ライフサイエンスコーパス: thrombin receptor

1 -rich fractions following stimulation of the thrombin receptor.

2 cells correlates with overexpression of the thrombin receptor.

3 sm that required proteolytic cleavage of the thrombin receptor.

4 These include Mas, G2A, and the PAR-1 thrombin receptor.

5 c brain damage, perhaps by activation of the thrombin receptor.

6 a type of activation different from that of thrombin receptor.

7 ith a lyophilized peptide that activates the thrombin receptor.

8 tinct chromosomal locations and encode a new thrombin receptor.

9 ma-1, a second messenger associated with the thrombin receptor.

10 implicating a functional role of the classic thrombin receptor.

11 ood candidate for the missing mouse platelet thrombin receptor.

12 ed cell death occurred via activation of the thrombin receptor.

13 isite for the formation of the high-affinity thrombin receptor.

14 ndidate for the sought-after second platelet thrombin receptor.

15 l neurons respond to thrombin via a neuronal thrombin receptor.

16 nesis and gene expression by the G12 coupled thrombin receptor.

17 ting that this regulation is mediated by the thrombin receptor.

18 clic analogs with excellent affinity for the thrombin receptor.

19 ling without altering the signaling of PAR-1 thrombin receptors.

20 Three of the family members are thrombin receptors.

21 t they activate a receptor distinct from the thrombin receptors.

22 ctivation of the classical G-protein-coupled thrombin receptors.

23 and for tissue-specific roles for different thrombin receptors.

24 hosphatidic acid and beta-adrenergic but not thrombin receptors.

25 talin and protease-activated receptor (PAR) thrombin receptors.

26 c (ATP), bradykinin, and protease-activated (thrombin) receptors.

27 The protease-activated thrombin receptor-1 (PAR-1) can be activated by both the

28 has the potential to activate both PAR-2 and thrombin receptors; 2) for PAR-2, this potential is real

29 ults were found with the nonspecific agonist thrombin receptor-activated peptide (relative increases

30 low and high adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP) concentratio

31 endent morphologic changes when activated by thrombin receptor activating peptide (TRAP) or when spre

32 were observed after platelet activation with thrombin receptor activating peptide (TRAP), collagen, a

33 ustment for platelet count, higher levels of thrombin receptor activating peptide (TRAP)-stimulated p

34 n between unactivated neutrophils and either thrombin receptor activating peptide (TRAP)-stimulated p

35 ng cascades in human platelets stimulated by thrombin receptor activating peptide (TRAP).

36 mu-thrombins but not to beta-thrombin or to thrombin receptor activating peptide (TRAP).

37 ide that imitates the fully active receptor, thrombin receptor activating peptide, was also found to

38 ed neuronal cultures exposed to thrombin and thrombin receptor activating peptides revealed rapid act

39 of cell death after exposure to thrombin or thrombin receptor activating peptides.

40 rachidonic acid, ADP, collagen, epinephrine, Thrombin receptor activating-peptide, U46619, and ristoc

41 mobility shift assay, thrombin (10 U/ml) or thrombin receptor-activating peptide (100 microM) stimul

42 Treatment of the cultures with a synthetic thrombin receptor-activating peptide (SFLLRNP) mimicked

43 Growth cone challenge with thrombin or thrombin receptor-activating peptide (TRAP) triggers col

44 rmation in human whole blood stimulated with thrombin receptor-activating peptide (TRAP) using ex viv

45 (ChA)(hR)Y-NH2 ([3H]haTRAP), a high affinity thrombin receptor-activating peptide (TRAP), and human p

46 hate and protease-activating peptide (PAR) 1 thrombin receptor-activating peptide (TRAP).

47 Platelet stimulation using either ADP or the thrombin receptor-activating peptide enhanced the access

48 U2-OS osteosarcoma cells with thrombin and a thrombin receptor-activating peptide induced pro-MMP-9 s

49 on of agonists including epinephrine and the thrombin receptor-activating peptide induced the alphaII

50 Platelet activation with thrombin receptor-activating peptide leads to the presen

51 because addition of calcium, fibrinogen, and thrombin receptor-activating peptide led to aggregation.

52 r ligands acetylcholine, serotonin, ATP, and thrombin receptor-activating peptide were similarly unaf

53 TR42-55, SFLLRNPNDKYEPF, also known as TRAP (thrombin receptor-activating peptide)], previously have

54 let aggregation induced by ADP, collagen, or thrombin receptor-activating peptide, suggesting that su

55 d a collagen-related peptide-induced but not thrombin receptor-activating peptide- or ADP-induced agg

56 We conclude that (1) thrombin- and thrombin receptor-activating peptide-induced inhibition

57 tathione have additive inhibitory effects on thrombin receptor-activating peptide-induced platelet ag

58 r LYN following the exposure of platelets to thrombin receptor-activating peptide.

59 hibitor, and was mimicked by a 14-amino acid thrombin receptor-activating peptide.

60 denosine diphosphate, thrombin, and the PAR4 thrombin receptor-activating peptide.

61 imal mechanical ventilation and injection of thrombin receptor-activating peptide.

62 These effects were mimicked by a thrombin receptor-activating peptide; preincubation of t

63 G(i) signaling pathways and (2) thrombin and thrombin receptor-activating peptides cause platelet agg

64 let aggregation induced by a TXA2 analog and thrombin receptor-activating peptides that were rescued

65 n-ADP-induced (arachidonic acid-, collagen-, thrombin receptor-activating, peptide-induced) platelet

66 Addition of platelets activated by thrombin-receptor-activating peptide enhanced IL-10 prod

67 This was a specific effect of thrombin receptor activation because peptides correspond

68 These data demonstrate that thrombin receptor activation may inhibit cellular spread

69 increase in clusterin mRNA, suggesting that thrombin receptor activation may regulate renal clusteri

70 The effect of thrombin receptor activation on monocyte conformation wa

71 but not FVIIIa binding; (b) thrombin and the thrombin receptor activation peptide (SFLLRN amide) are

72 n Willebrand factor release by HUVEC but not thrombin receptor activation peptide (SFLLRN-amide)-stim

73 , 8-Br-cGMP activation suppressed [Ca2+]i by thrombin receptor activation peptide (TRAP) by 98 +/- 1

74 A 14-mer thrombin receptor activation peptide (TRAP) of the tethe

75 ll as its PAR-1 receptor activation peptide [thrombin receptor activation peptide (TRAP)] as well as

76 n the presence of platelets activated by the thrombin receptor activation peptide but not with activa

77 Preactivation of platelets with the thrombin receptor activation peptide did not influence s

78 Activation of platelets with thrombin receptor activation peptide does not cause rele

79 Thrombin receptor activation peptide, a 14-amino-acid pe

80 second messenger role of PtdIns(3,4,5)P3 in thrombin receptor activation.

81 Like thrombin receptors, activation of PAR-2 caused pertussis

82 sine diphosphate (ADP), convulxin (CVX), and thrombin receptor activator peptide in only 150 muL of u

83 harvested from healthy volunteers induced by thrombin receptor activator peptide-6 amide (2 microM) i

84 e diphosphate-induced, and 15- and 25-microM thrombin receptor activator peptide-induced aggregation;

85 bleeding time, an increase in platelet PAR-1 thrombin receptor activity, and a decrease in the bindin

86 nding to alpha(IIb)beta(3) induced by a PAR4 thrombin receptor agonist (p < 0.01).

87 se to low concentrations of collagen or PAR4 thrombin receptor agonist AYPGKF, and reduced fibrinogen

88 ess of platelets to adenosine diphosphate or thrombin receptor agonist peptide (P >.4 in all cases);

89 alpha-Thrombin receptor agonist peptide (SFLLRN) induced its t

90 phologically, responded both to thrombin and thrombin receptor agonist peptide (TRAP 42-55) with elev

91 .5 +/- 3.8, p < 0.05) or 5 micromol/liter of thrombin receptor agonist peptide (TRAP) (65.7 +/- 6.8 v

92 ation epitopes induced by ADP, collagen, and thrombin receptor agonist peptide (TRAP) and to template

93 esponse to thrombin could be mimicked by the thrombin receptor agonist peptide (TRAP), implicating a

94 concentration-dependent increase in ADP and thrombin receptor agonist peptide (TRAP)-induced activat

95 peptide having the tethered ligand sequence (thrombin receptor agonist peptide or TRAP).

96 activity is duplicated by the 14-amino acid thrombin receptor agonist peptide that directly activate

97 The aggregation response was greater with thrombin receptor agonist peptide versus ADP stimulation

98 ore and after their being activated with the thrombin receptor agonist peptide, SFLLRN-amide.

99 alphaIIbbeta3 activation by ADP or a Par4 thrombin receptor agonist was also decreased in ADAP-/-

100 When platelets were stimulated with a thrombin receptor agonist, inhibition by GP IIb/IIIa ant

101 se to a protease activated receptor 4 (PAR4) thrombin receptor agonist.

102 cretion in response to low concentrations of thrombin receptor agonists and thromboxane A(2) (TXA(2))

103 ynthetic peptides that directly activate the thrombin receptor also induced apoptosis, indicating tha

104 agonist peptide that directly activates the thrombin receptor and is not inhibited by serum.

105 transfer between the protease-activated PAR1 thrombin receptor and membrane-associated heterotrimeric

106 e same cell and to compare the mechanisms of thrombin receptor and PAR-2 clearance and replacement in

107 ng compensatory up-regulation of alternative thrombin receptors and indicating that thrombin-PAR1 sig

108 and G(16)alphaX all inhibited the endogenous thrombin receptors and lysophosphatidic acid receptors i

109 results suggest that the expression of both thrombin receptors and PAR-2 on endothelial cells serves

110 idual response to SFLLRN after activation of thrombin receptors and PAR-2 raises the possibility that

111 Human endothelial cells express thrombin receptors and PAR-2, the two known members of t

112 ischemic tolerance is through activation of thrombin receptors and the p44/42 MAPK/p70S6K pathway.

113 (OGD), and whether the protection is through thrombin receptors and the p44/42 mitogen activated prot

114 PAR1 is a high-affinity thrombin receptor, and PAR4 is a low apparent affinity t

115 The metabolism of our prototypical thrombin receptor antagonist 1, Ki = 2.7 nM, was studied

116 g our earlier efforts in the himbacine-based thrombin receptor antagonist area, we have synthesized a

117 studied 12 635 patients with NSTE ACS in the Thrombin Receptor Antagonist for Clinical Event Reductio

118 New Jersey) versus placebo among the TRACER (Thrombin Receptor Antagonist for Clinical Event Reductio

119 let Inhibition and Patient Outcomes (PLATO), Thrombin Receptor Antagonist for Clinical Event Reductio

120 TRA2P-TIMI 50 (Thrombin Receptor Antagonist in Secondary Prevention of

121 5 years (median) in TRA 2 degrees P-TIMI 50 [Thrombin Receptor Antagonist in Secondary Prevention of

122 The Thrombin Receptor Antagonist in Secondary Prevention of

123 The Thrombin Receptor Antagonist in Secondary Prevention of

124 is effect in a subgroup of patients from the Thrombin Receptor Antagonist in Secondary Prevention of

125 s a reversible protease-activated receptor-1 thrombin receptor antagonist that interferes with platel

126 Vorapaxar, a novel thrombin receptor antagonist, reduces cardiovascular dea

127 otease activated receptor-1, the presumptive thrombin receptor, appeared to mediate ischemic neurovas

128 e proteins (e.g., thrombomodulin, functional thrombin receptor) are distributed about evenly between

129 opin-releasing factor (CRF) receptor and the thrombin receptor as a model, we present a ligand-depend

130 The results reveal several new aspects of thrombin receptor biology.

131 lial cells (P<0.001), which was reduced with thrombin receptor blockade (P=0.013).

132 plasma from each patient with or without the thrombin receptor blocker vorapaxar.

133 ide, (iso-S)FLLRN, that activates a platelet thrombin receptor but resists inactivation by plasma ami

134 o platelets or CHRF-288 cells, which express thrombin receptors but not PAR-2, tryptase caused neithe

135 n the presence of hirudin (an antagonist for thrombin receptors) but persisted in the presence of amp

136 lore a desensitization mechanism of the PAR1 thrombin receptor by anticoagulant proteases and provide

137 , in COS-7 cells, a chimeric D2R bearing the thrombin receptor C2 loop gained the ability to trigger

138 These observations suggest that the thrombin receptor C2 loop specifies Gq coupling by direc

139 The ability of the thrombin receptor C2 loop to function in the context of

140 Thus, the thrombin receptor C2 loop was able to confer Gq-like cou

141 Moreover, we show that thrombin receptors can stimulate [(35)S]guanosine-5'-O-(

142 Activation of thrombin receptors caused an increase in ligand affinity

143 Unlike thrombin receptors, co-expression of the anchored EC reg

144 Thrombin receptors couple to G(i/o), G(q), and G(12/13)

145 This study identifies thrombin receptors coupled to calcium, ERK, and Akt sign

146 ng properties of chimeric receptors in which thrombin receptor cytoplasmic sequences replaced the cog

147 omplexes within the regulatory region of the thrombin receptor demonstrates that AP-2 binds the proxi

148 We recently identified a new thrombin receptor designated protease-activated receptor

149 cloning and characterization of a new human thrombin receptor, designated protease-activated recepto

150 and establish Rho as a critical mediator of thrombin receptor effects on DNA synthesis and cell migr

151 Here, we found that the activation of thrombin receptors endogenously expressed in HEK-293T ce

152 we conclude that 1) PAR1 is the predominant thrombin receptor expressed in HUVEC and cleavage of PAR

153 PAR3 and PAR4 are thrombin receptors expressed in mouse platelets.

154 n hypersensitivity was not due to changes in thrombin receptor expression (GPIbalpha or PAR1) but is

155 These data support a thrombin receptor function for the platelet membrane GP

156 Thrombin receptor function in the human lens was determi

157 ward identifying the domains responsible for thrombin receptor-G protein interactions, we examined th

158 Cathepsin G, which disables thrombin receptors, had no effect on PAR-2, while urokin

159 ntiates TRPM7 currents, whereas G(q)-coupled thrombin receptors have little effect.

160 tion of the heterotrimeric G protein-coupled thrombin receptor in 1321N1 cells activates Rho-dependen

161 daptor protein in mitogenic signaling by the thrombin receptor in 1321N1 cells.

162 PAR4, a low-affinity thrombin receptor in human platelets, participates in su

163 1 (PAR-1) has been proposed as the principal thrombin receptor in humans, although its actions in viv

164 This review focuses on the role of the thrombin receptor in melanoma and its regulation by AP-2

165 Thus PAR1 is the major thrombin receptor in mouse endothelial cells, but PAR4 a

166 or provided definitive evidence for a second thrombin receptor in mouse platelets and for tissue-spec

167 itive evidence for the existence of a second thrombin receptor in mouse platelets.

168 the nervous system that is identical to the thrombin receptor in platelets, fibroblasts, and endothe

169 activated receptor-1 (PAR1) is the principal thrombin receptor in the vasculature, and antagonists ag

170 ontrast, although tryptase clearly activates thrombin receptors in COS-1 cells, it does not appear to

171 Using endogenous and transfected thrombin receptors in NIH 3T3 cells, ectopic expression

172 lls, it does not appear to cleave endogenous thrombin receptors in platelets or CHRF-288 cells.

173 ent studies we have examined the location of thrombin receptors in resting platelets and followed the

174 ed by protease-activated receptor (PAR)-4 (a thrombin receptor) in human platelets.

175 Thus, activation of thrombin receptors increases Galphaq association with th

176 contrast to previous reports, e.g., for the thrombin receptor, inhibition of matrix metalloproteases

177 ternalization and in part to the shedding of thrombin receptors into membrane microparticles, especia

178 Thus, the prototypical thrombin receptor is the target for EPCR-dependent APC s

179 fibroblasts, Erk 1/2 activation via LPA and thrombin receptors is completely insensitive to both age

180 gh PAR-3 is postulated to represent a second thrombin receptor, its modest endothelial cell and plate

181 ide (CpG) site within coagulation factor II (thrombin) receptor-like 3 (F2RL3) was recently found to

182 of cg03636183 in the coagulation factor II (thrombin) receptor-like 3 gene (F2RL3) (M = -0.64, 95% c

183 gest that thrombin and/or podocyte-expressed thrombin receptors may be novel therapeutic targets for

184 EK-293 human embryonic kidney cells, LPA and thrombin receptor-mediated Erk 1/2 activation is partial

185 Like alpha-thrombin receptor-mediated Erk activation, the effect of

186 ectable increase in the expression of aortic thrombin receptor mRNA.

187 G protein activation strategies used by the thrombin receptor must be very similar to those used by

188 activation of protease-activated receptor 4 thrombin receptors noted in black subjects compared with

189 eceptor, and PAR4 is a low apparent affinity thrombin receptor of uncertain function.

190 ies, indicating that PAR1 is the predominant thrombin receptor on EVTs.

191 al studies revealed specific staining of the thrombin receptor on neurons, with intense labeling alon

192 lized fibrinogen, or (2) activating the PAR1 thrombin receptor on platelets in suspension.

193 suggest that formation of the high-affinity thrombin receptor on the platelet surface has complex al

194 especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor

195 th altered specificities and with ligands of thrombin receptors on platelets.

196 whether these responses could be mediated by thrombin receptors or PAR-2, two G-protein-coupled recep

197 Stimulation of platelet thrombin receptors or protein kinase C causes fibrinogen

198 lial cells, which normally express PAR-2 and thrombin receptors, or keratinocytes, which express only

199 ar permeability induced by activation of the thrombin receptor PAR-1.

200 a-adrenergic receptor), as well as the human thrombin receptor (PAR-1) and the C-C chemokine receptor

201 scovery of an exceptionally potent series of thrombin receptor (PAR-1) antagonists based on the natur

202 eptors (such as muscarinic receptor, m1, and thrombin receptor, PAR-1) and constitutively active Galp

203 The thrombin receptor, PAR-1, and MMP-9 are expressed in ost

204 ently reported upregulation of an additional thrombin receptor, PAR-4, in human vascular smooth muscl

205 B16F10 cells did not contain the two other thrombin receptors, PAR-3 and glycoprotein Ib.

206 f a cell line, B16F10, devoid of the 3 other thrombin receptors, PAR-3, PAR-4, and GPIb; and (2) grea

207 of thrombin-bound fibrinogen Aalpha (7-16), thrombin receptor PAR1 (38-60), and factor XIII (28-37).

208 The thrombin receptor PAR1 becomes rapidly phosphorylated up

209 otease (leishmanolysin or gp63) activate the thrombin receptor PAR1 in the macrophages.

210 The thrombin receptor PAR1 is activated when thrombin cleave

211 to thrombin in a manner more similar to the thrombin receptor PAR1 than to fibrinogen Aalpha.

212 r development and that PAR2, rather than the thrombin receptor PAR1, plays a crucial role in the angi

213 The thrombin receptors PAR1 and PAR4 can be effectively targ

214 lar domain of the seven transmembrane domain thrombin receptor (PAR1) was determined using site-direc

215 ein coupled receptors (GPCRs), including the thrombin receptor (PAR1), elicits mitogenic responses.

216 The thrombin receptor, PAR1, has recently emerged as a promi

217 After stimulation of the thrombin receptor, PAR1, or overexpression of a constitu

218 Human platelets express two thrombin receptors, PAR1 and PAR4, both of which signal

219 tudying differences between the two platelet thrombin receptors, PAR1 and PAR4, in mediating thrombin

220 ors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as w

221 The recent identification of two new thrombin receptors, PAR3 and PAR4, led us to re-examine

222 brain microglia is mediated through another thrombin receptor, PAR4.

223 ) on platelets activated with ADP, thrombin, thrombin receptor peptide (SFLLRN amide), or collagen at

224 Tryptase also cleaved the analogous thrombin receptor peptide at the activating site but les

225 The thrombin receptor peptide SFLLRNP also induces cell roun

226 nd 72 hours, and was also demonstrable using thrombin receptor peptide TR42-47.

227 platelets (3.5 x 10(8)/mL) activated by the thrombin receptor peptide, SFLLRN (25 microM), were incu

228 inus of the cleaved receptor; however, these thrombin receptor peptides (TRPs) fail to induce sustain

229 ces in the rate of cleavage of the PAR-2 and thrombin receptor peptides by tryptase.

230 ese studies illustrate that specific LPA and thrombin receptors promote inositol lipid signaling via

231 The thrombin receptor protease activated receptor-1 (PAR-1)

232 r (TF)-dependent thrombin generation and the thrombin receptor protease activated receptor-1 (PAR-1)

233 have defined a new signaling pathway for the thrombin receptor protease activated receptor-1 (PAR1) i

234 Deficiency in the thrombin receptor protease activated receptor-1 reduces

235 e through a mechanism dependent on the major thrombin receptor protease-activated receptor (PAR) 1.

236 rn diet-induced NAFLD, we tested whether the thrombin receptor protease-activated receptor 1 (PAR-1)

237 Here we show that the thrombin receptor protease-activated receptor 4 agonist

238 that PKGI-alpha attenuates signaling by the thrombin receptor protease-activated receptor-1 (PAR-1)

239 bility increase induced by activation of the thrombin receptor protease-activated receptor-1.

240 Structurally novel thrombin receptor (protease activated receptor 1, PAR-1)

241 nists), anti-von Willebrand factor aptamers, thrombin receptor (protease-activated receptor-1) antago

242 Increasing evidence demonstrates that the thrombin receptor (protease-activated receptor-1, PAR-1)

243 activation of the EGF receptor (EGFR) and a thrombin receptor (protease-activated receptor-1, PAR-1)

244 sis and thrombosis, we examined the roles of thrombin receptors (protease-activated receptors, PARs)

245 The thrombin receptor [protease-activated receptor-1 (PAR-1)

246 We have studied the involvement of the thrombin receptor [protease-activated receptor-1 (PAR-1)

247 ease in vascular permeability induced by the thrombin receptor, protease activated receptor 1 (PAR1).

248 thality, Tfpi(+/-) mice lacking the platelet thrombin receptor, protease activated receptor 4 (PAR4;

249 Proteolysis of the thrombin receptor, protease activated receptor-1 (PAR1),

250 The G protein-coupled thrombin receptor, protease-activated receptor 1 (PAR1),

251 Recent studies of mice deficient in the thrombin receptor, protease-activated receptor 1 (PAR1),

252 ects via proteolytic activation of the major thrombin receptor, protease-activated receptor-1 (PAR-1)

253 The thrombin receptor, protease-activated receptor-1 (PAR-1)

254 We previously identified the prototypical thrombin receptor, protease-activated receptor-1 (PAR1),

255 Human platelets express dual thrombin receptors, protease-activated receptor (PAR) 1

256 Human platelets express two thrombin receptors, protease-activated receptors 1 and 4

257 Human platelets express 2 thrombin receptors: protease-activated receptor (PAR)-1

258 he potential role of the major high-affinity thrombin receptor, proteinase-activated receptor 1 (PAR-

259 The high-affinity thrombin receptor, proteinase-activated receptor 1 (PAR1

260 against the N-terminal peptide of the human thrombin receptor, putative receptor proteins of 66 and

261 A thrombin receptor-radioligand binding assay was develope

262 An intracellular pool of thrombin receptors refreshes the cell surface with naive

263 amilies of heterotrimeric G proteins, m1 and thrombin receptors, respectively, but not those coupled

264 tion of chimeras between CCR2A and the human thrombin receptor revealed that the cytoplasmic retentio

265 hose used by the D2R and beta2AR despite the thrombin receptor's strikingly different liganding mecha

266 opus oocytes, a chimeric beta2AR bearing the thrombin receptor second cytoplasmic (C2) loop gained th

267 In contrast, only LPA and thrombin receptors significantly stimulate Shc tyrosine

268 As thrombin receptors stimulate focal adhesion kinase (FAK)

269 Both rPMT- and alpha-thrombin receptor- stimulated Erk phosphorylation were s

270 of resting platelets, but we confirm that in thrombin receptor-stimulated platelets enhanced levels o

271 cate that SFK phosphorylation in response to thrombin receptor stimulation is downstream from G(q)/Ca

272 specific RGS-rhoGEF expression, we show that thrombin receptor stimulation of rho is primarily mediat

273 arlier role in platelet activation following thrombin receptor stimulation than had been previously d

274 cytosolic leukotrieneC4 produced downstream thrombin receptor stimulation through the catalytic acti

275 [Ca2+]i following thrombin receptor stimulation was examined in the absenc

276 I isoforms to inhibit [Ca2+]i in response to thrombin receptor stimulation was examined.

277 teraction that is distinct from the platelet thrombin receptor/substrate, PAR-1.

278 SFLLRN-NH2, a thrombin receptor-tethered ligand analogue, and [3H]haTR

279 PAR3 is a thrombin receptor that is expressed in mouse megakaryocy

280 tes protease activated receptor-1 (PAR-1), a thrombin receptor that is highly expressed in endothelia

281 human beings because human platelets have 2 thrombin receptors that are each capable of mediating tr

282 re activated by ADP or a thromboxane analog, thrombin receptors that were initially in the surface co

283 he first to describe the localization of the thrombin receptor to dorsal root ganglion neurons.

284 ange factors in transducing signals from the thrombin receptor to Rho-dependent cytoskeletal response

285 The potential coupling of thrombin receptors to G(o) proteins was substantiated by

286 ar response to hypertension, we have studied thrombin receptor (TR) expression and regulation in hype

287 The proteolytically activated thrombin receptor (TR) is expressed by T lymphocytes, wh

288 f the proteolyzed seven-transmembrane domain thrombin receptor [TR42-55, SFLLRNPNDKYEPF, also known a

289 ugh the protease activated receptor 1 (PAR1) thrombin receptor (TRAP-stimulated P-selectin, activated

290 ies have shown that the biology of the human thrombin receptor varies according to the cell in which

291 by endogenous lysophosphatidic acid (LPA) or thrombin receptors was markedly enhanced by the expressi

292 ic or nonproteolytic activation, PAR-2, like thrombin receptors, was cleared from the endothelial cel

293 corresponding to the tethered ligand of the thrombin receptor were also able to increase clusterin m

294 and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black su

295 espective receptors, as well as endoglin and thrombin receptors, were present in all JRA tissue speci

296 of other platelet receptors such as the PAR4 thrombin receptor, which lacks a functional Hir sequence

297 AP-2 results in increased expression of the thrombin receptor, which subsequently contributes to the

298 te that rat primary hippocampal neurons have thrombin receptors whose responses to thrombin apparentl

299 4 was shown to be a potent antagonist of the thrombin receptor with a Ki = 11 nM.

300 activated receptor (PAR)-4 is a low affinity thrombin receptor with slow activation and desensitizati