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

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

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

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

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

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

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

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

10 relationship between synovial mast cells and PAR-2.

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

12 relationship between synovial mast cells and PAR-2.

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

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

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

16 eviously that protease-activated receptor-2 (PAR-2), a proinflammatory receptor that is highly expres

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 PAR-2 activation augments inflammatory and profibrotic p

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

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

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

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

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

26 We now show that PAR-2 activation promotes ERK1/2- and beta-arrestin-depe

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

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

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

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

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

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

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

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

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

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

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

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

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

40 11 agonist BAM8-22, but not chloroquine or a PAR-2 agonist.

41 -1 agonist; 0.05 to 15 nmol/min) and SLIGKV (PAR-2 agonist; 1.6 to 160 nmol/min) infusions.

42 PAR-2 agonists showed potent proinflammatory effects as

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

44 -1 (PAR-1) or protease activated receptor-2 (PAR-2) alone did not affect inflammation or survival.

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

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

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

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

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

50 arly embryo, that these phenotypes depend on par-2 and par-3 gene function, and that cdc-42 is requir

51 re required for the cortical localization of PAR-2 and PAR-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 PAR-1 and PAR-2 are down-regulated in acute inflammation whereas P

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

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

80 pressed in the urothelium, whereas PAR-1 and PAR-2 are predominant in the detrusor muscle, and PAR-4

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

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

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

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

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

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

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

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

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

90 PAR-2 blocking experiments provided evidence that elasta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 er, a combination of thrombin inhibition and PAR-2 deficiency reduced inflammation and mortality.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Our results demonstrate PAR-1 and PAR-2 expression in the tumor cells, mast cells, macroph

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

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

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

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

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

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

143 PAR-2 expression, normally limited to endothelial cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 Expression of PAR-2 in mouse distal colon was confirmed using RT-PCR a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 We conclude that functional basolateral PAR-2 is present in mouse distal colon and that its acti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 During this phase (maintenance), PAR-2 maintains anterior-posterior polarity by excluding

207 Proteinase-activated receptor-2 (PAR-2) may participate in epithelial ion transport regul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 lasts demonstrated the presence of PAR-1 and PAR-2 not detected in quiescent, SMA-negative cultures.

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

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

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

229 -1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhematopoietic cells.

230 ating peptide (mAP), a specific activator of PAR-2, on electrogenic transport of mouse distal colon u

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

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

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

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

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

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

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

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

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

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

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

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

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

244 strate that proteinase-activated receptor-2 (PAR-2) plays a pivotal role in mediating chronic inflamm

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

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

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

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

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

250 rotrimeric G protein signaling, and that the PAR-2 protein affects microtubule dynamics by restrictin

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

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

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

254 ly localized PAR proteins, such as PAR-1 and PAR-2, redistribute to the inner, basolateral surfaces.

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

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

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

258 beta-Arrestin-bound PAR-2 serves as a scaffold to sequester a pool of activa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 se acting via protease-activated receptor-2 (PAR-2) stimulates the development of DC from bone marrow

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

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

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

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

279 rby cortex, allowing the ring finger protein PAR-2 to accumulate in an expanding 'posterior' domain.

280 orces applied to MTs at each pole and allows PAR-2 to accumulate in the posterior cortex of a one-cel

281 es PAR-3 from the posterior cortex, allowing PAR-2 to accumulate there.

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

283 ate that LET-99 acts downstream of PAR-3 and PAR-2 to determine spindle positioning, potentially thro

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 symmetric cortical localization of PAR-1 and PAR-2 to the posterior, and PAR-3, PAR-6, and PKC-3 to t

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

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

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

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

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

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

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

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

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

297 4T1 cells expressed TF, PAR-1 and PAR-2 whereas 67NR cells expressed TF and PAR-1.

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

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

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