ライフサイエンスコーパス: PAR-1

1 activation of protease activated receptor-1 (PAR-1).

2 activation of protease-activated receptor 1 (PAR-1).

3 activation of protease-activated receptor-1 (PAR-1).

4 activation of protease-activated receptor-1 (PAR-1).

5 as potent platelet agonist that acts through PAR-1.

6 uced up-regulation of MMP-9 was mediated via PAR-1.

7 duced by activation of the thrombin receptor PAR-1.

8 depends on the polarity proteins Bazooka and Par-1.

9 e transport mechanism and phosphorylation by PAR-1.

10 s site can rescue the defects of kinase-dead PAR-1.

11 ar actions of thrombin through antagonism of PAR-1.

12 lets through the protease-activated receptor PAR-1.

13 terior inactivation of aPKC or activation of Par-1.

14 nd PAR-2 whereas 67NR cells expressed TF and PAR-1.

15 ing, which was abrogated after rescuing with PAR-1.

16 tivity, is a crucial molecular substrate for PAR-1.

17 sm for the regulation of Cx-43 expression by PAR-1.

18 ires the function of serine/threonine kinase Par-1.

19 oblasts induced by thrombin and mediated via PAR-1.

20 PAR-1 -506 ins/del (adjusted P value=0.011) and EGF +61

21 vorable alleles, high expression variants of PAR-1 -506 ins/del (any insertion allele) and EGF +61 A>

22 lial cells is protease-activated receptor-1 (PAR-1), a member of the G protein-coupled receptor super

23 NH(2)) of the protease-activated receptor-1 (PAR-1), a thrombin receptor expressed by vECs, neuronal

24 on of the Protorhabditis group and show that PAR-1, a kinase localized asymmetrically in C. elegans e

25 Here, we show that Par-1, a serine/threonine kinase that regulates polarity

26 ce knockdown of tao, suggesting that tao and par-1 act in a pathway to control microtubule dynamics d

27 strates that both the type I collagenase and PAR-1 activating functions of MMP-1 are required for mel

28 Attenuation of PAR-1 activation abrogates cathepsin G-mediated inductio

29 In summary, PAR-1 activation by plasmin induces PKC-mediated phospho

30 olved, GpIbalpha may serve as a cofactor for PAR-1 activation by thrombin.

31 PAR-1 activation enhanced transforming growth factor-bet

32 ns containing CARMA3, Bcl10, and MALT1 links PAR-1 activation to stimulation of the IkappaB kinase co

33 factor for the detection of coincident EGFR/PAR-1 activation.

34 dependent ubiquitination mechanism restrains PAR-1 activation.

35 eneration and protease activated receptor-1 (PAR-1) activation contribute to liver fibrosis induced b

36 Basolateral PAR-1 activity appears to act redundantly with the trans

37 el with phosphorylation by PKC-3 to suppress PAR-1 activity in the anterior cytoplasm.

38 he activation of PAR-1 by either thrombin or PAR-1 agonist peptide elicited a barrier-protective resp

39 Stimulation of platelets with the PAR-1 agonist SFLLRN resulted in rapid and transient pho

40 vity of the serine/threonine polarity kinase PAR-1 (also known as microtubule-associated regulatory k

41 endent thrombin generation and activation of PAR-1 amplify hepatic inflammation and injury during the

42 of endothelial cells through stimulation of PAR-1 and activation of NF-kappaB.

43 gonistic activities of the polarity proteins PAR-1 and aPKC.

44 Par-1 and Dia colocalize along extended regions of the b

45 This study supports the role of functional PAR-1 and EGF polymorphisms as independent prognostic ma

46 functional role for thrombin and its targets PAR-1 and fibrinogen in the pathogenesis of colonic aden

47 culating prothrombin, and tumor cell-derived PAR-1 and further indicate that one key mechanism of thr

48 ere, we show that Oskar is phosphorylated by Par-1 and GSK-3/Shaggy to create a phosphodegron that re

49 tly been identified as downstream targets of PAR-1 and have been shown to modulate interactions betwe

50 These studies indicate that PAR-1 and hematopoietic cell TF are required for liver i

51 PAR-1 and its activating factors, which are expressed on

52 tween the anterior Baz complex and posterior Par-1 and Lgl.

53 to the posterior of slmb mutant oocytes, and Par-1 and oskar mRNA are mislocalised.

54 In conclusion, PAR-1 and PAR-2 are involved in FXa-mediated intracellul

55 We discovered that the activation of both PAR-1 and PAR-2 in endothelial cells pretreated with fac

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

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

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

59 4T1 cells expressed TF, PAR-1 and PAR-2 whereas 67NR cells expressed TF and PAR-

60 ted by the receptor agonist peptides to both PAR-1 and PAR-2.

61 /6 act downstream of the polarity regulators PAR-1 and PAR-3 and in a concentration-dependent manner

62 In addition, we find that PAR-1 and PAR-3 are necessary for inhibiting movement of

63 p66(Shc) mRNA and protein in podocytes (via PAR-1 and PAR-3) and various endothelial cell lines, but

64 Agonists of PAR-1 and PAR-4 mimicked the effects of thrombin and red

65 primary rat neurons and thrombin upregulated PAR-1 and PAR-4 mRNA expression.

66 en for enhancers of lethality in conditional par-1 and par-4 mutants.

67 in the polarization process by showing that PAR-1 and PAR-6 do not localize appropriately in pam-1 m

68 of GpIbalpha which enhances IIa cleavage of PAR-1 and subsequent activation of platelets.

69 ity formation and that the conserved role of Par-1 and Tau is crucial for the establishment of an AP

70 ry CD4(+) and CD8(+) T lymphocytes expressed PAR-1 and that expression was increased in CD8(+) T cell

71 ults in the uniform cortical localisation of Par-1 and the loss of cortical microtubules.

72 We found that cooperative signaling between PAR-1 and TLR3 in mouse cardiac fibroblasts enhanced act

73 carinic receptor, m1, and thrombin receptor, PAR-1) and constitutively active GalphaqQL and Galpha(1)

74 l cells via a protease-activated receptor-1 (PAR-1) and endothelial protein C receptor-dependent mech

75 Proteinase-activated-receptor 1 (PAR-1) and epidermal growth factor (EGF) have been shown

76 mbin receptor protease-activated receptor 1 (PAR-1) and hematopoietic cell-derived tissue factor (TF)

77 bin activates protease-activated receptor 1 (PAR-1) and induces a myofibroblast phenotype in normal l

78 ependent of proteinase-activated receptor 1 (PAR-1) and instead reflected proteolytic activation and

79 oblasts via proteinase-activated receptor 1 (PAR-1) and mammalian target of rapamycin complex 1 (mTOR

80 ffects appear to be related to inhibition of PAR-1, and represents a novel neuroprotective strategy t

81 the oligomeric scaffold PAR-3 and the kinase PAR-1, and the other involves CDC-42 and its putative GA

82 ear determinant, raising the question of how PAR-1 antagonises aPKC activity to promote neurogenesis.

83 n of S. pneumoniae (D39 and EF3030) but that PAR-1 antagonism did not impair the ability of the host

84 PAR-1 antagonist treatment significantly decreased pulmo

85 Preincubation with a plasmin inhibitor, a PAR-1 antagonist, or a protein kinase C (PKC) inhibitor

86 In addition, we found that a PAR-1 antagonist, SCH, prevented LPS-induced excessive m

87 We used the most clinically advanced PAR-1 antagonist, SCH530348, and performed neutrophil de

88 l studies using the most clinically advanced PAR-1 antagonist, SCH530348, revealed a key contribution

89 is a new oral protease-activated-receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platele

90 nt mice, implicating stromal cell-associated PAR-1 as one thrombin target important for tumor outgrow

91 bin receptor, protease activated receptor-1 (PAR-1), as well as deficiency of PAR-1 in all nonhematop

92 ngs reveal that maintaining proper levels of Par-1 at correct position in the oocyte is key to oocyte

93 PAR-1, ATP, and PDGF receptor activation resulted in pro

94 Par-1 binds to myosin phosphatase and phosphorylates it

95 whom severe bleeding attributed to selective PAR-1 blockade or complete thrombin inhibition must be a

96 Cytosolic Par-1 bound, phosphorylated, and inactivated KSR scaffol

97 Thus, the activation of PAR-1 by either thrombin or PAR-1 agonist peptide elicit

98 dependent signaling pathway and involves the PAR-1/c-Src/Rho GTPases Rac1 and Cdc42/c-Jun N-terminal

99 These results reveal that Par-1 controls the timing of pole plasm assembly by prom

100 Inhibiting such interactions by targeting PAR-1 could potentially be a useful therapeutic modality

101 ChIP analyses revealed that PAR-1 decreases binding of Ets-1 and c-Jun transcription

102 To our surprise, PAR-1 deficiency also prevented leukemia development ind

103 PAR-1 deficiency also reduced leukemogenicity of AML1-ET

104 horylation were reduced by TF deficiency and PAR-1 deficiency in mice fed the ANIT diet.

105 In contrast, neither thrombin inhibition nor PAR-1 deficiency in nonhematopoietic cells affected plas

106 PAR-1 deficiency reduced hepatic inflammation, particula

107 PAR-1 deficiency was associated with reduced endothelial

108 In addition, PAR-1 deficiency was associated with reduced steatosis i

109 Similar to PAR-1 deficiency, hematopoietic cell TF deficiency was a

110 ls were greatly reduced by TF-deficiency and PAR-1-deficiency.

111 Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-dilution

112 Colonic adenocarcinoma growth was reduced in PAR-1-deficient mice, implicating stromal cell-associate

113 umulation was not affected in low TF mice or PAR-1-deficient mice.

114 marking the anterior and lateral cortex, and Par-1 defining the posterior.

115 Notably, PAR-1-deleted KPC cells (KPC-Par-1(KO)) failed to genera

116 PAR-1 directly phosphorylates MEX-5 and is antagonized b

117 ether, these data demonstrate a key role for PAR-1 during S. pneumoniae lung infection that is mediat

118 n receptor, proteinase-activated receptor 1 (PAR-1), during the development of pneumonia to the commo

119 l infiltration in the lung, independently of PAR-1 expressed by nonhematopoietic cells.

120 proteolysis, protease-activated receptor-1 (PAR-1) expressed by stromal cells and the extracellular

121 Herein, we report that up-regulation of PAR-1 expression, seen in melanoma progression, mediates

122 enotype completely rescued by restoration of Par-1 expression.

123 reased neutrophil recruitment, and increased PAR-1 expression.

124 Thrombin-activated receptor (PAR-1) expression is increased in HIV-infected ART recip

125 The mammalian Par-1 family consists of four members.

126 , including the CaMKK-like Ssp1 and the MARK/PAR-1 family kinase Kin1, that are required for polarize

127 icrotubule affinity-regulating kinase (MARK)/PAR-1 family kinases.

128 The MARK/PAR-1 family of kinases are conserved regulators of cell

129 LSCs, while a small number of LSCs required PAR-1 for their efficient growth.

130 the regulation of cyclin A localization via Par-1 function plays a critical role in the centrosome o

131 We further show that PAR-1 functions through phosphorylating the synaptic sca

132 olution, we conducted a temporal analysis of par-1 gene expression in early C. elegans embryos.

133 Active PAR-1 generated by LKB1-controlled phosphorylation is ta

134 Thus, the Par-1/GSK-3/Slimb pathway plays important roles in limit

135 ever, the effects of MMP-1 signaling through PAR-1 have not been examined in melanoma.

136 Par-1 helps establish or maintain these bundles in a cor

137 both HAM-1 and its target, the kinase PIG-1 [PAR-1(I)-like Gene], leads to abnormal dopaminergic head

138 id thrombin-antithrombin complex levels) and PAR-1 immunostaining were increased in this model of bac

139 receptor-1 (PAR-1), as well as deficiency of PAR-1 in all nonhematopoietic cells, also reduces stasis

140 gnificantly diminished by depletion of TF or Par-1 in cancer cells or by genetic or pharmacologic red

141 Transgenic mice overexpressing PAR-1 in cardiomyocytes had reduced CVB3-induced myocard

142 In this study, we analyzed the role of PAR-1 in coxsackievirus B3-induced (CVB3-induced) myocar

143 these data revealed a multifaceted role for PAR-1 in leukemogenesis, and highlight this receptor as

144 demonstrated the cell-dose-dependent role of PAR-1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemi

145 eriments identify novel roles for Wnt11R and PAR-1 in NC specification and reveal an unexpected conne

146 in different cellular processes, the role of PAR-1 in neuronal morphogenesis is less well understood.

147 ransplantation experiments demonstrated that PAR-1 in nonhematopoietic cells protected mice from CVB3

148 Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-

149 Together, our findings uncover a role of PAR-1 in spine morphogenesis in hippocampal neurons thro

150 provide new insights into the regulation of PAR-1 in various physiological processes and offer new t

151 or (EGFR) and protease-activated receptor 1 (PAR-1) in endothelial cells.

152 ther show that gain- and loss-of-function of PAR-1 increase and decrease, respectively, the proportio

153 Mechanistically, PAR-1 increased the adherence properties of MLL-AF9 cell

154 bin receptor (protease-activated receptor-1, PAR-1) increases the expression of multiple immediate ea

155 and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) entry.

156 rized through a combination of transport and PAR-1-induced dispersion from basolateral membranes.

157 Furthermore, AICAR pretreatment blocked PAR-1-induced increase in the permeability of mouse lung

158 dependent role of PAR-1 in MLL-AF9 leukemia: PAR-1 inhibited rapid leukemic proliferation when there

159 However, the use of PAR-1 inhibitors to suppress remodeling may be limited b

160 Conversely, PAR-1 inhibits local accumulation of PAR-3 oligomers, wh

161 Par-1 is an evolutionarily conserved protein kinase requ

162 The N1S isoform of Par-1 is enriched at the posterior cortex of the oocyte

163 Since non-phosphorylatable Par-1 is epistatic to uninhibitable Baz, Par-1 seems to

164 ing evidence suggests that signaling through PAR-1 is involved in inflammation, however, its function

165 The cell polarity kinase Par-1 is required for cells to form following syncytial

166 Here, we show that PAR-1 is required for normal spine morphogenesis in hipp

167 PAR-1 is therefore a crucial regulator of the balance be

168 Protease-activated receptor-1 (PAR-1) is a key player in melanoma metastasis with highe

169 Protease activated receptor-1 (PAR-1) is activated by MMP-1, and is also expressed by V

170 mbin receptor protease activated receptor-1 (PAR-1) is overexpressed in metastatic melanoma cell line

171 Proteinase-activated receptor-1 (PAR-1) is protective against Helicobacter-induced gastri

172 We find that, as in human MARK1, the PAR-1 KA1 domain is an auto-inhibitory domain that suppr

173 of PAR-1 protein is not essential, and that PAR-1 kinase activity is regulated spatially.

174 arity, to the plasma membrane and release of Par-1 kinase into the cytosol.

175 The MEX-5 diffusion gradient arises when the PAR-1 kinase stimulates the release of MEX-5 from slow-d

176 We identify a critical new role for Par-1 kinase: spatiotemporal regulation of Myo-II activi

177 tributes to robust symmetry breaking by MARK/PAR-1 kinases in diverse cell types.

178 Localization of MARK/PAR-1 kinases to specific regions of the cell cortex is

179 FR2 after MMP-1 stimulation was inhibited by PAR-1 knockdown and NF-kappaB specific inhibition.

180 Accordingly, KPC-Par-1(KO) cells failed to form tumors in immune-competen

181 Expression profiling of KPC and KPC-Par-1(KO) cells indicated that thrombin-PAR-1 signaling

182 al killer cells, mediated elimination of KPC-Par-1(KO) tumor cells in C57Bl/6 mice.

183 Notably, PAR-1-deleted KPC cells (KPC-Par-1(KO)) failed to generate sizable tumors, a phenotyp

184 we have demonstrated that the suppression of PAR-1 leads to down-regulation of inflammatory factors i

185 und that factor Xa or thrombin activation of PAR-1 led to a rapid release of stored intracellular uPA

186 is associated with a progressive decrease in Par-1 levels.

187 The dynamics of Baz, Par-6 and Par-1 localisation in the oocyte indicate that the axis

188 rotein trafficking, cytoskeletal polarity or Par-1 localization/function.

189 Furthermore, Par-1 localizes to and increases active Myo-II at the cl

190 In Caenorhabditis elegans zygotes, PAR-1 localizes to the posterior cortex under the influe

191 r demonstrate that the cell polarity protein Par-1 (MARK), a serine-threonine kinase, regulates the l

192 The conserved kinases PAR-1/MARK are critically involved in processes such as

193 herapeutic strategies for diseases involving PAR-1/MARK deregulation.

194 pecifically inhibiting the activities of all PAR-1/MARK family members.

195 Given the importance of PAR-1/MARK in health and disease, their activities need

196 /MARK kinases in AD pathogenesis and suggest PAR-1/MARK inhibitors as potential therapeutics for AD a

197 Our results reveal a critical role for PAR-1/MARK kinases in AD pathogenesis and suggest PAR-1/

198 a non-phosphorylatable form of tau with the PAR-1/MARK site mutated blocked the synaptic toxicity in

199 ned, including the kinases shaggy/GSK-3beta, par-1/MARK, CamKI and Mekk1.

200 Kbeta) or knockdown of AMPKalpha1 suppressed PAR-1-mediated phosphorylation of p38beta and hence STIM

201 hrombin level and activity, thrombin-induced PAR-1-mediated signaling, superoxide generation and lung

202 dothelial cells, p38beta knockdown prevented PAR-1-mediated STIM1 phosphorylation and potentiated SOC

203 indicate that one key mechanism of thrombin/PAR-1-mediated tumor growth is suppression of antitumor

204 Protease-activated receptor 1 (PAR-1) mediates thrombin signaling in human endothelial

205 liver fibrosis was significantly reduced in PAR-1(-/-) mice fed an ANIT diet.

206 , we show that the partitioning defective-1 (PAR-1)/microtubule affinity-regulating kinase (MARK) fam

207 This newly identified PAR-1-modifying module critically regulates synaptic mor

208 dimerization with PAR-2 (human podocytes) or PAR-1 (mouse podocytes).

209 Interestingly, TF and PAR-1 mRNA levels were increased in livers from patients

210 Vascular PAR-1 mRNA was not increased in diabetic mice.

211 ocalized to the spectrosome, is perturbed in par-1 mutant GSCs.

212 Egg chambers with excessive and ectopic Par-1 (N1S) kinase activity in the germline cells displa

213 Here we report that posterior restriction of Par-1 (N1S) kinase activity is critical for microtubule

214 alleviates the phenotypes caused by ectopic Par-1 (N1S) kinase activity, suggesting that Par-1 regul

215 Herein, we demonstrate a mechanism by which PAR-1 negatively regulates the expression of the Maspin

216 CDC-42 (shown previously), such that either PAR-1 or CHIN-1 can prevent recruitment of PAR-6/PKC-3,

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

218 more apparent in par-2 early embryos than in par-1 or par-4, except for strd-1(RNAi), which enhances

219 which depletion is synthetically lethal with par-1 or par-4, or both, but produces little embryo leth

220 ent in either protease activated receptor-1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhe

221 thus attributing an alternative function to PAR-1 other than coagulation.

222 imilar to the effect of Runx1/Cbfb deletion, PAR-1 overexpression induced CDKN1A/p21 expression and a

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

224 thrombin and factor Xa did not activate the PAR-1/PAR-2 complex.

225 These results indicate that a TF-PAR-1 pathway contributes to liver fibrosis induced by c

226 lts indicate that the tissue factor/thrombin/PAR-1 pathway enhances IFN-beta expression and contribut

227 The polarity protein PAR-1 plays an essential role in many cellular contexts,

228 The kinase MARK2/Par-1 plays key roles in several cell processes, includi

229 bin receptor, protease-activated receptor-1 (PAR-1), plays a key role in exerting this function durin

230 re excluded from the oocyte posterior by the Par-1 polarity kinase to generate the polarized microtub

231 two-cell stage embryo and that the PAR-4 and PAR-1 polarity proteins dampen DNA replication dynamics

232 es mammalian ste20 homologs 1/2 (MST1/2) and Par-1 polarity proteins microtubule affinity-regulating

233 ting in decreased Cx-43 promoter activity in PAR-1-positive cells.

234 This requirement stems from Par-1 promoting cortical actin caps that grow into dome-

235 ntified FXa as potent, direct agonist of the PAR-1 (protease-activated receptor 1), leading to platel

236 including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-del

237 PAR-1 protects NMY-2 from being moved across the cortex

238 e, we report that asymmetric localization of PAR-1 protein is not essential, and that PAR-1 kinase ac

239 that zyxin binds to the C-terminal domain of PAR-1, providing a possible mechanism of involvement of

240 In addition, an increase in the Bazooka/Par-1 ratio causes formation of ectopic dorsal folds.

241 let surface while leaving exosite I free for PAR-1 recognition.

242 f MDA-9/syntenin as an important TF.FVIIa.Xa/PAR-1-regulated gene that initiates a signaling circuit

243 ted in PAR-1-silenced cells, suggesting that PAR-1 regulates Cx-43 at the transcriptional level.

244 Par-1 (N1S) kinase activity, suggesting that Par-1 regulates oocyte polarity at least partly through

245 eed, Cx-43 expression was restored following PAR-1 rescue in PAR-1-silenced cells.

246 ells, with this effect being abrogated after PAR-1 rescue.

247 The phosphorylation of Mib by PAR-1 results in Mib degradation, repression of Notch si

248 mutation of the aPKC phosphorylation site in Par-1 results in the uniform cortical localisation of Pa

249 form reduction of the activity of Bazooka or Par-1 results in uniform apical or lateral positioning o

250 Consistent with this model, PAR-1 RNA rescues NC markers in embryos in which noncano

251 ble Par-1 is epistatic to uninhibitable Baz, Par-1 seems to function downstream of the other PAR prot

252 cally to recruit PAR-6/PKC-3, which inhibits PAR-1 (shown previously) and inhibits local growth/accum

253 Par-1 shows a cell cycle-dependent localization to the s

254 Here, we demonstrate that an MMP-1/PAR-1 signaling axis exists in VGP melanoma, and is nece

255 The tissue factor-thrombin-PAR-1 signaling axis in tumor cells promotes PDAC growth

256 , SCH530348, revealed a key contribution for PAR-1 signaling in influencing neutrophil recruitment to

257 a suggest that therapeutic targeting of both PAR-1 signaling in osteoclast precursors as well as cath

258 lial cells and provides evidence for a novel PAR-1 signaling pathway mediated by zyxin.

259 latory mechanism in which combinatorial EGFR/PAR-1 signaling regulates STAT3-dependent IEG induction

260 Coincident PAR-1 signaling resolves these conflicting EGF-activated

261 KPC-Par-1(KO) cells indicated that thrombin-PAR-1 signaling significantly altered immune regulation

262 Functionally, combinatorial EGFR/PAR-1 signaling suppresses EGF-induced proliferation and

263 Although it is known that PAR-1 signaling to NF-kappaB depends on initial PKC acti

264 ome activation and that mimicking biased aPC PAR-1 signaling using parmodulins may be a feasible ther

265 Targeting biased PAR-1 signaling via parmodulin-2 restricted mTORC1 and N

266 Accordingly, inhibiting PAR-1 signaling, but not the anticoagulant properties of

267 volvement of zyxin as a signal transducer in PAR-1 signaling.

268 Moreover, silencing Maspin in PAR-1-silenced cells reverted the inhibition of tumor gr

269 oter activity was significantly inhibited in PAR-1-silenced cells, suggesting that PAR-1 regulates Cx

270 thelial cells was significantly decreased in PAR-1-silenced cells, with this effect being abrogated a

271 ssion was restored following PAR-1 rescue in PAR-1-silenced cells.

272 40-fold increase in expression of Maspin in PAR-1-silenced metastatic melanoma cell lines.

273 PAR-1 silencing did not affect Ets-1 or c-Jun expression

274 lial cells, is significantly decreased after PAR-1 silencing in metastatic melanoma cell lines.

275 rowth and experimental lung metastasis after PAR-1 silencing via systemic delivery of siRNA encapsula

276 r activity was significantly increased after PAR-1 silencing, suggesting that PAR1 negatively regulat

277 invasive capability of melanoma cells after PAR-1 silencing, which was abrogated after rescuing with

278 n vitro, while pharmacological inhibition of PAR 1 similarly slowed both the growth and migration of

279 ear to promote detachment; in the absence of Par-1, spatially distinct active Myo-II is lost.

280 PAR-1-specific inhibitors and activating peptides indica

281 Knockdown of PAR-1 sporadically destabilizes cellularization furrows,

282 Here we show that PAR-1 stimulates the generation of deep cell progeny fro

283 We also show that mutations in par-1 suppress both the mushroom body morphology and beh

284 pt at the posterior end of the oocyte, where PAR-1 suppressed nucleation.

285 ating a novel signaling pathway regulated by PAR-1 that is not mediated by G-proteins.

286 A phosphorylation target of Par-1, the microtubule-associated protein Tau, is also i

287 Vertebrate PAR-1 thus antagonises the anti-neurogenic influence of

288 Par-1 thus promotes phosphorylated myosin regulatory lig

289 n of EPCR from caveolin-1 and recruitment of PAR-1 to a protective pathway.

290 receptor from caveolin-1 and recruitment of PAR-1 to a protective signaling pathway.

291 eraction with the Gla domain of FX, recruits PAR-1 to protective signaling pathways in endothelial ce

292 Protease-activated receptor-1 (PAR-1) was localized to amnion mesenchymal and decidual

293 s hypothesis, mice deficient in either TF or PAR-1 were fed a diet containing 0.025% alpha-naphthylis

294 ctor (TF) and protease-activated receptor-1 (PAR-1) were highly expressed in primary KPC pancreatic l

295 PKC complex and the posterior recruitment of Par-1, which induces a microtubule reorganisation that l

296 Polarity proteins such as Par-1, which intrinsically localize, can thus directly m

297 The conserved polarity protein PAR-1, which is basolaterally localised in epithelia, pr

298 timulation of the G-protein-coupled receptor PAR-1 with thrombin in human 1321N1 glioblastoma cells l

299 Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular

300 Data showing that disruption of PAR-1-zyxin interaction inhibited thrombin-induced stres