sc 28644 Search Results


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Santa Cruz Biotechnology ve cadherin
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Santa Cruz Biotechnology rabbit anti-ve-cadherin
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
Rabbit Anti Ve Cadherin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology sc 28644
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
Sc 28644, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology vascular endothelial ve cadherin
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
Vascular Endothelial Ve Cadherin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology ve-cadherin sc-28644
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
Ve Cadherin Sc 28644, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology rabbit anti mouse ve cadherin
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
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Santa Cruz Biotechnology ve cadherin polyclonal antibody
JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of <t>VE-cadherin</t> <t>and</t> <t>α-SMA</t> is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.
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Image Search Results


JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of VE-cadherin and α-SMA is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure

doi: 10.1016/j.jbc.2022.101816

Figure Lengend Snippet: JMJD3 mediates TGFβ1-induced EndMT. A , Western blot analysis of ECs overexpressing JMJD3 by lentivirus (JMJD3OE) for 2 days following treatment with 2 ng/ml TGFβ1 or solvent for another 5 days. ECs infected with lentivirus packaging with empty vector were used as negative control (Ctl). Photos are representative of three independent experiments. B , quantification of the expression of JMJD3 and H3K27me3 is shown as means ± SD. Statistical significance between two groups was analyzed by one-way ANOVA. C , quantification of the expression of VE-cadherin and α-SMA is shown as means ± SD. Statistical significance between groups was analyzed by two-way ANOVA. D and E , ECs were treated with 2 ng/ml TGFβ1 or solvent (Ctl) for 24 h. ChIP assays with rabbit anti-H3K27me3 or anti-H3K4me3 antibody were performed. Rabbit IgG was used as control. Real-time PCR amplified VE-cadherin promoter with specific primers, respectively. Quantitative PCR data were normalized to IgG negative control and displayed as fold enrichment and expressed as means ± SD. Statistical significance between groups was analyzed by one-way ANOVA. α-SMA, α-smooth muscle actin; ChIP, chromatin immunoprecipitation; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; H3K27, histone H3 lysine 27; IgG, immunoglobulin G; JMJD3, Jumonji domain–containing protein-3; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin.

Article Snippet: : A2363, A2362, and A2361), rabbit anti-UTX (GeneTex; catalog no.: GTX12146), rabbit anti-eNOS (Cell Signaling Technology; catalog no.: 32027), rabbit anti-VE-cadherin (Santa Cruz; catalog no.: sc-28644), mouse anti-α-SMA (Sigma; catalog no.: A5228), goat anti-Hes1 (Santa Cruz; catalog no.: sc-13844), rabbit anti-PCNA (Santa Cruz; catalog no.: sc-7907), mouse anti-β-actin (GeneTex; catalog no.: GTX629630), and mouse anti-GAPDH (Santa Cruz; catalog no.: sc-32233).

Techniques: Western Blot, Infection, Plasmid Preparation, Negative Control, Expressing, Real-time Polymerase Chain Reaction, Amplification, Chromatin Immunoprecipitation

Schematic showing that decreased endothelial JMJD3 regulates neointima hyperplasia of AVFs. In CKD, Hes1 expression is induced by TGFβ1 signaling in ECs. Hes1 binds to the JMJD3 promoter and inhibits JMJD3 transcription. Decreased JMJD3 expression epigenetically reduces transcription of genes (such as VE-cadherin, eNOS and PCNA, and others) leading to EC barrier dysfunction and EndMT. Moreover, decreased JMJD3 in ECs also suppresses eNOS-NO production, promoting VSMC proliferation. These responses result in inflammation and neointima hyperplasia in AVF. AVF, arteriovenous fistula; CKD, chronic kidney disease; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; eNOS, endothelial nitric oxide synthase; JMJD3, Jumonji domain–containing protein-3; NO, nitric oxide; PCNA, proliferating cell nuclear antigen; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin; VSMC, vascular smooth muscle cell.

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure

doi: 10.1016/j.jbc.2022.101816

Figure Lengend Snippet: Schematic showing that decreased endothelial JMJD3 regulates neointima hyperplasia of AVFs. In CKD, Hes1 expression is induced by TGFβ1 signaling in ECs. Hes1 binds to the JMJD3 promoter and inhibits JMJD3 transcription. Decreased JMJD3 expression epigenetically reduces transcription of genes (such as VE-cadherin, eNOS and PCNA, and others) leading to EC barrier dysfunction and EndMT. Moreover, decreased JMJD3 in ECs also suppresses eNOS-NO production, promoting VSMC proliferation. These responses result in inflammation and neointima hyperplasia in AVF. AVF, arteriovenous fistula; CKD, chronic kidney disease; EC, endothelial cell; EndMT, endothelial–mesenchymal transition; eNOS, endothelial nitric oxide synthase; JMJD3, Jumonji domain–containing protein-3; NO, nitric oxide; PCNA, proliferating cell nuclear antigen; TGFβ1, transforming growth factor beta 1; VE-cadherin, vascular endothelial-cadherin; VSMC, vascular smooth muscle cell.

Article Snippet: : A2363, A2362, and A2361), rabbit anti-UTX (GeneTex; catalog no.: GTX12146), rabbit anti-eNOS (Cell Signaling Technology; catalog no.: 32027), rabbit anti-VE-cadherin (Santa Cruz; catalog no.: sc-28644), mouse anti-α-SMA (Sigma; catalog no.: A5228), goat anti-Hes1 (Santa Cruz; catalog no.: sc-13844), rabbit anti-PCNA (Santa Cruz; catalog no.: sc-7907), mouse anti-β-actin (GeneTex; catalog no.: GTX629630), and mouse anti-GAPDH (Santa Cruz; catalog no.: sc-32233).

Techniques: Expressing

List of primer sequences used for genotyping, plasmid construction, or ChIP–PCR

Journal: The Journal of Biological Chemistry

Article Title: Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure

doi: 10.1016/j.jbc.2022.101816

Figure Lengend Snippet: List of primer sequences used for genotyping, plasmid construction, or ChIP–PCR

Article Snippet: : A2363, A2362, and A2361), rabbit anti-UTX (GeneTex; catalog no.: GTX12146), rabbit anti-eNOS (Cell Signaling Technology; catalog no.: 32027), rabbit anti-VE-cadherin (Santa Cruz; catalog no.: sc-28644), mouse anti-α-SMA (Sigma; catalog no.: A5228), goat anti-Hes1 (Santa Cruz; catalog no.: sc-13844), rabbit anti-PCNA (Santa Cruz; catalog no.: sc-7907), mouse anti-β-actin (GeneTex; catalog no.: GTX629630), and mouse anti-GAPDH (Santa Cruz; catalog no.: sc-32233).

Techniques: Plasmid Preparation, Real-time Polymerase Chain Reaction