ライフサイエンスコーパス: RAGE

1 RAGE binds and mediates the cellular response to a range

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

3 RAGE ectopic overexpression in breast cancer cells incre

4 RAGE exists as a membrane glycoprotein with an ectodomai

5 RAGE is expressed at low levels under normal physiology,

6 RAGE is phosphorylated at Serine376 and Serine389 by the

7 RAGE knockdown with multiple independent shRNAs in breas

8 RAGE signaling requires interaction of ctRAGE with the i

9 RAGE was abundant in the intestinal epithelial cells in

10 RAGE(-/-) mice were protected against CS-induced neutrop

11 RAGE-knockout mice displayed striking impairment of tumo

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

13 A RAGE small-molecule antagonist was used to determine the

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

15 n A4, resolvin D1, and resolvin D2 through a RAGE- and LAIR-1-dependent pathway.

16 GB1 induces leukotriene production through a RAGE-dependent pathway, while HMGB1 plus C1q induces spe

17 In addition, treatment with a RAGE-specific antagonist diminished the effects of type

18 strategies aimed at targeting the S100A8/A9-RAGE (receptor for advanced glycation end products) axis

19 ed by geminin-overexpressing cells activates RAGE and CXCR4 expression on mesenchymal stem cells (MSC

20 In adults, RAGE expression is normally high only in the lung where

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

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

23 Associations between protein intake and AGE-RAGE biomarkers were examined using linear regression mo

24 Moreover, we newly report enrichment of AGE-RAGE signaling pathway in diabetic complications, IL-17

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

26 osure to AGEs in the liver promotes an AGER1/RAGE imbalance and consequent redox, inflammatory, and f

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

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

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

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

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

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

33 inked to increased endothelial cell AGEs and RAGE levels.

34 e inflammatory signaling molecules HMGB1 and RAGE, as well as the activated phosphorylated transcript

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

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

37 ch their effects are independent of P2Y1 and RAGE receptors.

38 we describe how ERs (estrogen receptors) and RAGE (receptor for advanced glycation end-products) play

39 of infection-mediated release of S100A11 and RAGE-dependent induction of CCL2, a crucial chemokine re

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

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

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

43 ave all been shown to activate both TLRs and RAGE to varying degrees in order to induce inflammation

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

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

46 Wild-type (WT) and RAGE knockout (RAGE(-/-)) mice, were intranasally admini

47 AAI/VCAM-1 expression in wild-type (WT) and RAGE-knockout (RAGE-KO) mice.

48 were extremely sensitive to anti-c-Abl, anti-RAGE, and anti-AXL drugs.

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

50 HDM, AA, or rIL-33 exposure was found to be RAGE-dependent.

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

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

53 wn that there is extensive crosstalk between RAGE and TLRs.

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

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

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

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

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

59 to be important in signal transduction, but RAGE oligomeric structures and stoichiometries remain un

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

61 tic Gq signaling pathways were unaffected by RAGE deletion or inhibition.

62 The three canonical RAGE ligands, Advanced Glycation End products (AGEs), HM

63 rum levels of total soluble RAGE and cleaved RAGE (cRAGE) were significantly lower in periodontitis p

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

65 mage-associated molecular patterns" (DAMPs), RAGE has been shown to recognize a broad collection of D

66 , we mapped regions involved in TM-dependent RAGE oligomerization.

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

68 In diseases, RAGE levels increase in the affected tissues and sustain

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

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

71 evels of inflammatory mediators-including EN-RAGE, TNFSF14, and oncostatin M-which correlated with di

72 he impact of smoking status on AGER (encodes RAGE) and TLR4 bronchial gene expression in patients wit

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

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

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

76 receptor for advanced glycation endproducts (RAGE) has been implicated as a critical molecule in the

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) is critically involved in the pathobiology of chro

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

81 receptor for advanced glycation endproducts (RAGE) plays a significant role in the pathogenesis of as

82 receptor for advanced glycation endproducts (RAGE) receptor to promote NF-kappaB- and IRF3-dependent

83 receptor for advanced glycation endproducts (RAGE).

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

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

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

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

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

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

90 CS exposure also was observed in the AM from RAGE null mice.

91 g of alveolar macrophages (AM) obtained from RAGE null and C57BL/6 WT mice exposed to CS for one week

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

93 The response of small hairpin RAGE-infected cells to human recombinant HMGB1 was blunt

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

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

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

97 onary artery smooth muscle cells in an HMGB1/RAGE-dependent manner.

98 /hresistin-induced macrophage-specific HMGB1/RAGE expression and facilitated HMGB1 nucleus-to-cytopla

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

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

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

102 DS and NS for extracellular newly identified RAGE binding protein and between CS and NS for MPO.

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

104 ce, which was nearly completely abrogated in RAGE(-/-) mice.

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

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

107 studied, there has been renewed interest in RAGE for its potential role in sepsis, along with a host

108 ability of obtained oligomerization modes in RAGE fragments.

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

110 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in enteric neurons,

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

112 clinical studies demonstrate that increased RAGE ligands and signaling strongly correlate with asthm

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

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

115 the effects of pharmacologically inhibiting RAGE on type 2 cytokine-induced effects.

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

117 n- and cytokine-induced VCAM-1 expression is RAGE-dependent and contributes to lung ILC2 accumulation

118 Wild-type (WT) and RAGE knockout (RAGE(-/-)) mice, were intranasally administered rIL-5/rI

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

120 ression in wild-type (WT) and RAGE-knockout (RAGE-KO) mice.

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

122 the oligomerization patterns of full-length RAGE (including the transmembrane (TM) and cytosolic reg

123 te the expression of cell-bound, full-length RAGE and its antagonist AGER1 locally, in gingival tissu

124 tis patients, gene expression of full-length RAGE and of AGER1 were significantly higher in periodont

125 ed oligomerization properties of full-length RAGE.

126 form a tetramolecular complex cross-linking RAGE and LAIR-1 and directing monocytes to an antiinflam

127 r mimic of HMGB1 plus C1q, which cross-links RAGE and LAIR-1 and polarizes monocytes to an antiinflam

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

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

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

131 rkers needed for early intervention and MMP9/RAGE pathway modulation may lead to promising drug targe

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

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

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

135 pt, we showed that treatment with the mutant RAGE peptide S391A-RAGE362-404 was able to inhibit trans

136 -33 induced VCAM-1 expression in WT, but not RAGE-KO cells.

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

138 hogenesis of COPD impacted by the absence of RAGE.

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

140 Blockade of RAGE ameliorates elastase-induced emphysema development

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

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

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

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

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

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

147 ligands or the ligand-binding ectodomain of RAGE.

148 RAGE, suggesting that the major effector of RAGE activation was its transactivation.

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

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

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

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

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

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

155 Soluble forms of RAGE have been proposed as biomarkers of severity in inf

156 e circulating levels of the soluble forms of RAGE in periodontitis and to evaluate the expression of

157 Soluble forms of RAGE, particularly cRAGE, may serve as biomarkers for th

158 We examined the impact of RAGE and/or TLR4 gene deficiency in a mouse model of COP

159 etic ablation or pharmacologic inhibition of RAGE blocks the effects of IL-13 and IL-4 by inhibiting

160 Inhibition of RAGE but not TLR4 signalling may protect against airway

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

162 that deletion or pharmacologic inhibition of RAGE prevents development of CS-induced emphysema.

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

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

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

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

167 xpression independently of the liberation of RAGE ligands or the ligand-binding ectodomain of RAGE.

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

169 s responsible for binding to the majority of RAGE ligands including advanced glycation end products (

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

171 cated versions of the extracellular parts of RAGE.

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 However, the role of RAGE in directly mediating type 2 cytokine signaling has

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

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

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

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

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

181 red transactivation of the cytosolic tail of RAGE and NF-kappaB-driven proinflammatory gene expressio

182 2-404 was able to inhibit transactivation of RAGE and attenuate Ang II-dependent inflammation and ath

183 an overview of the current understandings of RAGE in asthma pathogenesis, its role as a biomarker of

184 r apoptosis with concomitant upregulation of RAGE itself.

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

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

187 Inhibition of AGEs or RAGE deletion in hepatocytes in vivo reversed these effe

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

189 by nuclear over-expression of phosphomimetic RAGE reduces DNA damage, inflammation, and fibrosis, the

190 kinase Czeta (PKCzeta), which phosphorylates RAGE.

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

192 These data position RAGE transactivation by the AT1 receptor as a target for

193 receptor for advanced glycation end product (RAGE) to direct monocytes to a proinflammatory phenotype

194 ptor for advanced glycosylation end product (RAGE), exhibited decreased expression of both HMGB1 and

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

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

197 eceptor for advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4) is implicated in C

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

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

200 eceptor for advanced glycation end products (RAGE) is a critical molecule in the pathogenesis of expe

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

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

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

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

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

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

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) plays a key role in mammal physiology and in the e

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

212 eceptor for advanced glycation end products (RAGE), a cell membrane receptor, recognizes ligands prod

213 eceptor for Advanced Glycation End products (RAGE), has been extensively studied, there has been rene

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).

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) revealed the involvement of alarmins in inflammato

221 eceptor for advanced glycation end-products (RAGE) shedding into soluble and nuclear forms, and subse

222 eceptor for advanced glycation end-products (RAGE), and most cells were negative for alkaline phospha

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

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

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

226 eceptor for advanced glycation end products [RAGE], MPO, uteroglobin/CC-10); between groups of DS and

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 sponse to T. gondii by engaging its receptor RAGE, and regulated monocyte recruitment in vivo by indu

230 models, whereas the proinflammatory receptor RAGE was induced.

231 The pattern recognition receptor RAGE (receptor for advanced glycation end-products) tran

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

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

234 ing via antagonism of its putative receptor, RAGE, also decreases scar formation.

235 bition of hDia1, but not scavenger receptors RAGE or CD36, attenuated AGE-ECM inhibition of adipocyte

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

237 In concert, geminin-overexpression, S100A4/RAGE and Gas6/AXL signaling promote the invasive and int

238 and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine, a S10

239 o investigate the participation of the S100B/RAGE/NFkappaB pathway in intestinal mucositis and enteri

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

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

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

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

244 ients revealed an increase in plasma soluble RAGE relative to healthy controls.

245 Serum levels of total soluble RAGE and cleaved RAGE (cRAGE) were significantly lower i

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

247 More specifically, RAGE expressed on stromal cells, rather than hematopoiet

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

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

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

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

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

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

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

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

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

257 f this study was to test the hypothesis that RAGE mediates type 2 cytokine-induced signal transductio

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 This study is the first to indicate that RAGE is a critical component of type 2 cytokine signal t

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

262 Current experimental data indicates that RAGE is a critical mediator of the type 2 inflammatory r

263 We propose that RAGE is involved in modulating blood coagulation presuma

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

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

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

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

268 It has been previously shown that RAGE acts both upstream of interleukin-33 (IL-33) releas

269 lished evidence has led us to speculate that RAGE may be physically interacting with TLRs on the cell

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

271 The RAGE ligand ODN2006, a synthetic oligodeoxynucleotide re

272 nt oligomerization contact regions along the RAGE sequence.

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

274 g suggest attenuated oxidative stress in the RAGE null mice despite comparable CS exposure and lung l

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

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

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

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

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

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

281 TLR4(-/-) RAGE(-/-) mice were not protected against CS-induced neu

282 ld-type, RAGE(-/-) , TLR4(-/-) and TLR4(-/-) RAGE(-/-) mice following acute exposure to cigarette smo

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

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

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

286 al inhibitory/excitatory imbalance linked to RAGE shedding.

287 ed airway inflammation and AHR in wild-type, RAGE(-/-) , TLR4(-/-) and TLR4(-/-) RAGE(-/-) mice follo

288 ation because of the accumulation of various RAGE ligands.

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

290 is that ILC2s are recruited to the lungs via RAGE-dependent vascular cell adhesion molecule 1 (VCAM-1

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

292 release and downstream of IL-33 release via RAGE-dependent IL-33-induced accumulation of type 2 inna

293 hout restoring ligand-mediated signaling via RAGE, suggesting that the major effector of RAGE activat

294 AT1 receptor activation were attenuated when RAGE was deleted or transactivation of its cytosolic tai

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

296 However, the mechanism by which RAGE mediates downstream IL-33-induced type 2 inflammato

297 To identify molecular pathways by which RAGE mediates smoking related lung injury we performed u

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

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

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