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selective par1 antagonist  (MedChemExpress)


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    MedChemExpress selective par1 antagonist
    Selective Par1 Antagonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p2518/Protease-Activated+Receptor-1%2C+PAR-1+Agonist/pm40088673-70-36-41
    Average 93 stars, based on 5 article reviews
    selective par1 antagonist - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    other:

    Article Title: Gastrodin attenuates diabetic cardiomyopathy characterized by myocardial fibrosis by inhibiting the KLK8-PAR1 signaling axis
    Article Snippet: Gastrodin (GAS) (G2129091, purity: ≥98%) was purchased from Shanghai Aladdin Biochemical Technology Co., Ltd. PAR1 (141136–83 − 6, 1:1000), pSmad3 (YT4334, 1:1000), Smad3 (HY-P80325, 1:1000), SCH79797 (HY-14993), FSLLRY-NH2 (HY-P1260), and TFLLR-NH2 (HY-P0226A) were purchased from MedChemExpress.

    Article Title: Gastrodin attenuates diabetic cardiomyopathy characterised by myocardial fibrosis by inhibiting the KLK8-PAR1 signalling axis
    Article Snippet: Materials and Methods 2.1 Reagents and antibodies GAS (G2129091, purity: ≥98%) was obtained from Shanghai Aladdin Biochemical Technology Co., Ltd. PAR1(141136-83-6, 1:1000), pSmad3(YT4334, 1:1000), Smad3 (HY-P80325, 1:1000), SCH79797(HY14993), FSLLRY-NH2 (HY-P1260), TFLLR-NH2(HY-P0226A) purchased from MedChemExpress.

    Cell Culture:

    Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression.
    Article Snippet: Philadelphia chromosome-negative myeloproliferative neoplasms (Ph-MPNs) are clonal disorders marked by high morbidity and mortality, driven by uncontrolled myeloid proliferation from hematopoietic stem/progenitor cells (HSCs) and associated with a significant risk of thrombosis.. This study explored the relationship between JAK2V617F and protease-activated receptor 1 (PAR1) by examining PAR1 expression and activation across various hematopoietic stem/progenitor cell (HSPC) subgroups, assessing their contribution to the hypercoagulable state in Ph-MPNs.. We investigated the effects of thrombin, a PAR1 antagonist (vorapaxar), and a JAK2 inhibitor (ruxolitinib) on Ph-MPN cells.

    Incubation:

    Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression.
    Article Snippet: Philadelphia chromosome-negative myeloproliferative neoplasms (Ph-MPNs) are clonal disorders marked by high morbidity and mortality, driven by uncontrolled myeloid proliferation from hematopoietic stem/progenitor cells (HSCs) and associated with a significant risk of thrombosis.. This study explored the relationship between JAK2V617F and protease-activated receptor 1 (PAR1) by examining PAR1 expression and activation across various hematopoietic stem/progenitor cell (HSPC) subgroups, assessing their contribution to the hypercoagulable state in Ph-MPNs.. We investigated the effects of thrombin, a PAR1 antagonist (vorapaxar), and a JAK2 inhibitor (ruxolitinib) on Ph-MPN cells.

    Analysis:

    Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression.
    Article Snippet: Philadelphia chromosome-negative myeloproliferative neoplasms (Ph-MPNs) are clonal disorders marked by high morbidity and mortality, driven by uncontrolled myeloid proliferation from hematopoietic stem/progenitor cells (HSCs) and associated with a significant risk of thrombosis.. This study explored the relationship between JAK2V617F and protease-activated receptor 1 (PAR1) by examining PAR1 expression and activation across various hematopoietic stem/progenitor cell (HSPC) subgroups, assessing their contribution to the hypercoagulable state in Ph-MPNs.. We investigated the effects of thrombin, a PAR1 antagonist (vorapaxar), and a JAK2 inhibitor (ruxolitinib) on Ph-MPN cells.



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    selective par1 antagonist  (MedChemExpress)
    93
    MedChemExpress selective par1 antagonist
    Selective Par1 Antagonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p2518/Protease-Activated+Receptor-1%2C+PAR-1+Agonist/pm40088673-70-36-41
    Average 93 stars, based on 1 article reviews
    selective par1 antagonist - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    par1  (MedChemExpress)
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    MedChemExpress par1
    KLK8 exerts biological effects through the activation of the <t>PAR1</t> receptor, which is involved in HG-PA-induced differentiation, collagen synthesis, and the migration of CFs. A–D OE-KLK8-treated CFs were continuously transfected for 12 h. Interventions were performed using the PAR1 and PAR2 antagonists SCH79797 and FSLLRY-NH2. E-G. The PAR1 antagonist SCH79797 was used to treat HG-PA-exposed CFs. A OE-KLK8-overexpressing CFs were treated with the PAR1 antagonist SCH79797 (10 µM) or the PAR2 antagonist FSLLRY-NH2 (1 µM). The MTT assay was performed to determine the proliferation rate of the cells; *P < 0.05 vs. control; # P < 0.05 vs. OE-KLK8. B Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. C Immunofluorescence staining of α-SMA (green); the nuclei were restained with DAPI (blue); scale bar = 50 μm. D Wound healing assay; scale bar = 50 μm. E Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. F Immunofluorescence staining of α-SMA (green). The cell nuclei were restained with DAPI (blue); scale bar = 50 μm. G Wound healing assay; scale bar = 50 μm. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.
    Par1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p2518/Protease-Activated+Receptor-1%2C+PAR-1+Agonist/pmc11583739-57-14-35
    Average 93 stars, based on 1 article reviews
    par1 - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    par 1 antagonist  (MedChemExpress)
    93
    MedChemExpress par 1 antagonist
    KLK8 exerts biological effects through the activation of the <t>PAR1</t> receptor, which is involved in HG-PA-induced differentiation, collagen synthesis, and the migration of CFs. A–D OE-KLK8-treated CFs were continuously transfected for 12 h. Interventions were performed using the PAR1 and PAR2 antagonists SCH79797 and FSLLRY-NH2. E-G. The PAR1 antagonist SCH79797 was used to treat HG-PA-exposed CFs. A OE-KLK8-overexpressing CFs were treated with the PAR1 antagonist SCH79797 (10 µM) or the PAR2 antagonist FSLLRY-NH2 (1 µM). The MTT assay was performed to determine the proliferation rate of the cells; *P < 0.05 vs. control; # P < 0.05 vs. OE-KLK8. B Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. C Immunofluorescence staining of α-SMA (green); the nuclei were restained with DAPI (blue); scale bar = 50 μm. D Wound healing assay; scale bar = 50 μm. E Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. F Immunofluorescence staining of α-SMA (green). The cell nuclei were restained with DAPI (blue); scale bar = 50 μm. G Wound healing assay; scale bar = 50 μm. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.
    Par 1 Antagonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p2518/Protease-Activated+Receptor-1%2C+PAR-1+Agonist/pm31175838-72-11-13
    Average 93 stars, based on 1 article reviews
    par 1 antagonist - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    KLK8 exerts biological effects through the activation of the PAR1 receptor, which is involved in HG-PA-induced differentiation, collagen synthesis, and the migration of CFs. A–D OE-KLK8-treated CFs were continuously transfected for 12 h. Interventions were performed using the PAR1 and PAR2 antagonists SCH79797 and FSLLRY-NH2. E-G. The PAR1 antagonist SCH79797 was used to treat HG-PA-exposed CFs. A OE-KLK8-overexpressing CFs were treated with the PAR1 antagonist SCH79797 (10 µM) or the PAR2 antagonist FSLLRY-NH2 (1 µM). The MTT assay was performed to determine the proliferation rate of the cells; *P < 0.05 vs. control; # P < 0.05 vs. OE-KLK8. B Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. C Immunofluorescence staining of α-SMA (green); the nuclei were restained with DAPI (blue); scale bar = 50 μm. D Wound healing assay; scale bar = 50 μm. E Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. F Immunofluorescence staining of α-SMA (green). The cell nuclei were restained with DAPI (blue); scale bar = 50 μm. G Wound healing assay; scale bar = 50 μm. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

    Journal: Chinese Medicine

    Article Title: Gastrodin attenuates diabetic cardiomyopathy characterized by myocardial fibrosis by inhibiting the KLK8-PAR1 signaling axis

    doi: 10.1186/s13020-024-01035-4

    Figure Lengend Snippet: KLK8 exerts biological effects through the activation of the PAR1 receptor, which is involved in HG-PA-induced differentiation, collagen synthesis, and the migration of CFs. A–D OE-KLK8-treated CFs were continuously transfected for 12 h. Interventions were performed using the PAR1 and PAR2 antagonists SCH79797 and FSLLRY-NH2. E-G. The PAR1 antagonist SCH79797 was used to treat HG-PA-exposed CFs. A OE-KLK8-overexpressing CFs were treated with the PAR1 antagonist SCH79797 (10 µM) or the PAR2 antagonist FSLLRY-NH2 (1 µM). The MTT assay was performed to determine the proliferation rate of the cells; *P < 0.05 vs. control; # P < 0.05 vs. OE-KLK8. B Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. C Immunofluorescence staining of α-SMA (green); the nuclei were restained with DAPI (blue); scale bar = 50 μm. D Wound healing assay; scale bar = 50 μm. E Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. F Immunofluorescence staining of α-SMA (green). The cell nuclei were restained with DAPI (blue); scale bar = 50 μm. G Wound healing assay; scale bar = 50 μm. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

    Article Snippet: Gastrodin (GAS) (G2129091, purity: ≥98%) was purchased from Shanghai Aladdin Biochemical Technology Co., Ltd. PAR1 (141136–83 − 6, 1:1000), pSmad3 (YT4334, 1:1000), Smad3 (HY-P80325, 1:1000), SCH79797 (HY-14993), FSLLRY-NH2 (HY-P1260), and TFLLR-NH2 (HY-P0226A) were purchased from MedChemExpress.

    Techniques: Activation Assay, Migration, Transfection, MTT Assay, Control, Western Blot, Immunofluorescence, Staining, Wound Healing Assay

    GAS attenuates fibrosis in CFs by inhibiting the KLK8-PAR1 signaling axis, a process in which TGF-β1/smad3 is involved. CFs were transfected with OE-KLK8 with or without GAS (5 µM) treatment for 12 h, followed by 36 h of exposure in the presence or absence of HG-PA. A Immunoblotting of KLK8, TGFBβ1, PAR1, and Smad3 proteins. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

    Journal: Chinese Medicine

    Article Title: Gastrodin attenuates diabetic cardiomyopathy characterized by myocardial fibrosis by inhibiting the KLK8-PAR1 signaling axis

    doi: 10.1186/s13020-024-01035-4

    Figure Lengend Snippet: GAS attenuates fibrosis in CFs by inhibiting the KLK8-PAR1 signaling axis, a process in which TGF-β1/smad3 is involved. CFs were transfected with OE-KLK8 with or without GAS (5 µM) treatment for 12 h, followed by 36 h of exposure in the presence or absence of HG-PA. A Immunoblotting of KLK8, TGFBβ1, PAR1, and Smad3 proteins. The data are expressed as the mean ± SEM of three independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

    Article Snippet: Gastrodin (GAS) (G2129091, purity: ≥98%) was purchased from Shanghai Aladdin Biochemical Technology Co., Ltd. PAR1 (141136–83 − 6, 1:1000), pSmad3 (YT4334, 1:1000), Smad3 (HY-P80325, 1:1000), SCH79797 (HY-14993), FSLLRY-NH2 (HY-P1260), and TFLLR-NH2 (HY-P0226A) were purchased from MedChemExpress.

    Techniques: Transfection, Western Blot