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plasminogen activator inhibitor 1  (Innovative Research Inc)


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    Innovative Research Inc plasminogen activator inhibitor 1
    Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
    Plasminogen Activator Inhibitor 1, supplied by Innovative Research Inc, used in various techniques. Bioz Stars score: 94/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Comparison of changes in blood cells and hemostatic biomarkers in mouse xenograft models of acute myeloid leukemia and acute promyelocytic leukemia"

    Article Title: Comparison of changes in blood cells and hemostatic biomarkers in mouse xenograft models of acute myeloid leukemia and acute promyelocytic leukemia

    Journal: Research and Practice in Thrombosis and Haemostasis

    doi: 10.1016/j.rpth.2025.103319

    Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.

    Techniques Used: Control



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    Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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    Image Search Results


    Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.

    Journal: Research and Practice in Thrombosis and Haemostasis

    Article Title: Comparison of changes in blood cells and hemostatic biomarkers in mouse xenograft models of acute myeloid leukemia and acute promyelocytic leukemia

    doi: 10.1016/j.rpth.2025.103319

    Figure Lengend Snippet: Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.

    Article Snippet: Levels of different biomarkers in plasma were measured using commercial enzyme-linked immunosorbent assays: TAT (Siemens, cat number OWMG15), fibrinogen (Immunology Consultation Laboratory Inc, cat number E-90FIB), PAP (MyBioSource, cat number MBS2512896), D-dimer (Diagnostica Stago, cat number 00947), and plasminogen activator inhibitor 1 (PAI-1; Molecular Innovations, cat number IMSPAI1KTA). cfDNA was measured using the Quant-iT PicoGreen dsDNA Assay Kit (Thermo Fisher Scientific, cat number P11496).

    Techniques: Control

    PLAU derived from SCAFs promotes PDAC progression in vitro and in vivo (A) Relative mRNA expression of genes in human CAFs treated with 400 μM H 2 O 2 was measured by qRT-PCR. (B) The mRNA expression levels of genes in various cell types in the TME of PDAC. (C) The relationship between PLAU expression and UCell senescence score in CAFs. (D) PLAU knockdown in human SCAFs was verified by ELISA. (E) The migration and invasion abilities of the indicated cells were assessed by Transwell assay. Scale bar, 20 μm. (F) PLAU overexpression in human CAFs was verified by ELISA. (G) The migration and invasion abilities of the indicated cells were assessed by Transwell assay. Scale bar, 20 μm. (H) The flow of the experimental design. (I) Bioluminescence images showing orthotopically transplanted PDAC tumors. (J) Photographs and volumes of tumors. (K and L) Representative flow cytometry images and statistical analysis of CD3 + (K) and CD8 + T cells (L) in tumors in different groups. (M and N) Representative flow cytometry images and statistical analysis of MDSCs (M) and M2 macrophage (N) in tumors in different groups. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: iScience

    Article Title: Revealing the role of cancer-associated fibroblast senescence in prognosis and immune landscape in pancreatic cancer

    doi: 10.1016/j.isci.2024.111612

    Figure Lengend Snippet: PLAU derived from SCAFs promotes PDAC progression in vitro and in vivo (A) Relative mRNA expression of genes in human CAFs treated with 400 μM H 2 O 2 was measured by qRT-PCR. (B) The mRNA expression levels of genes in various cell types in the TME of PDAC. (C) The relationship between PLAU expression and UCell senescence score in CAFs. (D) PLAU knockdown in human SCAFs was verified by ELISA. (E) The migration and invasion abilities of the indicated cells were assessed by Transwell assay. Scale bar, 20 μm. (F) PLAU overexpression in human CAFs was verified by ELISA. (G) The migration and invasion abilities of the indicated cells were assessed by Transwell assay. Scale bar, 20 μm. (H) The flow of the experimental design. (I) Bioluminescence images showing orthotopically transplanted PDAC tumors. (J) Photographs and volumes of tumors. (K and L) Representative flow cytometry images and statistical analysis of CD3 + (K) and CD8 + T cells (L) in tumors in different groups. (M and N) Representative flow cytometry images and statistical analysis of MDSCs (M) and M2 macrophage (N) in tumors in different groups. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: The Human PLAU ELISA Kit and Mouse PLAU ELISA kit were purchased from BOSTER (Wuhan, China) and Hengyuan Biological Technology (Shanghai, China).

    Techniques: Derivative Assay, In Vitro, In Vivo, Expressing, Quantitative RT-PCR, Knockdown, Enzyme-linked Immunosorbent Assay, Migration, Transwell Assay, Over Expression, Flow Cytometry

    Journal: iScience

    Article Title: Revealing the role of cancer-associated fibroblast senescence in prognosis and immune landscape in pancreatic cancer

    doi: 10.1016/j.isci.2024.111612

    Figure Lengend Snippet:

    Article Snippet: The Human PLAU ELISA Kit and Mouse PLAU ELISA kit were purchased from BOSTER (Wuhan, China) and Hengyuan Biological Technology (Shanghai, China).

    Techniques: Purification, Blocking Assay, Virus, Plasmid Preparation, Recombinant, Saline, Staining, Marker, Bicinchoninic Acid Protein Assay, CCK-8 Assay, Infection, Enzyme-linked Immunosorbent Assay, Gene Expression, Microarray, Expressing, Software