ライフサイエンスコーパス: RAGE

1 RAGE and HMGB1 coordinately enhanced tumor cell mitochon

2 RAGE binds and mediates the cellular response to a range

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

4 RAGE deficiency had no effect on genetic forms of obesit

5 RAGE ectopic overexpression in breast cancer cells incre

6 RAGE is a multifunctional receptor implicated in diverse

7 RAGE is expressed at low levels under normal physiology,

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

9 RAGE is highly expressed on immune cells, including macr

10 RAGE is mainly involved in tissue damage and chronic inf

11 RAGE is phosphorylated at Serine376 and Serine389 by the

12 RAGE knockdown with multiple independent shRNAs in breas

13 RAGE signaling requires interaction of ctRAGE with the i

14 RAGE was abundant in the intestinal epithelial cells in

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

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

17 RAGE-knockout mice displayed striking impairment of tumo

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

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

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

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

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

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

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

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

26 mmunohistochemistry of the receptor for AGE (RAGE).

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

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

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

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

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

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

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

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

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

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

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

38 inked to increased endothelial cell AGEs and RAGE levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 of ventricular tachycardia was abolished by RAGE silencing.

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

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

65 through HMGB1-mediated engagement of T cell RAGE.

66 Soluble circulating RAGE (sRAGE) may counteract the detrimental effects of R

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

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

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

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

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

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

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

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

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

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

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

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

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

80 of recombinase-assisted genome engineering (RAGE).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 However, RAGE deletion did not completely prevent inflammation or

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 disorder associated with the accumulation of RAGE ligands.

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

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

137 Blockade of RAGE ameliorates elastase-induced emphysema development

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

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

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

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

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

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

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

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

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

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

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

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

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

151 E) may counteract the detrimental effects of RAGE.

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

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

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

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

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

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

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

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

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

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

162 nature of the RAGE ligand, and the impact of RAGE on lung inflammation and antimicrobial resistance i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 was ameliorated by functional suppression of RAGE.

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

181 mplant therapy, there was an upregulation of RAGE and TLR4 levels that coincided with a downregulatio

182 r apoptosis with concomitant upregulation of RAGE itself.

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

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

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

186 tro models to study the impact of hypoxia on RAGE expression and activity in human and murine CF, the

187 as dramatically inhibited by soluble RAGE or RAGE siRNA.

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

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

190 kinase Czeta (PKCzeta), which phosphorylates RAGE.

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

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

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

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

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

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

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

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

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

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

201 eceptor for advanced glycation end products (RAGE) is a pattern recognition receptor for many damage-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 eceptor for advanced glycation end products (RAGE).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 The RAGE ligand ODN2006, a synthetic oligodeoxynucleotide re

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

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

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

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

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

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

275 ty in human and murine CF, the nature of the RAGE ligand, and the impact of RAGE on lung inflammation

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

277 The binding of the RAGE-V1C1 domain to peanut allergens was assessed by PAG

278 ifferentiation of NPCs via activation of the RAGE/NF-kappaB axis.

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

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

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

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

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

284 were reduced in diabetic macrophages through RAGE.

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

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

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

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

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

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

291 ation because of the accumulation of various RAGE ligands.

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

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

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

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

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

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

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

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

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