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1 nduces A549 IL-8 secretion via activation of protease-activated receptor 2.
2 against transforming growth factor beta1 and protease-activated receptor 2.
3 ates nociceptors to induce visceral pain via protease-activated receptor-2.
4 ic nociceptors, which required expression of protease-activated receptor-2.
11 ected protective mechanisms, mediated by the protease activated receptor 2 and heat shock protein 70,
12 sm that was dependent upon the activation of protease activated receptor-2 and adenosine triphosphate
15 -activated receptor is distinct from that of protease-activated receptor-2, because the response to t
16 inhibitor and Bowman-Birk inhibitor inhibit protease-activated receptor 2 cleavage, affect cytoskele
18 s)-coupled receptor Taar1, respectively, and protease-activated receptor-2 could negatively regulate
21 tors on skin pigmentation and found that the protease-activated receptor 2, expressed on keratinocyte
23 d human keratinocytes showed upregulation in protease-activated receptor 2 expression as determined b
26 iated skin 24 and 96 h after irradiation and protease-activated receptor 2 expression was detected us
28 h skin type I showed delayed upregulation of protease-activated receptor 2 expression, however, compa
30 e dependent on subtilisin protease activity, protease-activated receptor-2, IL-33R ST2, and MyD88 sig
31 These results suggest an important role for protease-activated receptor-2 in pigmentation in vivo.
32 onse to activation of the B-cell receptor or protease-activated receptor 2, intracellular dialysis wi
34 imental arthritis model was not dependent on protease-activated receptor-2, it was dependent on the c
35 ydroxytryptamine [5-HT]), histamine, SLIGRL (protease-activated receptors 2/mas-related G-protein-cou
37 se the response to trypsin was unaffected by protease-activated receptor-2 overexpression or knockdow
38 her protease activated receptor-1 (PAR-1) or protease activated receptor-2 (PAR-2) alone did not affe
39 her protease activated receptor-1 (PAR-1) or protease activated receptor-2 (PAR-2) on nonhematopoieti
41 erated during injury and inflammation cleave protease-activated receptor 2 (PAR(2)) on primary sensor
43 ubiquitinates the G protein-coupled receptor protease-activated receptor 2 (PAR(2)), which is require
45 n the mechanisms that terminate signaling by protease-activated receptor 2 (PAR(2)), which mediated t
46 st the hypothesis that in vivo activation of protease-activated receptor 2 (PAR-2) in humans would me
48 ptase released from these cells can activate protease-activated receptor 2 (PAR-2), which was recentl
50 tivation of two Galpha(q)-coupled receptors, protease-activated receptor-2 (PAR(2)) and neurokinin-1
60 re we show that a serine protease acting via protease-activated receptor-2 (PAR-2) stimulates the dev
63 rthermore, matriptase elicited signaling via protease-activated receptor-2 (PAR-2), and promoted fibr
67 odels, we identified the interaction between protease-activated receptor 2 (PAR2) and serine protease
70 lation, and the EPCR-dependent activation of protease-activated receptor 2 (PAR2) by the ternary TF-V
74 rated during inflammation and disease cleave protease-activated receptor 2 (PAR2) on afferent nerves
75 hypothesized that mast cell tryptase cleaves protease-activated receptor 2 (PAR2) on colonocytes to i
76 leased during inflammation and injury cleave protease-activated receptor 2 (PAR2) on primary afferent
77 ses (mast cell tryptase and trypsins) cleave protease-activated receptor 2 (PAR2) on spinal afferent
79 ger signaling through the G protein-coupled, protease-activated receptor 2 (PAR2) relevant to inflamm
81 d scaffold of coagulation proteases cleaving protease-activated receptor 2 (PAR2) that plays pivotal
82 Neutrophils from aPL-treated mice expressed protease-activated receptor 2 (PAR2), and stimulation of
83 F) conditions induced KLK5 and activated the protease-activated receptor 2 (PAR2), resulting in thymi
87 y was carried out to determine the effect of protease-activated receptor-2 (PAR2) activation on the p
89 in turn cleaved the pericellular substrates protease-activated receptor-2 (PAR2) and pro-urokinase.
90 uch as trypsin and mast cell tryptase cleave protease-activated receptor-2 (PAR2) at R(36) downward a
91 This study sought to evaluate the role of protease-activated receptor-2 (PAR2) in coxsackievirus B
94 at degrades elastic fibers and activates the protease-activated receptor-2 (PAR2) on endothelial cell
97 on of beta2-adrenergic receptor (beta2AR) or Protease-activated-receptor-2 (PAR2) results in relief f
98 keratinocyte-melanocyte interactions via the protease-activated receptor 2 pathway affects melanosome
99 These results imply that inhibition of the protease-activated receptor 2 pathway by soymilk may be
103 onditions induced kallikrein 5 and activated protease-activated receptor 2, resulting in thymic strom
105 er dysfunction, itch, and dermatitis via the protease-activated receptor 2-thymic stromal lymphopoiet
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