ライフサイエンスコーパス: rage

1 receptor for advanced glycation endproducts (RAGE).

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

3 eceptor for advanced glycation end products (RAGE).

4 eceptor for advanced glycation end products (RAGE).

5 kinase Czeta (PKCzeta), which phosphorylates RAGE.

6 hogenesis of COPD impacted by the absence of RAGE.

7 ed oligomerization properties of full-length RAGE.

8 ligands or the ligand-binding ectodomain of RAGE.

9 cated versions of the extracellular parts of RAGE.

10 4-hour chest drainage (median, interquartile rage: 28.9, 12.6-150.0 vs 47.4, 15.2-145.0 ml/kg for DHC

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

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

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

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

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

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

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

22 Blockade of RAGE ameliorates elastase-induced emphysema development

23 2-404 was able to inhibit transactivation of RAGE and attenuate Ang II-dependent inflammation and ath

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 RAGE binds and mediates the cellular response to a range

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 ial world: when we see someone flying into a rage, does our brain automatically predict their social

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

90 RAGE ectopic overexpression in breast cancer cells incre

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

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

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

94 RAGE exists as a membrane glycoprotein with an ectodomai

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

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

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

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

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

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

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

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

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

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

105 ability of obtained oligomerization modes in RAGE fragments.

106 The proposed method provided a working rage from 0.36 to 5 mg L(-1) of Fe(II), with a detection

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 RAGE is expressed at low levels under normal physiology,

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

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

150 RAGE is phosphorylated at Serine376 and Serine389 by the

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

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

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

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

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

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

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

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

159 receptor for advanced glycation endproducts (RAGE) is critically involved in the pathobiology of chro

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

161 r apoptosis with concomitant upregulation of RAGE itself.

162 RAGE knockdown with multiple independent shRNAs in breas

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

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

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

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

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

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

169 RAGE-knockout mice displayed striking impairment of tumo

170 -33 induced VCAM-1 expression in WT, but not RAGE-KO cells.

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

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

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

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

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

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

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

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

179 inked to increased endothelial cell AGEs and RAGE levels.

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

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

182 The RAGE ligand ODN2006, a synthetic oligodeoxynucleotide re

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

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

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

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

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

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

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

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

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

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

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

194 ation because of the accumulation of various RAGE ligands.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 While debates have raged over the relationship between trance and rock art,

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

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

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

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

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

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

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

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

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

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

242 eceptor for advanced glycation end products (RAGE) plays a key role in mammal physiology and in the e

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

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

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

246 n of S100a9, S100a8, or its cognate receptor Rage prevented monocytosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 nt oligomerization contact regions along the RAGE sequence.

265 al inhibitory/excitatory imbalance linked to RAGE shedding.

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

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

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

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

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

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

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

273 RAGE signaling requires interaction of ctRAGE with the i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 RAGE was abundant in the intestinal epithelial cells in

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

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

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

299 models, whereas the proinflammatory receptor RAGE was induced.

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