ライフサイエンスコーパス: PAR-2

1 onists of the protease-activated receptor-2 (PAR-2).

2 eases, termed protease-activated receptor-2 (PAR-2).

3 st cells, and protease-activated receptor 2 (PAR-2).

4 aling through protease-activated receptor-2 (PAR-2).

5 cond pathway depends on the polarity protein PAR-2.

6 receptor agonist peptides to both PAR-1 and PAR-2.

7 n of protease-activated receptor (PAR)-1 and PAR-2.

8 antly with a worm-specific polarity protein, PAR-2.

9 BEAS-2B cells with small interfering RNA for PAR-2.

10 duction by papain was partially dependent on PAR-2.

11 relationship between synovial mast cells and PAR-2.

12 proteinase-activated receptor (PAR) subtype PAR-2.

13 relationship between synovial mast cells and PAR-2.

14 ility has not been addressed with respect to PAR-2.

15 fumigatus activates heterologously-expressed PAR-2.

16 Protease-activated receptor-2 (PAR-2), a Galpha(q/11)-coupled receptor, which has been

17 Protease-activated receptor 2 (PAR-2), a receptor for tryptase, was expressed on RASFs

18 The RING finger protein PAR-2 accumulates in a complementary pattern in the post

19 Stimulation of PAR-2 activates Nf-kappaB signaling, resulting in RelA n

20 firm whether EA attenuates VH through spinal PAR-2 activation and CGRP release, goats received an inj

21 PAR-2 activation augments inflammatory and profibrotic p

22 riptase was a potent activator of PAR-2, and PAR-2 activation by matriptase caused robust induction o

23 m plethysmography, we studied the effects of PAR-2 activation in human blood vessels and investigated

24 Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI-H5

25 uman stellate cells, indicating that hepatic PAR-2 activation increases profibrogenic cytokines and c

26 PAR-2 activation induces G protein-alpha-mediated signal

27 Per a 10 leads to PAR-2 activation on BMDCs resulting in downstream activa

28 e data support a model wherein KLK5-mediated PAR-2 activation regulates the expression of inflammatio

29 Our findings demonstrate the capacity of PAR-2 activation to augment TGFbeta production and promo

30 thogenesis of inflammatory arthritis through PAR-2 activation via release of mast cell tryptase.

31 PAR-2 activation was blocked in murine model by administ

32 tripping-induced barrier abrogation provokes PAR-2 activation, as shown by receptor internalization (

33 We show that, in response to PAR-2 activation, beta-arrestins scaffold cofilin with i

34 ing mast cells induced synovial hyperemia by PAR-2 activation.

35 Trypsin and the PAR-2 agonist (PAR2-AP) activated PAR-2 in an in vitro f

36 ining hemagglutinin and neuraminidase with a PAR-2 agonist peptide (PAR-2AP) in an intranasal prime b

37 Thirdly, topical applications of PAR-2 agonist peptide, SLIGRL, delay permeability barrie

38 ibitor, but this inhibition is overcome by a PAR-2 agonist peptide.

39 Intradermal (i.d.) injection of the PAR-2 agonist SLIGRL-NH(2) in the rostral back evoked bo

40 cular injection of ASKH95, a novel synthetic PAR-2 agonist, induced prolonged joint swelling and syno

41 PAR-1 binding sites, but not SLIGRL-amide, a PAR-2 agonist.

42 11 agonist BAM8-22, but not chloroquine or a PAR-2 agonist.

43 -1 agonist; 0.05 to 15 nmol/min) and SLIGKV (PAR-2 agonist; 1.6 to 160 nmol/min) infusions.

44 PAR-2 agonists showed potent proinflammatory effects as

45 sponded to apically or basolaterally applied PAR-2 agonists.

46 BSM cell proliferation and migration through PAR-2-, AKT-, ERK-, and p38-dependent mechanisms.

47 -1 (PAR-1) or protease activated receptor-2 (PAR-2) alone did not affect inflammation or survival.

48 e blocking anti-PAR-1 antibody, whereas anti-PAR-2 and -PAR-3 antibodies were without effect.

49 ruited into a scaffolding complex containing PAR-2 and beta-arrestins.

50 Downregulation of spinal PAR-2 and CGRP levels by EA attenuates the ileitis and r

51 nsitized by peptide and protease ligands for PAR-2 and inhibited by a PAR-2 antagonistic peptide.

52 We find that PAR-2 and LGL-1 affect cortical myosin accumulation by d

53 CDC-42, and the posterior cortical proteins PAR-2 and LGL-1 on the posterior cortex.

54 y emerging evidence for an interplay between PAR-2 and membrane-anchored serine proteases, which may

55 Meanwhile, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics on the cortex.

56 ll migration through autocrine activation of PAR-2 and this correlates with constitutive localization

57 Our results revealed strong increase in PAR-2 and tryptase expression in the lungs of idiopathic

58 diate synovial proinflammatory responses via PAR-2 and whether degranulating mast cells induced synov

59 tors, influences whether fibroblasts express PAR-2 and, thus, would be responsive to protease signali

60 PAR-2(+/+) and PAR-2(-/-) C57BL/6J mice were used to inv

61 signaling via protease-activated receptor-2 (PAR-2), and promoted fibroblast activation, proliferatio

62 direct effects of matriptase are mediated by PAR-2, and a more detailed understanding of these mechan

63 recipitation studies showed that secretases, PAR-2, and CXCR1 colocalize and physically interact in a

64 d FVIIa, and specific antibodies against TF, PAR-2, and IL-8 inhibited TF-FVIIa-induced cell migratio

65 he pro-inflammatory mediators HMGB-1, MMP-9, PAR-2, and IL-8.

66 signaling pathways, Rgp acting on PAR-1 and PAR-2, and LPS on TLR2 and TLR4.

67 assays, matriptase was a potent activator of PAR-2, and PAR-2 activation by matriptase caused robust

68 Because it has been reported that PAR-1, PAR-2, and PAR-3 may also be involved in the processes o

69 atinocytes through the involvement of MMP-9, PAR-2, and the NF-kappaB pathway.

70 ion data confirmed that matriptase activates PAR-2, and we demonstrated that matriptase-dependent enh

71 ronectin and matrix metalloproteinase-2 in a PAR-2- and ERK1/2-dependent manner, suggesting that PAR-

72 re protected against hypoxia-induced PH, and PAR-2 antagonist application reversed established PH in

73 ssion and to determine the effect of a novel PAR-2 antagonist on synovial cytokine production, in ord

74 The novel PAR-2 antagonist, ENMD-1068, was added to primary cultur

75 rotease ligands for PAR-2 and inhibited by a PAR-2 antagonistic peptide.

76 PAR-2 antagonists have recently been developed and may r

77 Once on the cortex, PAR-2 antagonizes PAR-3-dependent recruitment of myosin,

78 us, fungal aspartate protease and eosinophil PAR-2 appear critical for the eosinophils' innate immune

79 When testisin and PAR-2 are co-expressed in HeLa cells, GPI-anchored testi

80 del that in wild-type embryos both PAR-3 and PAR-2 are essential for nuclear rotation in asymmetrical

81 In conclusion, PAR-1 and PAR-2 are involved in FXa-mediated intracellular Ca(2+)

82 esearch using PAR-2 knockout mice identified PAR-2 as a key mediator of chronic joint inflammation.

83 rrier homeostasis, and second, they identify PAR-2 as a novel signaling mechanism of permeability bar

84 These findings identify PAR-2 as a novel upstream regulator of proinflammatory c

85 The RING-finger protein PAR-2 becomes enriched on the posterior cortex and preve

86 correlates with constitutive localization of PAR-2, beta-arrestin-2, and activated ERK1/2 to pseudopo

87 e demonstrate that the previously identified PAR-2/beta-arrestin/ERK1/2 scaffolding complex is enrich

88 a 10-administered mice and was reduced upon PAR-2 blockage.

89 evels in mouse lungs, which was reduced upon PAR-2 blockage.

90 otease-activated receptor-4 (PAR-4), but not PAR-2, blocked the effects of MET-1.

91 PAR-2 blocking experiments provided evidence that elasta

92 Peptide agonist of PAR-2, but not PAR-1 activator, also induced hBD-2 in GE

93 pernatant and purified RgpB was mediated via PAR-2, but not via PAR-1, and that proteases play a role

94 es from carious teeth specifically activated PAR-2, but those from healthy teeth failed to do so.

95 can be maintained independently of LGL-1 and PAR-2 by a redundant pathway that includes the CDC-42 GA

96 Although activation of PAR-1 or PAR-2 by agonist peptides induced calcium mobilization,

97 or testisin and that proteolytic cleavage of PAR-2 by recombinant testisin activates downstream signa

98 ity and suggest that autocrine activation of PAR-2 by secreted proteases may contribute to the migrat

99 The cleavage of PAR-2 by testisin induces activation of the intracellula

100 Furthermore, the activation of PAR-2 by testisin results in the loss and internalizatio

101 PAR-2(+/+) and PAR-2(-/-) C57BL/6J mice were used to investigate the PA

102 Here we demonstrate that PAR-2 can increase PI3K activity through a Galphaq/Ca(2+

103 We hypothesized that PAR-2 can trigger specific responses by differential act

104 active-cells and expression-levels of spinal PAR-2, CGRP and c-Fos in the EA group were greater (P <

105 2, and distribution and expression-levels of PAR-2, CGRP and c-Fos on day 22.

106 Ocular tissue from diabetic patients shows PAR-2 colocalization with phosphorylated TF specifically

107 PAR-1 and PAR-2 colocalize at the posterior cortex of the embryo.

108 Second, thrombin transactivation of a PAR-1/PAR-2 complex resulted in increases in PAI-1 mRNA and pr

109 bin and factor Xa did not activate the PAR-1/PAR-2 complex.

110 band, the predicted molecular weight for the PAR-2 core protein.

111 ase-2 (COX-2), providing a mechanism whereby PAR-2 could modulate pulpal inflammation.

112 FXa inhibition and PAR-2 deficiency in nonhematopoietic cells attenuated sy

113 ombin signaling through PAR-1 and PAR-4 with PAR-2 deficiency reduced lipopolysaccharide-induced inte

114 osis in PAR-2 knockout mice, and showed that PAR-2 deficiency reduced the progression of liver fibros

115 ctions in a murine model of arthritis, since PAR-2-deficient mice exhibit strikingly reduced articula

116 oint swelling was substantially inhibited in PAR-2-deficient mice, being reduced by more than fourfol

117 pontaneously develop from the bone marrow of PAR-2-deficient mice, but can be stimulated to do so by

118 of the chronic inflammatory response in the PAR-2-deficient mice, our findings demonstrate a key rol

119 noblots of cell lysates with polyclonal anti-PAR-2 demonstrated a 44 kDa band, the predicted molecula

120 ) C57BL/6J mice were used to investigate the PAR-2 dependence of compound 48/80-induced synovial hype

121 een deleted (TF Delta CT mice) show enhanced PAR-2-dependent angiogenesis, in synergy with platelet-d

122 M cell proliferation and migration through a PAR-2-dependent mechanism.

123 zygote is initiated by redundant ECT-2- and PAR-2-dependent mechanisms that lower PAR-3 levels local

124 by the protease ligand VIIa, known to induce PAR-2-dependent phosphorylation of TF.

125 and ERK1/2-dependent manner, suggesting that PAR-2-dependent signaling contributes to vascular remode

126 cription of symmetry breaking, wherein local PAR-2-dependent weakening of the actin cortex, together

127 thrombin or a deficiency in either PAR-1 or PAR-2 did not affect interleukin-6 expression or mortali

128 rected cortical flows and a single posterior PAR-2 domain.

129 mes entirely usually establish two posterior PAR-2 domains, one at each pole.

130 genes, polarity defects are more apparent in par-2 early embryos than in par-1 or par-4, except for s

131 We also found that activated PAR-2 enhanced tumor angiogenesis through the release of

132 (b) PAR-2-evoked cofilin dephosphorylation requires both the

133 lel with C. elegans axis formation, in which PAR-2 excludes the anterior PAR complex from the posteri

134 In contrast, a less metastatic PAR-2 expressing breast cancer cell line does not exhibi

135 Mast cell proximity to PAR-2-expressing cells was investigated in RA synovium.

136 e aim of this study was to determine whether PAR-2 expression and activation were increased in dental

137 Here, we assess PAR-2 expression and function in OSCC cell lines and tis

138 his study was undertaken to examine synovial PAR-2 expression and to determine the effect of a novel

139 -derived growth factor (PDGF)-BB upregulated PAR-2 expression in PASMC.

140 We also silenced PAR-1 or PAR-2 expression in the 4T1 cells.

141 may explain the previous inconsistencies in PAR-2 expression observed on tissue fibroblasts.

142 Previous studies describing PAR-2 expression on fibroblasts have been conflicting.

143 In this report, we investigated in vitro PAR-2 expression on several fibroblast cell lines using

144 Attenuation of PAR-2 expression was also observed in smooth muscle cell

145 Consistent PAR-2 expression was detected in cultured fibroblasts, a

146 ulated receptor expression whereas increased PAR-2 expression was observed by the addition of fibrobl

147 PAR-2 expression, normally limited to endothelial cells

148 itis, neither of which exhibited significant PAR-2 expression.

149 Using a monoclonal antibody to human PAR-2, expression in RA synovium and cultured synovial f

150 Cells lacking PAR-2 failed to express PAI-1 in response to thrombin an

151 Selective ablation of PAR-2 from bone marrow-derived cells did not prevent mat

152 Importantly, genetic elimination of PAR-2 from mice completely prevented matriptase-induced

153 n results in the loss and internalization of PAR-2 from the cell surface.

154 ion of LGL-1 is sufficient to rescue loss of PAR-2 function.

155 kt-mTor proliferation/survival signaling and PAR-2-Galphai-NFkappaB inflammatory signaling.

156 Mice heterozygous for PAR-2 gene disruption showed an intermediate phenotype.

157 NA expression was significantly decreased in PAR-2 gene knockdown cells, whereas no change was detect

158 P = 0.024, respectively), and was blocked in PAR-2 gene knockdown cells.

159 eed, recent evidence suggests that targeting PAR-2 helps reduce joint swelling observed in animal mod

160 requires aPC-induced heterodimerization with PAR-2 (human podocytes) or PAR-1 (mouse podocytes).

161 transport the anterior PAR complex away from PAR-2 in a positive-feedback loop.

162 st a novel and previously overlooked role of PAR-2 in airway physiology, adding to our understanding

163 in and the PAR-2 agonist (PAR2-AP) activated PAR-2 in an in vitro functional assay.

164 ar cell types, demonstrating upregulation of PAR-2 in cells from an inflammatory background compared

165 overed that the activation of both PAR-1 and PAR-2 in endothelial cells pretreated with factor FX (FX

166 Further research examined the role of PAR-2 in human articular cell types, demonstrating upreg

167 ice, our findings demonstrate a key role for PAR-2 in mediating chronic inflammation, thereby identif

168 rize the emerging data regarding the role of PAR-2 in neuroinflammation and ischaemic injury and disc

169 he initiation/spread of the polarity protein PAR-2 in regions distant from microtubule organizing cen

170 Here we investigate the role of PAR-2 in the constitutive migration of a metastatic brea

171 Cortical PAR-2 in turn prevents PAR-3/PAR-6/PKC-3 from returning

172 Our study identified a novel role of PAR-2 in vascular remodeling in the lung.

173 The activation of PAR-2 in vitro was shown to increase the expression of t

174 there is no clinical evidence of a role for PAR-2 in vivo in humans, although recent studies utilizi

175 activation of protease-activated receptor 2 (PAR-2) in humans would mediate vasodilatation.

176 ds a detrimental role for PARs, particularly PAR-2, in arthritis.

177 ignaling responses through the activation of PAR-2 independent of EPCR mobilization.

178 nsistent with microarray analysis, activated PAR-2 induced TGF-A and VEGF-A gene expression.

179 nishing ILK by siRNA decreased the levels of PAR-2-induced p-AKT, HIFs-alpha, and TGF-alpha; our resu

180 -dependent scaffolding and suggest that many PAR-2-induced processes may be independent of Galpha(q/1

181 llagenolysis from OA cartilage is blocked by PAR-2 inhibition.

182 endent NMY-2 in the anterior cortex, whereas PAR-2 inhibits CDC-42-dependent NMY-2 in the posterior d

183 Here, we show that the N-terminal domain of PAR-2 is a substrate for testisin and that proteolytic c

184 PAR-2 is a target of the PKC-3 kinase and is excluded fr

185 PAR-2 is activated by proteases secreted by airway neutr

186 PAR-2 is activated via proteolytic cleavage by trypsin-l

187 We found that PAR-2 is expressed basolaterally, where it stimulates bo

188 Firstly, PAR-2 is expressed in the outer nucleated layers of the

189 osure to allergen-derived proteases and that PAR-2 is involved in the process.

190 PAR-2 is known to exert proinflammatory actions in a mur

191 mation, or trypsin secretion; in these cells PAR-2 is more uniformly distributed around the cell peri

192 PAR-2 is normally expressed basolaterally in differentia

193 The RING domain of PAR-2 is required to overcome inhibition by PKC-3 and st

194 We further demonstrate that PAR-2 is stored in mobilizable compartments in neutrophi

195 PAR-2 is widely expressed in cells of the gastrointestin

196 Protease-activated receptor-2 (PAR-2) is a G-protein-coupled receptor (GPCR) activated

197 Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune ce

198 Protease-activated receptor-2 (PAR-2) is activated by trypsin-like serine proteases and

199 Protease-activated receptor 2 (PAR-2) is expressed in various tissues, including lung,

200 The proteinase-activated receptor 2 (PAR-2) is important for skin pigmentation because activa

201 and inhibit LB secretion, while, conversely, PAR-2 knockout mice display accelerated barrier recovery

202 Initial research using PAR-2 knockout mice identified PAR-2 as a key mediator o

203 lopment of CCl(4) -induced liver fibrosis in PAR-2 knockout mice, and showed that PAR-2 deficiency re

204 One strong enhancer of par-1 and par-2 lethality, F25B5.2, corresponds to nop-1, a regula

205 d compared with non-inflammatory cells, with PAR-2 levels being further upregulated by pro-inflammato

206 is study, we investigate the interplay among PAR-2, LGL-1, myosin, the anterior PAR proteins and CDC-

207 several ASM mitogenic factors, including the PAR-2 ligands, mast cell tryptase, trypsin, tissue facto

208 By contrast, PAR-2 likely has separate roles in regulating cortical m

209 PAR-3 and PAR-2 localize LET-99 to a posterior cortical band throu

210 We show that PAR-2 localizes to the cortex nearest the sperm centroso

211 tase as a model, we show gluten-independent, PAR-2 mediated upregulation of inflammatory pathways in

212 ate a requirement for both beta-arrestins in PAR-2-mediated motility and suggest that autocrine activ

213 olving aberrant expression and activation of PAR-2-mediated pathways, characterizes younger patients

214 -treated mice and BMDCs indicating a role of PAR-2-mediated signalling.

215 results suggest that ILK is involved in the PAR-2-mediated TGF-alpha via an HIF-alpha-dependent path

216 ponse with methysergide unveiled an enhanced PAR-2-mediated vasodilatation to compound 48/80 in PAR-2

217 Our data suggest that PAR-2 mediates cutaneous pigmentation both through incre

218 Protease-activated receptor-2 (PAR-2) mediates pro-inflammatory signals in a number of

219 mediated vasodilatation to compound 48/80 in PAR-2(+/+) mice and ablated the vasoconstrictor response

220 administration resulted in vasodilatation in PAR-2(+/+) mice but not in PAR-2(-/-) mice, which showed

221 oint swelling and synovial vasodilatation in PAR-2(+/+) mice but not PAR-2(-/-) mice.

222 Furthermore, PAR-2(-/-) mice were protected against hypoxia-induced P

223 vasodilatation in PAR-2(+/+) mice but not in PAR-2(-/-) mice, which showed a vasoconstrictor response

224 al vasodilatation in PAR-2(+/+) mice but not PAR-2(-/-) mice.

225 and ablated the vasoconstrictor response in PAR-2(-/-) mice.

226 and 11 of them also increase lethality in a par-2 mutant.

227 n in NCI/ADR-Res ovarian tumor cells reduces PAR-2 N-terminal proteolytic cleavage.

228 ies, our data suggest that dual induction of PAR-2-NFkappaB inflammatory signaling and PI3K-Akt-mTor

229 st cells leads to the binding of tryptase to PAR-2 on RASFs and inhibits the apoptosis of RASFs via t

230 o overcome inhibition by PKC-3 and stabilize PAR-2 on the posterior cortex.

231 Our results reveal how PAR-1 and PAR-2 on tumor cells mediate crosstalk between coagulati

232 -1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhematopoietic cells.

233 nduced the migration on angiostatin, whereas PAR-2 or PAR-4 agonist peptides were without effect.

234 d remodeling, whereas it was associated with PAR-2 overexpression and higher alveolar tryptase (P </=

235 ence or absence of antibodies against PAR-1, PAR-2, PAR-3, or EPCR.

236 The asymmetry is dependent on PAR-2, PAR-5 and PAR-6.

237 e have analyzed the localization dynamics of PAR-2, PAR-6, MEX-5, MEX-6 and PIE-1 in wild-type and mu

238 Here we present evidence that PAR-2 participates in a feedback loop to stabilize polar

239 inhibitors, trypsin inhibitors, a scrambled PAR-2 peptide, and silencing of beta-arrestins with smal

240 y knockdown or pharmacological inhibition of PAR-2, PKC-alpha, Raf-1, or p44/42.

241 Tryptase stimulated HLF growth in a PAR-2/PKC-alpha/Raf-1/p44/42-dependent manner and potent

242 We hypothesized here that PAR-2 plays a central role in epidermal permeability bar

243 in order to investigate the hypothesis that PAR-2 plays a critical role in the pathogenesis of rheum

244 growing that protease-activated receptor-2 (PAR-2) plays a key role in epithelial inflammation.

245 pled receptor protease-activated receptor-2 (PAR-2) plays a key role in inflammation.

246 Altered PAR-2 polarization in disease-remodeled epithelia may en

247 polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium response

248 ilial loss and squamous metaplasia may alter PAR-2 polarization.

249 Some fibroblast lines expressed PAR-2 predominantly as an intracellular protein with dif

250 ns, whereas other fibroblast lines displayed PAR-2 primarily as a cell surface receptor.

251 At the cellular level, PAR-2 promotes activation of the actin filament-severing

252 (a) PAR-2 promotes beta-arrestin-dependent dephosphorylation

253 co-immunoprecipitation, we demonstrate that PAR-2 promotes the formation of a complex containing bet

254 d GEC, and this induction partially uses the PAR-2 receptor and signaling pathway.

255 studies, an activating peptide for the human PAR-2 receptor was synthesized and administered to healt

256 Activation of PAR-2 receptors in vivo dilated human blood vessels in a

257 Antagonism of PAR-1 and PAR-2 reduced FXa-induced Ca(2+) release.

258 Little is known, however, about PAR-2 regulation of inflammation-related microRNAs.

259 Thus, PAR-2 represents an important interface linking coagulat

260 ility of different protease agonists to bias PAR-2 signaling and the newly emerging evidence for an i

261 releases its negative regulatory control of PAR-2 signaling in angiogenesis.

262 was to investigate the pathological role of PAR-2 signaling in pancreatic cancer.

263 In conclusion, the activation of PAR-2 signaling induced human pancreatic cancer progress

264 e TF cytoplasmic domain negatively regulates PAR-2 signaling.

265 ntracellular presenilin-1 expression through PAR-2 signaling.

266 nesis through protease-activated receptor-2 (PAR-2) signaling.

267 PAR-2-specific antibodies fully attenuated TF-FVIIa-indu

268 In addition, PAR-2 stimulated activation, proliferation, collagen pro

269 dependent signaling scaffold is required for PAR-2-stimulated activation of extracellular signal regu

270 Inhibition of PI3K activity blocks PAR-2-stimulated chemotaxis, and beta-arrestin-1 colocal

271 this localized inhibition may be crucial for PAR-2-stimulated chemotaxis.

272 , and that this pathway may be important for PAR-2-stimulated immune cell migration.

273 negative fragment of beta-arrestin-1 reduces PAR-2-stimulated internalization, ERK1/2 activation, and

274 ort, we show that activation of keratinocyte PAR-2 stimulates release of PGE(2) and PGF(2alpha) and t

275 mentation because activation of keratinocyte PAR-2 stimulates uptake of melanosomes through phagocyto

276 pithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, incre

277 binates, exhibit apical calcium responses to PAR-2 stimulation.

278 miR-23b, and miR-200c was observed following PAR-2 stimulation.

279 res responded to both apical and basolateral PAR-2 stimulation.

280 -anchored testisin specifically releases the PAR-2 tethered ligand.

281 ctional network of elastase, secretases, and PAR-2 that regulate CXCR1 expression on neutrophils.

282 Furthermore, PAR-2, through integrin-linked kinase (ILK) signaling, i

283 Using immunohistochemistry, we showed PAR-2 to be localized to pulp cells subjacent to caries

284 matriptase activates keratinocyte stem cell PAR-2 to elicit its pro-inflammatory and pro-tumorigenic

285 rnaria-derived aspartate protease(s) cleaved PAR-2 to expose neo-ligands; these neo-ligands activated

286 ndent manner, and functions redundantly with PAR-2 to maintain polarity.

287 p was strongly suggested to cleave PAR-1 and PAR-2 to up-regulate CCR5.

288 Furthermore, the culture medium from PAR-2-treated pancreatic cancer cells enhanced human umb

289 We first demonstrated that activated PAR-2 up-regulated the protein expression of both hypoxi

290 d receptor, proteinase-activated receptor 2 (PAR-2), via cleavage and exposure of a tethered ligand.

291 Furthermore, we noted that expression of PAR-2 was subject to regulation.

292 PAR-2 was substantially up-regulated in RA synovium comp

293 to activate proteinase-activated receptor 2 (PAR-2) was determined using a synovial perfusion assay i

294 signal certain downstream responses through PAR-2, we assessed its potential role in mediating the n

295 cells and synovial lining cells staining for PAR-2 were colocalized in RA articular tissue.

296 4T1 cells expressed TF, PAR-1 and PAR-2 whereas 67NR cells expressed TF and PAR-1.

297 nase C, and proteinase-activated receptor-2 (PAR-2), which is consistent with the expression patterns

298 can activate protease-activated receptor 2 (PAR-2), which was recently shown to have proinflammatory

299 roles of one of four mammalian PARs, namely PAR-2, which is overexpressed in advanced stage tumors a

300 PAR-2, which localizes to the posterior cortex, inhibits