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human jagged 1 antibody  (Bio-Techne corporation)


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    Bio-Techne corporation human jagged 1 antibody
    Human Jagged 1 Antibody, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 94/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+jagged+1+antibody/Human+Jagged+1+Antibody/custom%40af1277%4041650956
    Average 94 stars, based on 37 article reviews
    human jagged 1 antibody - by Bioz Stars, 2026-10
    94/100 stars

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    NCF2 regulates OPN expression via <t>Notch1</t> signaling in GBM. (A) Western blot analysis showing NCF2 and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. (B) qRT-PCR analysis confirming changes in NCF2 and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. qPCR was performed in triplicate for each sample. (C) Western blot analysis of NCF2, Notch1, and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. (D) qRT-PCR analysis of NCF2 , Notch1 , and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. qPCR was performed in triplicate for each sample. (“*”represents P<0.05).
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    Figure 8. CAVIN3 deficiency downregulates <t>JAG1</t> by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.
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    Figure 8. CAVIN3 deficiency downregulates <t>JAG1</t> by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.
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    Figure 8. CAVIN3 deficiency downregulates <t>JAG1</t> by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.
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    Figure 8. CAVIN3 deficiency downregulates <t>JAG1</t> by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.
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    Image Search Results


    NCF2 regulates OPN expression via Notch1 signaling in GBM. (A) Western blot analysis showing NCF2 and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. (B) qRT-PCR analysis confirming changes in NCF2 and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. qPCR was performed in triplicate for each sample. (C) Western blot analysis of NCF2, Notch1, and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. (D) qRT-PCR analysis of NCF2 , Notch1 , and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. qPCR was performed in triplicate for each sample. (“*”represents P<0.05).

    Journal: Frontiers in Immunology

    Article Title: NCF2 facilitates M2 macrophage polarization in glioblastoma through activation of the notch1–osteopontin axis

    doi: 10.3389/fimmu.2026.1743950

    Figure Lengend Snippet: NCF2 regulates OPN expression via Notch1 signaling in GBM. (A) Western blot analysis showing NCF2 and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. (B) qRT-PCR analysis confirming changes in NCF2 and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, and in U87 and U251 cells with NCF2 overexpression. qPCR was performed in triplicate for each sample. (C) Western blot analysis of NCF2, Notch1, and OPN protein expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. (D) qRT-PCR analysis of NCF2 , Notch1 , and OPN mRNA expression in LN229 and T98G cells with NCF2 knockdown, with or without Notch1 agonist (N1A) treatment, and in U87 and U251 cells with NCF2 overexpression, with or without Notch1 inhibitor (N1i) treatment. qPCR was performed in triplicate for each sample. (“*”represents P<0.05).

    Article Snippet: To investigate the involvement of the Notch1 signaling pathway, NCF2-knockdown or NCF2-overexpressing GBM cells were treated with either a Notch1 agonist (recombinant human Jagged1, 2 μg/mL; AF1277;R&D Systems) or a Notch1 inhibitor (DAPT, 10 μM; 2634; R&D Systems) for 48 h. Following treatment, the protein and mRNA expression levels of Notch1 and OPN were analyzed by western blot and qRT-PCR.

    Techniques: Expressing, Western Blot, Knockdown, Over Expression, Quantitative RT-PCR

    Figure 8. CAVIN3 deficiency downregulates JAG1 by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.

    Journal: JCI insight

    Article Title: CAVIN3 deficiency promotes vascular normalization in ocular neovascular disease via ERK/JAG1 signaling pathway.

    doi: 10.1172/jci.insight.187836

    Figure Lengend Snippet: Figure 8. CAVIN3 deficiency downregulates JAG1 by inhibiting ERK phosphorylation. (A) A volcano plot displays DEGs of CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (B) GO analysis revealed the enrichment of significant DEGs in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (C) A heatmap illustrates the expression of NOTCH signaling pathway ligand receptors, including JAG1, in CAVIN3-siRNA–treated HUVECs versus scramble siRNA–treated HUVECs. (D) mRNA levels of JAG1 in HUVECs and HRMECs after control or hypoxic treatment. n = 3 per group.

    Article Snippet: For anti-JAG1 treatment, HRMECs were maintained in a complete medium supplemented with anti-JAG1 antibody (60 μg/mL; R&D Systems, catalog AF1277) for 24 hours before collection.

    Techniques: Phospho-proteomics, Expressing, Control

    Figure 10. Jag1 is regulated by endothelial Cavin3. (A) Experimental protocols for B and C. (B) Immunofluorescent staining of IB4 in retinas from PBS-treated OIR mice injected with AAV-Cavin3/AAV-blank or anti-JAG1–treated OIR mice injected with AAV-Cavin3/AAV-blank on P17. n = 6 per group. Blue areas indicate NVT areas, while orange areas mark avascular areas. Scale bars: 50 μm. (C) Immunofluorescent staining of IB4 and FITC-dextran in the RPE-choroid-sclera complex of PBS-treated CNV mice injected with AAV-Cavin3/AAV-blank or anti-JAG1–treated CNV mice injected with AAV-Cavin3/AAV-blank. n = 12 burns per group. Scale bars: 100 μm. Data are presented as mean ± SD. *P < 0.05; **P < 0.01 by 1-way ANOVA with Tukey’s multiple-comparison test.

    Journal: JCI insight

    Article Title: CAVIN3 deficiency promotes vascular normalization in ocular neovascular disease via ERK/JAG1 signaling pathway.

    doi: 10.1172/jci.insight.187836

    Figure Lengend Snippet: Figure 10. Jag1 is regulated by endothelial Cavin3. (A) Experimental protocols for B and C. (B) Immunofluorescent staining of IB4 in retinas from PBS-treated OIR mice injected with AAV-Cavin3/AAV-blank or anti-JAG1–treated OIR mice injected with AAV-Cavin3/AAV-blank on P17. n = 6 per group. Blue areas indicate NVT areas, while orange areas mark avascular areas. Scale bars: 50 μm. (C) Immunofluorescent staining of IB4 and FITC-dextran in the RPE-choroid-sclera complex of PBS-treated CNV mice injected with AAV-Cavin3/AAV-blank or anti-JAG1–treated CNV mice injected with AAV-Cavin3/AAV-blank. n = 12 burns per group. Scale bars: 100 μm. Data are presented as mean ± SD. *P < 0.05; **P < 0.01 by 1-way ANOVA with Tukey’s multiple-comparison test.

    Article Snippet: For anti-JAG1 treatment, HRMECs were maintained in a complete medium supplemented with anti-JAG1 antibody (60 μg/mL; R&D Systems, catalog AF1277) for 24 hours before collection.

    Techniques: Staining, Injection, Comparison