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1 redefines the concept of what constitutes a protease-activated receptor.
2 endothelial cell protein C receptor but not protease activated receptors.
3 and thus is independent of interaction with protease-activated receptors.
6 et age (IPF, FSC) and activation through the protease activated receptor 1 (PAR1) thrombin receptor (
7 us-encoded glycoprotein C (gC) can stimulate protease activated receptor 1 (PAR1)-enhanced infection
13 viously demonstrated that the stimulation of protease activated receptor 1 promotes alphavbeta6 integ
14 g to several Gq-coupled receptors, including protease activated receptor 1, muscarinic acetylcholine
16 ing activities mediated by the activation of protease-activated receptor 1 (F2R, also known as PAR1)
17 FLD, we tested whether the thrombin receptor protease-activated receptor 1 (PAR-1) and hematopoietic
18 previously reported that thrombin activates protease-activated receptor 1 (PAR-1) and induces a myof
19 epidermal growth factor receptor (EGFR) and protease-activated receptor 1 (PAR-1) in endothelial cel
23 -1 has been shown to cleave and activate the protease-activated receptor 1 (PAR1) in noncardiac cells
30 onstrate a novel signaling mechanism whereby protease-activated receptor 1 (PAR1) mediates expression
32 using variants of human APC with or without protease-activated receptor 1 (PAR1) signaling function
33 of thrombin, and is associated with altered protease-activated receptor 1 (PAR1) signaling, as PAR1
35 t protease that initiates cell signaling via protease-activated receptor 1 (PAR1) to regulate vascula
38 by cleaving its G-protein-coupled receptors, protease-activated receptor 1 (PAR1), PAR4, or both.
39 CFs express 190 GPCRs and that activation of protease-activated receptor 1 (PAR1), the most highly ex
40 othelial cytoprotective actions that require protease-activated receptor 1 (PAR1), whereas thrombin a
41 coagulation cascade and a potent trigger of protease-activated receptor 1 (PAR1)-mediated platelet a
42 ated through G(i)-coupled receptors, such as protease-activated receptor 1 and CXC chemokine receptor
43 otease-activated receptor 4, and between rat protease-activated receptor 1 and protease-activated rec
44 d receptor 4 in human podocytes, and between protease-activated receptor 1 and protease-activated rec
45 larization and neurogenesis were mediated by protease-activated receptor 1 and were independent of th
47 population with symptomatic PAD and whether protease-activated receptor 1 antagonism with vorapaxar
49 tory of myocardial infarction, inhibition of protease-activated receptor 1 with vorapaxar reduces the
54 an platelets express two thrombin receptors, protease-activated receptors 1 and 4 (PAR1 and PAR4) and
55 activates platelets by binding and cleaving protease-activated receptors 1 and 4 (PAR1 and PAR4).
56 telets revealed that DXA3 formation requires protease-activated receptors 1 and 4, cytosolic phosphol
58 actor (TF)-dependent thrombin generation and protease activated receptor-1 (PAR-1) activation contrib
59 hrombin generation and the thrombin receptor protease activated receptor-1 (PAR-1) contribute to live
62 to generate sickle mice deficient in either protease activated receptor-1 (PAR-1) or protease activa
66 R on endothelial cells, activates endogenous protease activated receptor-1 (PAR1) and induces PAR1-me
67 pose that APC-mediated signaling through the protease activated receptor-1 (PAR1) can favorably regul
68 enase and activator of the G protein-coupled protease activated receptor-1 (PAR1), is an emerging new
70 l cell protein C receptor (EPCR, PROCR), and protease activated receptor-1 (PAR1, F2R) on the growth
72 fferences at the transcript level, including protease activated receptor-1, protease activated recept
74 by proteolytic cleavage on activation of the protease activated receptor-1, with antiangiogenic prope
77 eruli, aPC preserves endothelial cells via a protease-activated receptor-1 (PAR-1) and endothelial pr
78 wo targets of thrombin-mediated proteolysis, protease-activated receptor-1 (PAR-1) expressed by strom
81 eceptor for thrombin on endothelial cells is protease-activated receptor-1 (PAR-1), a member of the G
83 phorylation on serine residues and prevented protease-activated receptor-1 (PAR-1)-induced Ca(2+) ent
87 signaling function of aPC, mediated through protease-activated receptor-1 (PAR1) and endothelial pro
88 synthesis in neuronal cells by APC required protease-activated receptor-1 (PAR1) and PAR3, which inh
92 rect oncogenic activity by signaling through protease-activated receptor-1 (PAR1) in carcinoma cells;
93 lood, Aisiku et al describe a novel class of protease-activated receptor-1 (PAR1) inhibitors that blo
100 activation of the G protein-coupled receptor protease-activated receptor-1 (PAR1) is an important sti
101 and thermodynamic parameters for individual protease-activated receptor-1 (PAR1) molecules in the ab
104 llular (i3) loop agonist, pepducin, based on protease-activated receptor-1 (PAR1) was solved by NMR a
108 tein ALIX regulates lysosomal degradation of protease-activated receptor-1 (PAR1), a GPCR for thrombi
109 d facilitated APC cleavage and activation of protease-activated receptor-1 (PAR1), leading to enhance
111 ar cell recruitment in vivo was dependent on protease-activated receptor-1 activation of the MEK/ERK/
112 of thrombin was attenuated by application of protease-activated receptor-1 and protein kinase C antag
116 elets by alternate mechanisms, including the protease-activated receptor-1 antagonist vorapaxar, have
118 itor leupeptin or two structurally different protease-activated receptor-1 antagonists (SCH79797 and
120 llebrand factor aptamers, thrombin receptor (protease-activated receptor-1) antagonists, and thrombox
121 ing the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted ML
122 or, low-density lipoprotein-related protein, protease-activated receptor-1, or matrix metalloproteina
123 EGF receptor (EGFR) and a thrombin receptor (protease-activated receptor-1, PAR-1) increases the expr
125 thermore, MMP-1 induced vasoconstriction via protease-activated receptor-1, whose expression was sign
129 is externalized via calcium mobilization and protease-activated receptors-1 and -4, and 48% is contai
130 ected protective mechanisms, mediated by the protease activated receptor 2 and heat shock protein 70,
131 erated during injury and inflammation cleave protease-activated receptor 2 (PAR(2)) on primary sensor
133 ubiquitinates the G protein-coupled receptor protease-activated receptor 2 (PAR(2)), which is require
136 odels, we identified the interaction between protease-activated receptor 2 (PAR2) and serine protease
138 lation, and the EPCR-dependent activation of protease-activated receptor 2 (PAR2) by the ternary TF-V
143 d scaffold of coagulation proteases cleaving protease-activated receptor 2 (PAR2) that plays pivotal
144 F) conditions induced KLK5 and activated the protease-activated receptor 2 (PAR2), resulting in thymi
149 We also provide molecular evidence that protease-activated receptor 2 activation followed by PI3
151 nization of the skin could be blocked by the protease-activated receptor 2 antagonist ENMD-1068.
154 onditions induced kallikrein 5 and activated protease-activated receptor 2, resulting in thymic strom
156 er dysfunction, itch, and dermatitis via the protease-activated receptor 2-thymic stromal lymphopoiet
158 ydroxytryptamine [5-HT]), histamine, SLIGRL (protease-activated receptors 2/mas-related G-protein-cou
159 her protease activated receptor-1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhematopoieti
160 sm that was dependent upon the activation of protease activated receptor-2 and adenosine triphosphate
161 tivation of two Galpha(q)-coupled receptors, protease-activated receptor-2 (PAR(2)) and neurokinin-1
167 rthermore, matriptase elicited signaling via protease-activated receptor-2 (PAR-2), and promoted fibr
170 in turn cleaved the pericellular substrates protease-activated receptor-2 (PAR2) and pro-urokinase.
171 uch as trypsin and mast cell tryptase cleave protease-activated receptor-2 (PAR2) at R(36) downward a
172 This study sought to evaluate the role of protease-activated receptor-2 (PAR2) in coxsackievirus B
174 at degrades elastic fibers and activates the protease-activated receptor-2 (PAR2) on endothelial cell
178 e dependent on subtilisin protease activity, protease-activated receptor-2, IL-33R ST2, and MyD88 sig
179 imental arthritis model was not dependent on protease-activated receptor-2, it was dependent on the c
183 on of beta2-adrenergic receptor (beta2AR) or Protease-activated-receptor-2 (PAR2) results in relief f
184 isms for these contrasting cellular effects, protease activated receptor 3 (PAR3) activation by APC a
185 ptors endothelial protein C receptor (EPCR), protease-activated receptor 3 (PAR3), and macrophage-1 a
186 ed injury depended upon interactions between protease-activated receptor 3 and protease-activated rec
187 hrombin-dependent interactions between human protease-activated receptor 3 and protease-activated rec
188 el, including protease activated receptor-1, protease activated receptor-3, platelet activating facto
189 versible fibrinogen binding in response to a protease activated receptor 4 (PAR4) thrombin receptor a
190 mice lacking the platelet thrombin receptor, protease activated receptor 4 (PAR4; Par4(-/-)), or its
194 Here we show that the thrombin receptor protease-activated receptor 4 agonist peptide AYPGKF eli
195 etween rat protease-activated receptor 1 and protease-activated receptor 4 in cultured podocytes.
196 ns between protease-activated receptor 3 and protease-activated receptor 4 in human podocytes, and be
198 ncreased platelet responses on activation of protease-activated receptor 4 thrombin receptors noted i
200 ing Gbeta1) in murine megakaryocytes reduced protease-activated receptor 4, activating peptide-induce
201 ween human protease-activated receptor 3 and protease-activated receptor 4, and between rat protease-
202 other antiplatelet compounds (antagonists of protease-activated receptor 4, MRS 2179, and clopidogrel
204 ur previous study, surface modification with protease-activated receptor 4-activating peptide (PAR4-A
209 ts in blood from mice lacking cathepsin G or protease-activated receptor-4 (PAR4), indicating that ca
213 Stimulation of washed human platelets with protease-activated receptor agonists caused translocatio
214 cates to the membrane after stimulation with protease-activated receptor agonists in a Gq-dependent m
217 can cleave a number of substrates, including protease-activated receptors, and may play an important
218 ith the endothelial cell protein C receptor, protease-activated receptors, and other receptors to exe
220 f other GPCRs, such as the ADP receptors and protease-activated receptors, can also potentiate CLEC-2
221 n contrast to its activation of conventional protease-activated receptors, cathepsin S-mediated activ
222 gand, coagulation factor VIIa, TF influences protease-activated receptor-dependent tumor cell behavio
223 eceptors such as the Toll-like receptors and protease-activated receptors, endogenous proteins with p
224 ping revealed that rat podocytes express the protease-activated receptor family of coagulation recept
226 e proteases, serine protease inhibitors, and protease-activated receptors have been intensively inves
227 ad no effect on the Ca(2+) signals evoked by protease-activated receptors, heterologously expressed m
233 is was not seen in platelets stimulated by a protease activated receptor (PAR)-4 peptide, which is un
235 atelet aggregation to arachidonic acid, ADP, protease-activated receptor (PAR) 1 activation peptide (
241 ain directly activated naive T cells through protease-activated receptor (PAR) 2 to initiate a chemok
243 a is activated by glycoprotein VI (GPVI) and protease-activated receptor (PAR) agonists, but not by a
247 sent study we investigated the importance of protease-activated receptor (PAR)-2 and its ligand mast
250 protease-sensing G protein-coupled receptor, protease-activated receptor (PAR)-2; TSLP induction by p
251 following i.d. 5-HT (5-hydroxytryptamine), a protease-activated receptor (PAR)-4 agonist, and an Mrgp
252 lood, Miyakawa et al show that platelets and protease-activated receptor (PAR)-4 contribute to acetam
253 et accumulation were reduced in mice lacking protease-activated receptor (PAR)-4, which mediates thro
254 botic disorders, we compared the efficacy of protease-activated receptor (PAR)1 and PAR4 in the gener
262 synthetic peptides and pepducins to describe protease-activated receptor PAR1 and PAR4 signaling.
264 (m) values for the hydrolysis of fibrinogen, protease-activated receptor PAR1, and protein C that spa
265 mediator thrombin proteolytically activates protease-activated receptor (PAR1) eliciting a transient
267 atomic force microscopy (AFM) to image human protease-activated receptors (PAR1) in the functionally
268 y be caused by thrombin acting on astrocytic protease-activated receptors (PAR1) in the hindbrain.
269 GPCRs and other membrane proteins, including protease-activated receptors (PAR1, PAR2, and PAR4), che
270 h as the epithelial sodium channel ENaC, the protease-activated receptor PAR2, the tight junction pro
272 ng the proteolytic activity of allergens via protease-activated receptors (PAR2) to initiate inflamma
273 cate that TF signaling via G protein-coupled protease-activated receptors (PAR2, PAR1) additionally d
274 cts appeared to be mediated through specific protease activated receptors (PARs) and sphingosine-1-ph
276 likrein directly activates G protein-coupled protease-activated receptors (PARs) 1 and 2, which posse
278 sed in platelets and activated downstream of protease-activated receptors (PARs) and glycoprotein VI
288 e protease-mediated activation of epithelial protease-activated receptors (PARs) has been shown to in
290 mation through the proteolytic activation of protease-activated receptors (PARs), fibrinogen, factor
295 we examined the roles of thrombin receptors (protease-activated receptors, PARs) and the ADP receptor
296 Together, our results suggest a role for protease-activated receptor signaling in neural tube clo
297 ulation-activated osteopontin, chemerin, and protease-activated receptor signaling, as well as platel
298 thrombin contributes to podocyte injury in a protease-activated receptor-specific manner during nephr
299 o-l-arginine methyl ester (100 mumol/L) or a protease-activated receptor type 1 blocker (BMS 200261,
300 otype among an unusual group of GPCRs called protease activated receptors, which self-activate after
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