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primary antibodies against plau  (Proteintech)


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    Proteintech primary antibodies against plau
    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
    Primary Antibodies Against Plau, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against plau/product/Proteintech
    Average 94 stars, based on 44 article reviews
    primary antibodies against plau - by Bioz Stars, 2026-03
    94/100 stars

    Images

    1) Product Images from "Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling"

    Article Title: Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.67.1.31

    In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
    Figure Legend Snippet: In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.

    Techniques Used: In Vitro, Western Blot, Expressing, Irradiation



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    primary antibodies against plau  (Proteintech)
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    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
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    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
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    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
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    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
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    urokinase type plasminogen activator upa  (MedChemExpress)
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    In vitro experiments confirming ellagic acid (EA) target on <t>PLAU</t> to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.
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    Image Search Results


    UPA inhibits inflammation by silencing IFIT3 in LPS-stimulated macrophages. ( A ) mRNA levels of IFIT3, TNF-α, IL-1β and IL-6 in 100 ng/mL LPS-stimulated macrophages with untreated or treated with 100 nM and 400 nM UPA. ( B ) Protein levels of STAT1, pSTAT1, STAT2, pSTAT2 and IFIT3 among cell-groups. ( C ) Schematic diagram of relation among UPA, IFIT3 and STAT1/2 pathways. Data was presented as mean ± SD from 3 independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Journal of Inflammation Research

    Article Title: Downregulation of IFIT3 Relieves the Inflammatory Response in Ulcerative Colitis via Selectively Regulating Macrophage M1 Polarization and the STAT1/2 Signaling Pathway

    doi: 10.2147/JIR.S542033

    Figure Lengend Snippet: UPA inhibits inflammation by silencing IFIT3 in LPS-stimulated macrophages. ( A ) mRNA levels of IFIT3, TNF-α, IL-1β and IL-6 in 100 ng/mL LPS-stimulated macrophages with untreated or treated with 100 nM and 400 nM UPA. ( B ) Protein levels of STAT1, pSTAT1, STAT2, pSTAT2 and IFIT3 among cell-groups. ( C ) Schematic diagram of relation among UPA, IFIT3 and STAT1/2 pathways. Data was presented as mean ± SD from 3 independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Additionally, M0 THP-1 macrophages were pretreated with 100 nM and 400 nM UPA (#HY-19569, Medchemexpress, New Jersey, USA) for 1 hour prior to stimulation with 100 ng/mL LPS.

    Techniques:

    In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling

    doi: 10.1167/iovs.67.1.31

    Figure Lengend Snippet: In vitro experiments confirming ellagic acid (EA) target on PLAU to regulate NF-κB signaling pathway in corneal endothelial cells. ( A – C ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in H 2 O 2 -treated B4G12 cells, with or without EA treatment. The relative protein expression levels are shown for B PLAU and C the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( D – F ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 in UVA-irradiated B4G12 cells, with or without EA treatment. Relative protein expression levels are shown for E PLAU and F the ratio of phospho-NF-κB p65 to total NF-κB p65 ( n = 3). ( G – I ) Western blot analysis of PLAU, NF-κB p65, and phospho-NF-κB p65 following siPLAU treatment in H 2 O 2 -treated B4G12 cells, with or without EA. Relative protein expression levels are presented for G PLAU and I the ratio of phospho-NF-κB p65 to NF-κB p65 ( n = 3 for PLAU, and n = 4 for phospho-NF-κB p65 to NF-κB p65). ( J ) Schematic diagram illustrating the proposed anti-inflammatory and anti-oxidant mechanisms of EA in FECD, highlighting its role in modulating the NF-κB pathway. All data are presented as mean ± SD. * P < 0.05, ** P < 0.01 by 1-way ANOVA with Tukey’s post hoc test.

    Article Snippet: Primary antibodies against PLAU (Proteintech, China; #17968-1-AP), NF-κB p65 (Abcam, UK; #ab32536), phospho-NF-κB p65 (S536; Abcam, UK; #ab76302), GAPDH (ABclonal, China; #AC002), and β-Actin (ABclonal, China; #AC004) were applied overnight at 4°C.

    Techniques: In Vitro, Western Blot, Expressing, Irradiation