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  • 93
    MedChemExpress pf 4136309 pf
    Pf 4136309 Pf, 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
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    91
    Cusabio platelet factor 4 pf 4 elisa kits
    Blood compatibility of the insulation materials. (A) and (C). SEM morphology images of the platelets adhering to the ANF/epoxy nanocomposite. (B) and (D) SEM morphology images of the platelets adhering to the Parylene C film. (E) The average number of the adhered platelets onto the substrates from platelet-rich plasma estimated by 5 SEM images. (F) The generated Platelet Factor <t>(PF-4)</t> and thrombin–antithrombin (TAT) of the insulation substrates with 2 h blood incubation. The normal whole blood without exposure to insulation materials was applied as the control group. Values are expressed as means ± SD, n = 3.
    Platelet Factor 4 Pf 4 Elisa Kits, supplied by Cusabio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/platelet factor 4 pf 4 elisa kits/product/Cusabio
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    platelet factor 4 pf 4 elisa kits - by Bioz Stars, 2024-02
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    93
    Tocris pf670462
    Blood compatibility of the insulation materials. (A) and (C). SEM morphology images of the platelets adhering to the ANF/epoxy nanocomposite. (B) and (D) SEM morphology images of the platelets adhering to the Parylene C film. (E) The average number of the adhered platelets onto the substrates from platelet-rich plasma estimated by 5 SEM images. (F) The generated Platelet Factor <t>(PF-4)</t> and thrombin–antithrombin (TAT) of the insulation substrates with 2 h blood incubation. The normal whole blood without exposure to insulation materials was applied as the control group. Values are expressed as means ± SD, n = 3.
    Pf670462, supplied by Tocris, 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/result/pf670462/product/Tocris
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    95
    Selleck Chemicals fak
    Sema7A upregulates endothelial cell migration and tube formation through <t>FAK/MAPK</t> signaling pathway. (A) Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor <t>(PF573228,</t> 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h and then subjected to wound healing assay at selected time points. Phase contrast images are from the start of the assay (0 h) and after 24 h. Location of initial scratch margins indicated by dashed green lines. Bar = 100 μm. (B) Quantified migration distances from A for 24 h migration ability. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (C) Representative images of transwell membranes with cells stained by crystal violet. Cells were prepared as in (A) . Bar = 50 μm. (D) Quantified numbers of migrated cells in Sema7A-pCDH-HUVECs and control pCDH-HUVECs. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (E) Sema7A-pCDH-HUVECs and control pCDH-HUVECs subjected to tube formation assay after pretreatment same as in (A) . Bar = 50 μm. (F) Quantified data from (E) for tube formation numbers. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (G–I) P-FAK (G,H) , P-ERK1/2 proteins (G,I) were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. Sema7A-pCDH-HUVECs and control pCDH-HUVECs were pretreated same as in (A) . Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001.
    Fak, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Selleck Chemicals pf 562271
    Sema7A upregulates endothelial cell migration and tube formation through <t>FAK/MAPK</t> signaling pathway. (A) Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor <t>(PF573228,</t> 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h and then subjected to wound healing assay at selected time points. Phase contrast images are from the start of the assay (0 h) and after 24 h. Location of initial scratch margins indicated by dashed green lines. Bar = 100 μm. (B) Quantified migration distances from A for 24 h migration ability. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (C) Representative images of transwell membranes with cells stained by crystal violet. Cells were prepared as in (A) . Bar = 50 μm. (D) Quantified numbers of migrated cells in Sema7A-pCDH-HUVECs and control pCDH-HUVECs. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (E) Sema7A-pCDH-HUVECs and control pCDH-HUVECs subjected to tube formation assay after pretreatment same as in (A) . Bar = 50 μm. (F) Quantified data from (E) for tube formation numbers. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (G–I) P-FAK (G,H) , P-ERK1/2 proteins (G,I) were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. Sema7A-pCDH-HUVECs and control pCDH-HUVECs were pretreated same as in (A) . Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001.
    Pf 562271, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pf 562271/product/Selleck Chemicals
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    Image Search Results


    Blood compatibility of the insulation materials. (A) and (C). SEM morphology images of the platelets adhering to the ANF/epoxy nanocomposite. (B) and (D) SEM morphology images of the platelets adhering to the Parylene C film. (E) The average number of the adhered platelets onto the substrates from platelet-rich plasma estimated by 5 SEM images. (F) The generated Platelet Factor (PF-4) and thrombin–antithrombin (TAT) of the insulation substrates with 2 h blood incubation. The normal whole blood without exposure to insulation materials was applied as the control group. Values are expressed as means ± SD, n = 3.

    Journal: bioRxiv

    Article Title: Graph Theoretical Design of Biomimetic Aramid Nanofiber Nanocomposites as Insulation Coatings for Implantable Bioelectronics

    doi: 10.1101/2020.12.28.424604

    Figure Lengend Snippet: Blood compatibility of the insulation materials. (A) and (C). SEM morphology images of the platelets adhering to the ANF/epoxy nanocomposite. (B) and (D) SEM morphology images of the platelets adhering to the Parylene C film. (E) The average number of the adhered platelets onto the substrates from platelet-rich plasma estimated by 5 SEM images. (F) The generated Platelet Factor (PF-4) and thrombin–antithrombin (TAT) of the insulation substrates with 2 h blood incubation. The normal whole blood without exposure to insulation materials was applied as the control group. Values are expressed as means ± SD, n = 3.

    Article Snippet: Platelet Factor 4 (PF-4) ELISA kits were purchased from Cusabio Biotech Co., Ltd, China; the thrombin-antithrombin III complex (TAT) ELISA kit, Enzygnost TAT micro, was purchased from Assay Pro, USA.

    Techniques: Generated, Incubation

    Sema7A upregulates endothelial cell migration and tube formation through FAK/MAPK signaling pathway. (A) Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor (PF573228, 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h and then subjected to wound healing assay at selected time points. Phase contrast images are from the start of the assay (0 h) and after 24 h. Location of initial scratch margins indicated by dashed green lines. Bar = 100 μm. (B) Quantified migration distances from A for 24 h migration ability. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (C) Representative images of transwell membranes with cells stained by crystal violet. Cells were prepared as in (A) . Bar = 50 μm. (D) Quantified numbers of migrated cells in Sema7A-pCDH-HUVECs and control pCDH-HUVECs. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (E) Sema7A-pCDH-HUVECs and control pCDH-HUVECs subjected to tube formation assay after pretreatment same as in (A) . Bar = 50 μm. (F) Quantified data from (E) for tube formation numbers. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (G–I) P-FAK (G,H) , P-ERK1/2 proteins (G,I) were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. Sema7A-pCDH-HUVECs and control pCDH-HUVECs were pretreated same as in (A) . Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001.

    Journal: Frontiers in Physiology

    Article Title: Semaphorin 7A Promotes VEGFA/VEGFR2-Mediated Angiogenesis and Intraplaque Neovascularization in ApoE -/- Mice

    doi: 10.3389/fphys.2018.01718

    Figure Lengend Snippet: Sema7A upregulates endothelial cell migration and tube formation through FAK/MAPK signaling pathway. (A) Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor (PF573228, 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h and then subjected to wound healing assay at selected time points. Phase contrast images are from the start of the assay (0 h) and after 24 h. Location of initial scratch margins indicated by dashed green lines. Bar = 100 μm. (B) Quantified migration distances from A for 24 h migration ability. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (C) Representative images of transwell membranes with cells stained by crystal violet. Cells were prepared as in (A) . Bar = 50 μm. (D) Quantified numbers of migrated cells in Sema7A-pCDH-HUVECs and control pCDH-HUVECs. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (E) Sema7A-pCDH-HUVECs and control pCDH-HUVECs subjected to tube formation assay after pretreatment same as in (A) . Bar = 50 μm. (F) Quantified data from (E) for tube formation numbers. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗∗∗∗ P < 0.0001. (G–I) P-FAK (G,H) , P-ERK1/2 proteins (G,I) were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. Sema7A-pCDH-HUVECs and control pCDH-HUVECs were pretreated same as in (A) . Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001.

    Article Snippet: Human umbilical vein endothelial cells expressing hSema7A-pCDH-GFP or pCDH-GFP were seeded in 24-well plates and allowed to attach for 24 h. When HUVEC monolayer cultures reached approximately 95–100% confluence, the cells were pre-treated with blocking antibody or inhibitors (blocking antibodies for β1 (P5D2, ab24693, Abcam, United States), inhibitors for VEGFR2 (ZM323881, HY-15467, MCE, United States), FAK (PF573228, S2013, Selleck Chemicals, United States) and MAPK (U0126, 662005, Merck Millipore, Germany).

    Techniques: Migration, Wound Healing Assay, Staining, Tube Formation Assay, Western Blot

    ROCK1 and MYPT1 are involved in Sema7A induced endothelial cell migration and tube formation through FAK/MAPK signaling pathway in a β1 integrin-dependent manner. ROCK1 (A,B) and MYPT1 (C,D) proteins were analyzed by western blotting normalized to β actin and displayed as fold-changes relative to pCDH-HUVECs. Sema7A pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor (PF573228, 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. (E,F) P-ERK1/2 proteins were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. (G,H) ROCK1 proteins were analyzed by western blotting normalized to β actin and displayed as fold-changes relative to pCDH-HUVECs. Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with integrin β1 blocking antibody (P5D2, 1 μg/mL) or VEGFR2 inhibitor (ZM323881, 10 μM) for 24 h. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. (I) Sema7A-pCDH-HUVEC and control pCDH-HUVECs cytoskeleton were stained by Phalloidin following pretreatment with blocking antibody or inhibitors as shown in figures. Bar = 10 μm. Results are representative of ≥ 3 independent experiments.

    Journal: Frontiers in Physiology

    Article Title: Semaphorin 7A Promotes VEGFA/VEGFR2-Mediated Angiogenesis and Intraplaque Neovascularization in ApoE -/- Mice

    doi: 10.3389/fphys.2018.01718

    Figure Lengend Snippet: ROCK1 and MYPT1 are involved in Sema7A induced endothelial cell migration and tube formation through FAK/MAPK signaling pathway in a β1 integrin-dependent manner. ROCK1 (A,B) and MYPT1 (C,D) proteins were analyzed by western blotting normalized to β actin and displayed as fold-changes relative to pCDH-HUVECs. Sema7A pCDH-HUVECs and pCDH-HUVECs were treated with FAK inhibitor (PF573228, 10 μM) or MAPK inhibitor (U0126, 20 μM) for 24 h. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. (E,F) P-ERK1/2 proteins were analyzed by western blotting normalized to total FAK/ERK1/2 and displayed as fold-changes relative to control pCDH-HUVECs. (G,H) ROCK1 proteins were analyzed by western blotting normalized to β actin and displayed as fold-changes relative to pCDH-HUVECs. Sema7A-pCDH-HUVECs and pCDH-HUVECs were treated with integrin β1 blocking antibody (P5D2, 1 μg/mL) or VEGFR2 inhibitor (ZM323881, 10 μM) for 24 h. Data are shown as mean ± SEM. Results are representative of ≥ 3 independent experiments. A.U = arbitrary unit. ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. (I) Sema7A-pCDH-HUVEC and control pCDH-HUVECs cytoskeleton were stained by Phalloidin following pretreatment with blocking antibody or inhibitors as shown in figures. Bar = 10 μm. Results are representative of ≥ 3 independent experiments.

    Article Snippet: Human umbilical vein endothelial cells expressing hSema7A-pCDH-GFP or pCDH-GFP were seeded in 24-well plates and allowed to attach for 24 h. When HUVEC monolayer cultures reached approximately 95–100% confluence, the cells were pre-treated with blocking antibody or inhibitors (blocking antibodies for β1 (P5D2, ab24693, Abcam, United States), inhibitors for VEGFR2 (ZM323881, HY-15467, MCE, United States), FAK (PF573228, S2013, Selleck Chemicals, United States) and MAPK (U0126, 662005, Merck Millipore, Germany).

    Techniques: Migration, Western Blot, Blocking Assay, Staining