which is resistant to ecto

242 sphorylated Tau (p-Tau(Ser-202)) levels; and RAGE, RAGE ligands, and RAGE intracellular signaling.

243 dying or stressed cells, HMGB1 binds to the RAGE receptor and activates the p42/44 MAP kinase (MAPK)

244 ulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end products) are

245 rmational alterations and protein binding to RAGE receptors were assessed by Congo red binding assay

246 ouse model of idiopathic pulmonary fibrosis (RAGE-/-), reconstitution of RAGE efficiently restored DS

247 This suggests that RAGE rescues the apoptosis of T lymphocytes when the dea

248 eceptor for advanced glycation end-products (RAGE) revealed the involvement of alarmins in inflammato

249 RAGE's lung-specific role in type 2 responses was explor

250 In this model, we found that RAGE/S100A7 conditioned the tumor microenvironment by dr

251 TNBCs, and they reveal a functional role for RAGE/S100A7 signaling in linking inflammation to aggress

252 t of Toll-like receptor (TLR) 2 or TLR4, and RAGE shRNA inhibited HMGB1-induced EMT in human airway e

253 In vivo, targeting RAGE shRNA knockdown in human and mouse breast cancer ce

254 In murine models of A. baumannii pneumonia, RAGE signaling alters neither inflammation nor bacterial

255 reperfusion (IR) injury, and the blockade of RAGE signaling has been considered as a potential therap

256 Blocking RAGE signaling in cell and animal models has revealed th

257 The role of RAGE signaling in response to opportunistic bacterial in

258 RAGE signaling requires interaction of ctRAGE with the i

259 Furthermore, HMGB1-RAGE signaling resulted in functional exhaustion of matu

260 f the dominant-negative form of RAGE lacking RAGE signalling targeted to microglia (DNMSR) in mhAPP m

261 eceptor for advanced glycation end products (RAGE) signals.

262 of ventricular tachycardia was abolished by RAGE silencing.

263 nduced upregulation of RAGE, siRNA targeting RAGE (siRAGE) was delivered to myocardium by using deoxy

264 as dramatically inhibited by soluble RAGE or RAGE siRNA.

265 To inhibit the IR-induced upregulation of RAGE, siRNA targeting RAGE (siRAGE) was delivered to myo

266 models, we investigated the efficacy of the RAGE-specific antagonist FPS-ZM1 administration in in vi

267 -dependent cell migration but did not affect RAGE splice variant 4 cell migration.

268 ic expression of the splice variant of RAGE (RAGE splice variant 4), which is resistant to ectodomain

269 creased local and systemic HMGB1 and soluble RAGE (sRAGE) expression.

270 because inhibition of HMGB1 and ablation of RAGE suppressed inflammation in the heart.

271 Here, we tested the hypothesis that RAGE suppresses effective axonal regeneration in superim

272 We tested the hypothesis that RAGE suppresses macrophage cholesterol efflux and probed

273 We further found that RAGE suppression led to the activation of Wnt signaling,

274 dy, we primarily investigated the effects of RAGE suppression particularly on IR-induced ventricular

275 short-term stress was sufficient to increase RAGE surface expression as well as anhedonic behavior, r

276 alarmin HMGB1 via CD24 and presenting it to RAGE(+) T cells.

277 Transcriptome analysis of RAGE(+) versus RAGE(-) T cells from patients with T1D showed difference

278 age-matched healthy controls received an MP-RAGE T1-weighted MRI.

279 rexpression of the dominant-negative form of RAGE targeted to microglia (DNMSR) protects against OGD-

280 sphate-deoxyribose backbone is recognized by RAGE through well-defined interactions.

281 NLCs can be prevented by blocking the HMGB1-RAGE-TLR9 pathway.

282 .Increased retinal immunoreactivity of GFAP, RAGE, TNF-alpha, VEGF and 5-LO was seen in diabetic anim

283 protein O10 (FBXO10), which associates with RAGE to mediate its ubiquitination and degradation.

284 eceptor for advanced glycation end products (RAGE) to reverse apoptosis-induced tolerance.

285 ced glycation end product-specific receptor (RAGE), trigger various intracellular events, such as oxi

286 Epithelial HMGB1, through its receptor RAGE, triggered recruitment of neutrophils, but not macr

287 Persistent RAGE upregulation was noted in both the LD and HD groups

288 er cells, or inhibiting S100A8/A9 binding to RAGE (using paquinimod), all reduced diabetes-induced th

289 ligands, longistatin specifically bound the RAGE V domain, and stimulated cultured HUVECs adhered to

290 Transcriptome analysis of RAGE(+) versus RAGE(-) T cells from patients with T1D sh

291 eceptor for advanced glycation end products (RAGE) via nuclear factor erythroid-2-related-factor-2 (N

292 MP-RAGE volumes were segmented into 1015 regions of interes

293 lycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis a

294 RAGE was abundant in the intestinal epithelial cells in

295 Ectodomain shedding of both human and mouse RAGE was dependent on ADAM10 activity and induced with c

296 Cellular expression of RAGE was determined in protein, serum, and bronchoalveol

297 RAGE was found to drive AAI by promoting IL-33 expressio

298 either RAGE neutralizing antibody or soluble RAGE was sufficient to inhibit tumor progression and met

299 MGB1 downstream signaling, particularly with RAGE, was studied in various transgenic animal models an

300 the non-tumor cell microenvironment role of RAGE, we performed syngeneic studies with orthotopically