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anti bfgf  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti bfgf
    Anti Bfgf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; <t>bFGF,</t> basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin <t>6;</t> <t>MMP,</t> matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.
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    Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; <t>bFGF,</t> basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin <t>6;</t> <t>MMP,</t> matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.
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    Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; <t>bFGF,</t> basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin <t>6;</t> <t>MMP,</t> matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.
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    Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; <t>bFGF,</t> basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin <t>6;</t> <t>MMP,</t> matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.
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    Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; bFGF, basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin 6; MMP, matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.

    Journal: TH Open: Companion Journal to Thrombosis and Haemostasis

    Article Title: Effects of DOACs on Mouse Melanoma Metastasis and the Inhibitory Mechanism of Edoxaban, a Factor Xa-Specific DOAC

    doi: 10.1055/a-2701-4242

    Figure Lengend Snippet: Possible mechanism of melanoma metastasis mediated by FXa-PAR2 and FXa-PAR2-TGFβ pathways in mice implanted with B16 melanoma cells. ( A ) In the absence of EDX, FXa produced by activation of the blood coagulation system and/or cancer-associated FXa-like protease in hosts implanted with melanoma cells activates the FXa-PAR2 and FXa-PAR2-TGFβ pathways in living tissue and melanoma cells, resulting in a decrease in tight junction-associated factors (claudin 5 and E-cadherin) between tissue cells, and an increase in other tumor-associated factors, thereby promoting inflammation, tumor angiogenesis, tissue invasion, and EMT in the host body, and promoting metastasis of melanoma cells. ( B ) In mice treated with EDX, activation of the FXa-PAR2 and FXa-PAR2-TGFβ pathways is suppressed, tight junction-associated factors are increased, and other angiogenic, invasion, and EMT-associated factors are decreased, resulting in the suppression of inflammation, angiogenesis, tissue invasion, and EMT, and the inhibition of melanoma cell metastasis. Ang-2, angiopoietin-2; bFGF, basic fibroblast growth factor; EDX, edoxaban; EMT, epithelial–mesenchymal transition; FXa, factor Xa; IL-6, interleukin 6; MMP, matrix metalloproteinase; PAR, protease-activated receptor; PDGF, platelet-derived growth factor; SMAD, small mothers against decapentaplegic; Snail-1, small family zinc finger 1; TGFβ1, transforming growth factor β1; TGFβR I, TGFβ receptor type I; TGFβR II, TGFβR type II; VEGFA, vascular endothelial growth factor A; Wnt3a, wingless MMTV integration site family, member 3a; ZEB1, zinc finger E-box binding homeobox 1.

    Article Snippet: The levels of interleukin 6 (IL-6), protease-activated receptor (PAR) 1 (PAR1), PAR2, transforming growth factor β1 (TGFβ1), TGFβ receptor type I (TGFβR I), small mothers against decapentaplegic (SMAD) family member 2 (SMAD2), SMAD3, SMAD4, matrix metalloproteinase (MMP)-2 (MMP-2), MMP-9, angiopoietin-2, basic fibroblast growth factor (bFGF), vimentin, fibronectin, snail family transcriptional repressor 1 (Snail-1), inducible nitric oxide synthase (iNOS), and arginase-1 in the lung were determined using commercially available enzyme-linked immunosorbent assay kits per manufacturers' instructions: IL-6 (M6000B, R&D Systems) and angiopoietin-2 (MANG20, R&D Systems), PAR1 (MBS753326, MyBioSoutce, San Diego, CA), PAR2 (MBS4501658; MyBioSource), TGFβ1 (E-EL-M0051, Elabscience, Houston, TX), TGFβR I ( Q64729 , RayBiotech Life, Peachtree Corners, GA), SMAD2 (OKEH03472, Aviva Systems Biology, San Diego, CA), SMAD3 (OKEH03473, Aviva Systems Biology), SMAD4 (OKEH03425, Aviva Systems Biology), fibronectin (OKCD05702, Aviva Systems Biology), MMP-2 (ab254516, Abcam), MMP-9 (ab253227, Abcam), bFGF (bs-0217R, Bioss Antibodies), vimentin (ELK3731, ELK Biotechnology, Denver, CO), Snail-1 (LS-F2317-1, LS Bio, Shirley, MA), iNOS (CSB-E08326m, Wuhan Fine Biotech, Hubei, China), and arginase-1 (MBS2882661, MyBioSource).

    Techniques: Produced, Activation Assay, Coagulation, Inhibition, Derivative Assay, Binding Assay