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par4 antagonist tcy nh2  (Tocris)


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    Tocris par4 antagonist tcy nh2
    PAR1–4 mRNA expression in GBM specimen and its association with patients´ overall survival time. (A) Comparison of PAR1, PAR2, PAR3 and <t>PAR4</t> mRNA expression in non-malignant brain (NMB, n=7) and all analyzed GBM samples (both primary and relapsed GBM, n=118). (B) Subdivision of GBM specimen in primary GBM (prGBM, n=78), first (1 st , n=33) and second (2 nd , n=7) relapses and comparison with NMB. (A+B) Gene expression was measured by qPCR. Each mRNA level of the target genes (PAR1-4) was normalized to the mean of GAPDH and β-actin using the 2 -ΔΔct method. Data are shown as scatter plots representing the median as horizontal bars. Mann Whitney U test, *p < 0.05 and ***p < 0.001 for (A) and OneWay ANOVA/Kruskal Wallis test with Dunn’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and *** p < 0.001 for (B) . (C) Kaplan Meier survival analyses of PAR1–4 mRNA expression in GBM patients. Association of the relative mRNA expression of each single PAR receptor with the survival time of patients with primary GBM. The patients were divided into two subgroups depending on the median gene expression. No significant association was found.
    Par4 Antagonist Tcy Nh2, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/par4+antagonist+tcy+nh2/tcY-NH2/pmc12321897-285-16-21
    Average 94 stars, based on 29 article reviews
    par4 antagonist tcy nh2 - by Bioz Stars, 2026-10
    94/100 stars

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    1) Product Images from "The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells"

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2025.1582996

    PAR1–4 mRNA expression in GBM specimen and its association with patients´ overall survival time. (A) Comparison of PAR1, PAR2, PAR3 and PAR4 mRNA expression in non-malignant brain (NMB, n=7) and all analyzed GBM samples (both primary and relapsed GBM, n=118). (B) Subdivision of GBM specimen in primary GBM (prGBM, n=78), first (1 st , n=33) and second (2 nd , n=7) relapses and comparison with NMB. (A+B) Gene expression was measured by qPCR. Each mRNA level of the target genes (PAR1-4) was normalized to the mean of GAPDH and β-actin using the 2 -ΔΔct method. Data are shown as scatter plots representing the median as horizontal bars. Mann Whitney U test, *p < 0.05 and ***p < 0.001 for (A) and OneWay ANOVA/Kruskal Wallis test with Dunn’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and *** p < 0.001 for (B) . (C) Kaplan Meier survival analyses of PAR1–4 mRNA expression in GBM patients. Association of the relative mRNA expression of each single PAR receptor with the survival time of patients with primary GBM. The patients were divided into two subgroups depending on the median gene expression. No significant association was found.
    Figure Legend Snippet: PAR1–4 mRNA expression in GBM specimen and its association with patients´ overall survival time. (A) Comparison of PAR1, PAR2, PAR3 and PAR4 mRNA expression in non-malignant brain (NMB, n=7) and all analyzed GBM samples (both primary and relapsed GBM, n=118). (B) Subdivision of GBM specimen in primary GBM (prGBM, n=78), first (1 st , n=33) and second (2 nd , n=7) relapses and comparison with NMB. (A+B) Gene expression was measured by qPCR. Each mRNA level of the target genes (PAR1-4) was normalized to the mean of GAPDH and β-actin using the 2 -ΔΔct method. Data are shown as scatter plots representing the median as horizontal bars. Mann Whitney U test, *p < 0.05 and ***p < 0.001 for (A) and OneWay ANOVA/Kruskal Wallis test with Dunn’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and *** p < 0.001 for (B) . (C) Kaplan Meier survival analyses of PAR1–4 mRNA expression in GBM patients. Association of the relative mRNA expression of each single PAR receptor with the survival time of patients with primary GBM. The patients were divided into two subgroups depending on the median gene expression. No significant association was found.

    Techniques Used: Expressing, Comparison, Gene Expression, MANN-WHITNEY

    Impact of PAR subtype specific inhibitors and agonists on viability of LN-18 GBM cells. Adherent and neurospheric LN-18 cells of passage 1 or 3 were treated for 48 or 72h with the respective compounds followed by measurement of cell viability using the Resazurin assay. (A+B) Treatment of adherent (A) and neurospheric (B) LN-18 cells with inhibitors of PAR1 (RWJ), PAR2 (FSLLRY) and PAR4 (tcY) (each 5 and 20 µM), n=3-4. (C+D) Incubation of adherent (C) and neurospheric (D) LN-18 cells with Thrombin (TB, 30 U/ml), Factor Xa (FXa, 30 nM) or PAR subtype specific agonists (AP1 to AP4, each 100 and 200 µM), n=3-4. OneWay ANOVA Dunnett’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Con.
    Figure Legend Snippet: Impact of PAR subtype specific inhibitors and agonists on viability of LN-18 GBM cells. Adherent and neurospheric LN-18 cells of passage 1 or 3 were treated for 48 or 72h with the respective compounds followed by measurement of cell viability using the Resazurin assay. (A+B) Treatment of adherent (A) and neurospheric (B) LN-18 cells with inhibitors of PAR1 (RWJ), PAR2 (FSLLRY) and PAR4 (tcY) (each 5 and 20 µM), n=3-4. (C+D) Incubation of adherent (C) and neurospheric (D) LN-18 cells with Thrombin (TB, 30 U/ml), Factor Xa (FXa, 30 nM) or PAR subtype specific agonists (AP1 to AP4, each 100 and 200 µM), n=3-4. OneWay ANOVA Dunnett’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Con.

    Techniques Used: Resazurin Assay, Incubation, Comparison

    Related Articles

    Expressing:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Comparison:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Gene Expression:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    MANN-WHITNEY:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Resazurin Assay:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Incubation:

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells.
    Article Snippet: As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).As specific PAR agonists we used the following PAR activating peptides: PAR1 activating peptide AP1 (TFLLR-NH2), PAR2 activating peptide AP2 (SLIGKV-NH2), PAR3 activating peptide AP3 (1-6) amide trifluoroacetate salt (TFAGAP-NH2), PAR4 activating peptide AP4 (AYPGKF-NH2) frontiersin.org (all from Bachem AG).. As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).. Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).Furthermore, we used Factor Xa (human plasma) as activator of PAR1, PAR2 and PAR4, as well as Thrombin as activator of PAR1, PAR3 and PAR4 (both from Enzo Life Sciences GmbH Lörrach, Deutschland).



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    A . C4a desArg concentration-dependently enhances ERK phosphorylation. B. <t>PAR4</t> antagonist tcY-NH2 (300 μM, 30 min), but not pertussis toxin (0.3 μg/ml, 10 h) and RWJ56110 (10 μM, 30 min) inhibit C4a desArg -induced ERK activation. The data are expressed as –fold change in densitometry of Western blots from control group and represent the mean ± SE of three independent experiments (n=3; * p < 0.05 vs. control; pairwise two-sided Student’s t test).
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    A . C4a desArg concentration-dependently enhances ERK phosphorylation. B. <t>PAR4</t> antagonist tcY-NH2 (300 μM, 30 min), but not pertussis toxin (0.3 μg/ml, 10 h) and RWJ56110 (10 μM, 30 min) inhibit C4a desArg -induced ERK activation. The data are expressed as –fold change in densitometry of Western blots from control group and represent the mean ± SE of three independent experiments (n=3; * p < 0.05 vs. control; pairwise two-sided Student’s t test).
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    Image Search Results


    PAR1–4 mRNA expression in GBM specimen and its association with patients´ overall survival time. (A) Comparison of PAR1, PAR2, PAR3 and PAR4 mRNA expression in non-malignant brain (NMB, n=7) and all analyzed GBM samples (both primary and relapsed GBM, n=118). (B) Subdivision of GBM specimen in primary GBM (prGBM, n=78), first (1 st , n=33) and second (2 nd , n=7) relapses and comparison with NMB. (A+B) Gene expression was measured by qPCR. Each mRNA level of the target genes (PAR1-4) was normalized to the mean of GAPDH and β-actin using the 2 -ΔΔct method. Data are shown as scatter plots representing the median as horizontal bars. Mann Whitney U test, *p < 0.05 and ***p < 0.001 for (A) and OneWay ANOVA/Kruskal Wallis test with Dunn’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and *** p < 0.001 for (B) . (C) Kaplan Meier survival analyses of PAR1–4 mRNA expression in GBM patients. Association of the relative mRNA expression of each single PAR receptor with the survival time of patients with primary GBM. The patients were divided into two subgroups depending on the median gene expression. No significant association was found.

    Journal: Frontiers in Oncology

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells

    doi: 10.3389/fonc.2025.1582996

    Figure Lengend Snippet: PAR1–4 mRNA expression in GBM specimen and its association with patients´ overall survival time. (A) Comparison of PAR1, PAR2, PAR3 and PAR4 mRNA expression in non-malignant brain (NMB, n=7) and all analyzed GBM samples (both primary and relapsed GBM, n=118). (B) Subdivision of GBM specimen in primary GBM (prGBM, n=78), first (1 st , n=33) and second (2 nd , n=7) relapses and comparison with NMB. (A+B) Gene expression was measured by qPCR. Each mRNA level of the target genes (PAR1-4) was normalized to the mean of GAPDH and β-actin using the 2 -ΔΔct method. Data are shown as scatter plots representing the median as horizontal bars. Mann Whitney U test, *p < 0.05 and ***p < 0.001 for (A) and OneWay ANOVA/Kruskal Wallis test with Dunn’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and *** p < 0.001 for (B) . (C) Kaplan Meier survival analyses of PAR1–4 mRNA expression in GBM patients. Association of the relative mRNA expression of each single PAR receptor with the survival time of patients with primary GBM. The patients were divided into two subgroups depending on the median gene expression. No significant association was found.

    Article Snippet: As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).

    Techniques: Expressing, Comparison, Gene Expression, MANN-WHITNEY

    Impact of PAR subtype specific inhibitors and agonists on viability of LN-18 GBM cells. Adherent and neurospheric LN-18 cells of passage 1 or 3 were treated for 48 or 72h with the respective compounds followed by measurement of cell viability using the Resazurin assay. (A+B) Treatment of adherent (A) and neurospheric (B) LN-18 cells with inhibitors of PAR1 (RWJ), PAR2 (FSLLRY) and PAR4 (tcY) (each 5 and 20 µM), n=3-4. (C+D) Incubation of adherent (C) and neurospheric (D) LN-18 cells with Thrombin (TB, 30 U/ml), Factor Xa (FXa, 30 nM) or PAR subtype specific agonists (AP1 to AP4, each 100 and 200 µM), n=3-4. OneWay ANOVA Dunnett’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Con.

    Journal: Frontiers in Oncology

    Article Title: The protease-activated receptors are expressed in glioblastoma and differentially modulate adherent versus stem-like growth of LN-18 GBM cells

    doi: 10.3389/fonc.2025.1582996

    Figure Lengend Snippet: Impact of PAR subtype specific inhibitors and agonists on viability of LN-18 GBM cells. Adherent and neurospheric LN-18 cells of passage 1 or 3 were treated for 48 or 72h with the respective compounds followed by measurement of cell viability using the Resazurin assay. (A+B) Treatment of adherent (A) and neurospheric (B) LN-18 cells with inhibitors of PAR1 (RWJ), PAR2 (FSLLRY) and PAR4 (tcY) (each 5 and 20 µM), n=3-4. (C+D) Incubation of adherent (C) and neurospheric (D) LN-18 cells with Thrombin (TB, 30 U/ml), Factor Xa (FXa, 30 nM) or PAR subtype specific agonists (AP1 to AP4, each 100 and 200 µM), n=3-4. OneWay ANOVA Dunnett’s Multiple Comparison Test, *p < 0.05, **p < 0.01 and ***p < 0.001 vs. Con.

    Article Snippet: As specific PAR antagonists the following compounds were used: PAR1 antagonist RWJ, PAR2 antagonist FSLLRY-NH2, and PAR4 antagonist tcY-NH2 (all from Tocris Bioscience).

    Techniques: Resazurin Assay, Incubation, Comparison

    A . C4a desArg concentration-dependently enhances ERK phosphorylation. B. PAR4 antagonist tcY-NH2 (300 μM, 30 min), but not pertussis toxin (0.3 μg/ml, 10 h) and RWJ56110 (10 μM, 30 min) inhibit C4a desArg -induced ERK activation. The data are expressed as –fold change in densitometry of Western blots from control group and represent the mean ± SE of three independent experiments (n=3; * p < 0.05 vs. control; pairwise two-sided Student’s t test).

    Journal: bioRxiv

    Article Title: Divergent effects of C4a, C4a desArg , and thrombin on platelet aggregation and phosphorylation of ERK and Akt in human endothelial cells

    doi: 10.1101/2024.03.13.584877

    Figure Lengend Snippet: A . C4a desArg concentration-dependently enhances ERK phosphorylation. B. PAR4 antagonist tcY-NH2 (300 μM, 30 min), but not pertussis toxin (0.3 μg/ml, 10 h) and RWJ56110 (10 μM, 30 min) inhibit C4a desArg -induced ERK activation. The data are expressed as –fold change in densitometry of Western blots from control group and represent the mean ± SE of three independent experiments (n=3; * p < 0.05 vs. control; pairwise two-sided Student’s t test).

    Article Snippet: PAR1 antagonist RWJ65110 (Catalog no. 2614) and PAR4 antagonist tcY-NH 2 (Catalog no. 1488) were purchased from Tocris Bioscience (Minneapolis, MN).

    Techniques: Concentration Assay, Phospho-proteomics, Activation Assay, Western Blot, Control

    In HMEC-1 ECs, C4a-induced Akt phosphorylation (Ser473) can be inhibited by both PAR1 and PAR4 antagonists. However, C4a desArg -induced Akt phosphorylation (Ser473) can be inhibited by PAR4 antagonist but not PAR1 antagonist. A . Western blotting results show pretreatment of antagonists of PAR1 ( lane 5 ) and PAR4 (lane 6) significantly inhibit C4a-induced Akt phosphorylation (Ser473) ( lane 4 ). C4a desArg -induced Akt phosphorylation (Ser473) ( lane 7 ) can be inhibited by the pretreatment of PAR4 antagonist ( lane 9 ), but not inhibited by PAR1 antagonist ( lane 8 ). One experiment from three separate experiments is shown. B . Densitometry analyses represent the mean ± SE of four independent experiments (n=4; * p < 0.05 vs. control; pairwise two-sided Student’s t test).

    Journal: bioRxiv

    Article Title: Divergent effects of C4a, C4a desArg , and thrombin on platelet aggregation and phosphorylation of ERK and Akt in human endothelial cells

    doi: 10.1101/2024.03.13.584877

    Figure Lengend Snippet: In HMEC-1 ECs, C4a-induced Akt phosphorylation (Ser473) can be inhibited by both PAR1 and PAR4 antagonists. However, C4a desArg -induced Akt phosphorylation (Ser473) can be inhibited by PAR4 antagonist but not PAR1 antagonist. A . Western blotting results show pretreatment of antagonists of PAR1 ( lane 5 ) and PAR4 (lane 6) significantly inhibit C4a-induced Akt phosphorylation (Ser473) ( lane 4 ). C4a desArg -induced Akt phosphorylation (Ser473) ( lane 7 ) can be inhibited by the pretreatment of PAR4 antagonist ( lane 9 ), but not inhibited by PAR1 antagonist ( lane 8 ). One experiment from three separate experiments is shown. B . Densitometry analyses represent the mean ± SE of four independent experiments (n=4; * p < 0.05 vs. control; pairwise two-sided Student’s t test).

    Article Snippet: PAR1 antagonist RWJ65110 (Catalog no. 2614) and PAR4 antagonist tcY-NH 2 (Catalog no. 1488) were purchased from Tocris Bioscience (Minneapolis, MN).

    Techniques: Phospho-proteomics, Western Blot, Control