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protease activated receptor par 1 agonist thrombin receptor activator peptide  (Tocris)


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    Structured Review

    Tocris protease activated receptor par 1 agonist thrombin receptor activator peptide
    Protease Activated Receptor Par 1 Agonist Thrombin Receptor Activator Peptide, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/thrombin+receptor+agonist+peptide+sfllrn/TRAP-6/pm32788114-39-18-16
    Average 94 stars, based on 49 article reviews
    protease activated receptor par 1 agonist thrombin receptor activator peptide - by Bioz Stars, 2026-08
    94/100 stars

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    Protease-activated receptor 1 (PAR1) activation induces FN-dependent rat pulmonary microvascular endothelial cell (RPMVEC) migration. Modified Boyden chamber filters were coated on both sides with the indicated extracellular matrix (ECM) protein. A: activation of the PAR1 receptor with PAR1 agonist peptide (SFLLRN, PAR1-AP) stimulated dose-dependent chemotaxis of RPMVEC when the cells were interacting with FN, but not with any other ECM protein tested. Migration in response to 10% FBS (positive control) did not differ significantly among the ECM proteins (*P < 0.05 vs. no agonist, n = 3). B: checkerboard assay performed by including PAR1-AP in the lower well (analogous to 2A), upper well (with cells), or both. PAR1-induced migration has both chemotactic and chemokinetic components (*P < 0.01 vs. no PAR1-AP; #P < 0.02 vs. PAR1-AP above and below, n = 3). C: modified Boyden assay with varying concentrations of FN coating. Increasing concentration of FN coating potentiated migration in response to low amounts of PAR1-AP (*P < 0.05 vs. DMEM, n = 3). HPF, high-powered field.

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Thrombin induces fibronectin-specific migration of pulmonary microvascular endothelial cells: requirement of calcium/calmodulin-dependent protein kinase II

    doi: 10.1152/ajplung.90598.2008

    Figure Lengend Snippet: Protease-activated receptor 1 (PAR1) activation induces FN-dependent rat pulmonary microvascular endothelial cell (RPMVEC) migration. Modified Boyden chamber filters were coated on both sides with the indicated extracellular matrix (ECM) protein. A: activation of the PAR1 receptor with PAR1 agonist peptide (SFLLRN, PAR1-AP) stimulated dose-dependent chemotaxis of RPMVEC when the cells were interacting with FN, but not with any other ECM protein tested. Migration in response to 10% FBS (positive control) did not differ significantly among the ECM proteins (*P < 0.05 vs. no agonist, n = 3). B: checkerboard assay performed by including PAR1-AP in the lower well (analogous to 2A), upper well (with cells), or both. PAR1-induced migration has both chemotactic and chemokinetic components (*P < 0.01 vs. no PAR1-AP; #P < 0.02 vs. PAR1-AP above and below, n = 3). C: modified Boyden assay with varying concentrations of FN coating. Increasing concentration of FN coating potentiated migration in response to low amounts of PAR1-AP (*P < 0.05 vs. DMEM, n = 3). HPF, high-powered field.

    Article Snippet: PAR1 agonist peptide/thrombin receptor agonist peptide (SFLLRN-NH 2 ), PAR2 agonist peptide (SLIGRL-NH 2 ), VEGF, basic fibroblast growth factor, endothelin-1, KN-93, SCH-79797, W-7, RGD/RGE peptides, FN, vitronectin, and lectins were from Sigma Aldrich (St. Louis, MO).

    Techniques: Activation Assay, Migration, Modification, Chemotaxis Assay, Positive Control, Boyden Assay, Concentration Assay

    Thrombin induces PAR1-specific, FN-dependent RPMVEC migration. A: thrombin treatment resulted in dose-dependent RPMVEC chemotaxis that was inhibited by the PAR1-selective antagonist SCH79797 (*P < 0.05 vs. DMEM; #P < 0.05 vs. thrombin 10−2 U/ml, n = 3). B: migration was also prevented by blocking RPMVEC association with the FN arg-gly-asp (RGD) motif; using soluble RGD peptide soluble arg-gly-glut (RGE) peptide did not block migration (*P < 0.05 vs. thrombin, n = 3).

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Thrombin induces fibronectin-specific migration of pulmonary microvascular endothelial cells: requirement of calcium/calmodulin-dependent protein kinase II

    doi: 10.1152/ajplung.90598.2008

    Figure Lengend Snippet: Thrombin induces PAR1-specific, FN-dependent RPMVEC migration. A: thrombin treatment resulted in dose-dependent RPMVEC chemotaxis that was inhibited by the PAR1-selective antagonist SCH79797 (*P < 0.05 vs. DMEM; #P < 0.05 vs. thrombin 10−2 U/ml, n = 3). B: migration was also prevented by blocking RPMVEC association with the FN arg-gly-asp (RGD) motif; using soluble RGD peptide soluble arg-gly-glut (RGE) peptide did not block migration (*P < 0.05 vs. thrombin, n = 3).

    Article Snippet: PAR1 agonist peptide/thrombin receptor agonist peptide (SFLLRN-NH 2 ), PAR2 agonist peptide (SLIGRL-NH 2 ), VEGF, basic fibroblast growth factor, endothelin-1, KN-93, SCH-79797, W-7, RGD/RGE peptides, FN, vitronectin, and lectins were from Sigma Aldrich (St. Louis, MO).

    Techniques: Migration, Chemotaxis Assay, Blocking Assay

    Microvascular and macrovascular pulmonary endothelial cells display contrasting migratory behavior

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Thrombin induces fibronectin-specific migration of pulmonary microvascular endothelial cells: requirement of calcium/calmodulin-dependent protein kinase II

    doi: 10.1152/ajplung.90598.2008

    Figure Lengend Snippet: Microvascular and macrovascular pulmonary endothelial cells display contrasting migratory behavior

    Article Snippet: PAR1 agonist peptide/thrombin receptor agonist peptide (SFLLRN-NH 2 ), PAR2 agonist peptide (SLIGRL-NH 2 ), VEGF, basic fibroblast growth factor, endothelin-1, KN-93, SCH-79797, W-7, RGD/RGE peptides, FN, vitronectin, and lectins were from Sigma Aldrich (St. Louis, MO).

    Techniques: