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goat anti human zonula occludens 1 zo 1 primary antibody  (Proteintech)


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    Structured Review

    Proteintech goat anti human zonula occludens 1 zo 1 primary antibody
    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein <t>ZO-1.</t> All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.
    Goat Anti Human Zonula Occludens 1 Zo 1 Primary Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 97/100, based on 2059 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/goat anti human zonula occludens 1 zo 1 primary antibody/product/Proteintech
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    Images

    1) Product Images from "MiR-21 modulates P.g- LPS induced apoptosis and inflammatory response in HUVECs via NF-κB/iNOS/NO pathway by targeting PDCD4"

    Article Title: MiR-21 modulates P.g- LPS induced apoptosis and inflammatory response in HUVECs via NF-κB/iNOS/NO pathway by targeting PDCD4

    Journal: Non-coding RNA Research

    doi: 10.1016/j.ncrna.2025.10.001

    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein ZO-1. All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.
    Figure Legend Snippet: Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein ZO-1. All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.

    Techniques Used: CCK-8 Assay, Incubation, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control, Immunofluorescence, Cell Counting, Standard Deviation



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    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein <t>ZO-1.</t> All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.
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    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein <t>ZO-1.</t> All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.
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    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein <t>ZO-1.</t> All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.
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    Image Search Results


    Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein ZO-1. All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.

    Journal: Non-coding RNA Research

    Article Title: MiR-21 modulates P.g- LPS induced apoptosis and inflammatory response in HUVECs via NF-κB/iNOS/NO pathway by targeting PDCD4

    doi: 10.1016/j.ncrna.2025.10.001

    Figure Lengend Snippet: Dose-and time-dependent induction of inflammation and apoptosis in HUVECs following P.g- LPS exposure. (a) CCK-8 assay demonstrating decreased cell viability after 12, 24, and 32-h incubation with P.g- LPS at concentrations ranging from 0 μg/mL to 1 μg/mL. (b–c) ELISA quantification of IL-6 and TNF-α in supernatants. (d–e) Western blot analysis showing increased expression of apoptotic markers Bax and cleaved caspase-3. β-actin was used as a loading control. (f–g) Immunofluorescence showed an increase in P.g -LPS and a decrease in the expression of tight junction protein ZO-1. All data are presented as the mean ± SD. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001. Abbreviations: HUVECs = Human umbilical vein endothelial cells; P.g -LPS = Porphyromonas gingivalis lipopolysaccharide; CCK-8 = Cell Counting Kit-8; IL-6 = Interleukin-6; TNF-α = Tumor necrosis factor-alpha; ZO-1 = Zonula Occludens-1; SD = Standard deviation.

    Article Snippet: The coverslips with cells were incubated with goat anti-human Zonula Occludens-1 (ZO-1) primary antibody (Proteintech, 21773-1-AP, 1:200) overnight at 4 °C.

    Techniques: CCK-8 Assay, Incubation, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control, Immunofluorescence, Cell Counting, Standard Deviation

    Assessment of morphological damage of RPE in MASP-1 and/or MASP-3 deficient mice 7 d after NaIO 3 injection. (A) RPE flat mounts were used to assess the central, middle, and peripheral regions of the retina. Central region is near the optic nerve. Middle and peripheral regions are 700 µm and 1400 µm from the central region, respectively. (B) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts at low magnification. The area of inside white lines shows the necrotic area of RPE flat mounts. Scale bars represent 500 µm. (C) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts high magnification images of the central, middle, and peripheral region. Scale bars represent 100 µm. (D) To quantify RPE damage, the percentage of necrotic RPE area to total RPE area in each mouse was calculated. Error bars indicate SEM of the mean (n = 3). Statistical comparisons were performed using Dunnett’s multiple comparisons test ( * P < 0.05 versus NaIO 3 -injected WT group).

    Journal: Frontiers in Immunology

    Article Title: Roles of MASP-1 and MASP-3 in the development of retinal degeneration in a murine model of dry age-related macular degeneration

    doi: 10.3389/fimmu.2025.1566018

    Figure Lengend Snippet: Assessment of morphological damage of RPE in MASP-1 and/or MASP-3 deficient mice 7 d after NaIO 3 injection. (A) RPE flat mounts were used to assess the central, middle, and peripheral regions of the retina. Central region is near the optic nerve. Middle and peripheral regions are 700 µm and 1400 µm from the central region, respectively. (B) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts at low magnification. The area of inside white lines shows the necrotic area of RPE flat mounts. Scale bars represent 500 µm. (C) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts high magnification images of the central, middle, and peripheral region. Scale bars represent 100 µm. (D) To quantify RPE damage, the percentage of necrotic RPE area to total RPE area in each mouse was calculated. Error bars indicate SEM of the mean (n = 3). Statistical comparisons were performed using Dunnett’s multiple comparisons test ( * P < 0.05 versus NaIO 3 -injected WT group).

    Article Snippet: They were then incubated overnight at 4˚C with a rabbit anti-zonula occludens-1 (ZO-1) polyclonal primary antibody (1:100; Proteintech, Rosemont, IL, USA).

    Techniques: Injection, Immunofluorescence

    Assessment of morphological damage of RPE in MASP-1 and/or MASP-3 deficient mice 7 d after NaIO 3 injection. (A) RPE flat mounts were used to assess the central, middle, and peripheral regions of the retina. Central region is near the optic nerve. Middle and peripheral regions are 700 µm and 1400 µm from the central region, respectively. (B) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts at low magnification. The area of inside white lines shows the necrotic area of RPE flat mounts. Scale bars represent 500 µm. (C) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts high magnification images of the central, middle, and peripheral region. Scale bars represent 100 µm. (D) To quantify RPE damage, the percentage of necrotic RPE area to total RPE area in each mouse was calculated. Error bars indicate SEM of the mean (n = 3). Statistical comparisons were performed using Dunnett’s multiple comparisons test ( * P < 0.05 versus NaIO 3 -injected WT group).

    Journal: Frontiers in Immunology

    Article Title: Roles of MASP-1 and MASP-3 in the development of retinal degeneration in a murine model of dry age-related macular degeneration

    doi: 10.3389/fimmu.2025.1566018

    Figure Lengend Snippet: Assessment of morphological damage of RPE in MASP-1 and/or MASP-3 deficient mice 7 d after NaIO 3 injection. (A) RPE flat mounts were used to assess the central, middle, and peripheral regions of the retina. Central region is near the optic nerve. Middle and peripheral regions are 700 µm and 1400 µm from the central region, respectively. (B) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts at low magnification. The area of inside white lines shows the necrotic area of RPE flat mounts. Scale bars represent 500 µm. (C) Representative images of immunofluorescence of ZO-1 (in green) on RPE flat mounts high magnification images of the central, middle, and peripheral region. Scale bars represent 100 µm. (D) To quantify RPE damage, the percentage of necrotic RPE area to total RPE area in each mouse was calculated. Error bars indicate SEM of the mean (n = 3). Statistical comparisons were performed using Dunnett’s multiple comparisons test ( * P < 0.05 versus NaIO 3 -injected WT group).

    Article Snippet: They were then incubated overnight at 4 ̊C with a rabbit anti-zonula occludens-1 (ZO-1) polyclonal primary antibody (1:100; Proteintech, Rosemont, IL, USA).

    Techniques: Injection, Immunofluorescence