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control viruses ad gfp  (R&D Systems)


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    R&D Systems control viruses ad gfp
    Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 <t>(rhCCN2)</t> increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.
    Control Viruses Ad Gfp, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rhccn2/pm36625347-202-46-55?v=R%26D+Systems
    Average 93 stars, based on 14 article reviews
    control viruses ad gfp - by Bioz Stars, 2026-07
    93/100 stars

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    1) Product Images from "CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development."

    Article Title: CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development.

    Journal: JCI insight

    doi: 10.1172/jci.insight.162987

    Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.
    Figure Legend Snippet: Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.

    Techniques Used: Expressing, Western Blot, Biomarker Discovery, Co-Immunoprecipitation Assay, Negative Control, Positive Control, Recombinant, Phospho-proteomics



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    Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 <t>(rhCCN2)</t> increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.
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    Image Search Results


    Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.

    Journal: JCI insight

    Article Title: CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development.

    doi: 10.1172/jci.insight.162987

    Figure Lengend Snippet: Figure 7. CCN2 interacts with and potentiates TGF-β1 receptor signaling. (A) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot (n = 3). Target protein levels were normalized to Vinculin. *P < 0.05, **P < 0.01, compared with time point 0, using 1-way ANOVA. (B) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). (C) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot (n = 3). Target protein levels were normalized to β-actin. **P < 0.01, ***P < 0.001; ****P < 0.0001 (compared with nontreatment [N] group); ##P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.

    Article Snippet: Adenoviruses used for CCN2 overexpression (Ad-GFP-hCTGF, ADV-206232) and knockdown (Ad-GFP-U6-h-CTGF-shRNA, shADV-206232) studies, henceforth AdCCN2 and shCCN2, and control viruses (Ad-GFP, Ad-GFP-U6-scrmb-shRNA), henceforth AdCtrl and shCtrl, were purchased from Vector Biolabs. siRNAs used for human TGF-β receptor knockdown (TGFBR1-7046, TGFFBR2-7048, and Nontargeting Pool) were purchased from Horizon. rhCCN2 (9190-cc) and TGF-β1 (rhTGF-β1, 240-B/CF) were purchased form R&D Systems and reconstituted in sterile PBS and 4 mM HCl-0.1% BSA, respectively, as recommended by the manufacturer.

    Techniques: Expressing, Western Blot, Biomarker Discovery, Co-Immunoprecipitation Assay, Negative Control, Positive Control, Recombinant, Phospho-proteomics

    ( A ) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot ( n = 3). Target protein levels were normalized to Vinculin. * P < 0.05, ** P < 0.01, compared with time point 0, using 1-way ANOVA. ( B ) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). ( C ) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot ( n = 3). Target protein levels were normalized to β-actin. ** P < 0.01, *** P < 0.001; **** P < 0.0001 (compared with nontreatment [N] group); ## P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.

    Journal: JCI Insight

    Article Title: CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development

    doi: 10.1172/jci.insight.162987

    Figure Lengend Snippet: ( A ) TGF-β1 (1 ng/mL) induces protein expression of CCN2, αSMA, and SM22 in HASMCs by Western blot ( n = 3). Target protein levels were normalized to Vinculin. * P < 0.05, ** P < 0.01, compared with time point 0, using 1-way ANOVA. ( B ) Validation of physical interaction between CCN2 and TGF-β1/TGF-β receptor II via Co-IP followed by Western blot. Column 3 indicate positive bands for TGFBR2 (75 kD) and TGF-β1 (25 kD) in sediment precipitated with anti-CCN2 antibody; column 1, 20% input; column 2, IgG (negative control); column 4, TGFBR2 (positive control); column 5, TGF-β1 (positive control). ( C ) Supplementation of recombinant human CCN2 (rhCCN2) increases TGF-β receptor II phosphorylation and potentiates TGF-β1–induced Smad-3 phosphorylation in HASMCs by Western blot ( n = 3). Target protein levels were normalized to β-actin. ** P < 0.01, *** P < 0.001; **** P < 0.0001 (compared with nontreatment [N] group); ## P < 0.01 (compared with TGF-β1-only [T] group); 1-way ANOVA.

    Article Snippet: Adenoviruses used for CCN2 overexpression (Ad-GFP-hCTGF, ADV-206232) and knockdown (Ad-GFP-U6-h-CTGF-shRNA, shADV-206232) studies, henceforth AdCCN2 and shCCN2, and control viruses (Ad-GFP, Ad-GFP-U6-scrmb-shRNA), henceforth AdCtrl and shCtrl, were purchased from Vector Biolabs. siRNAs used for human TGF-β receptor knockdown (TGFBR1-7046, TGFFBR2-7048, and Nontargeting Pool) were purchased from Horizon. rhCCN2 (9190-cc) and TGF-β1 (rhTGF-β1, 240-B/CF) were purchased form R&D Systems and reconstituted in sterile PBS and 4 mM HCl-0.1% BSA, respectively, as recommended by the manufacturer.

    Techniques: Expressing, Western Blot, Biomarker Discovery, Co-Immunoprecipitation Assay, Negative Control, Positive Control, Recombinant, Phospho-proteomics