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Gene Information
Gene symbol: MIRN146A
Gene name: microRNA 146a
HGNC ID: 31533
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | CCL2 | 1 hits |
| 2 | ERBB4 | 1 hits |
| 3 | NOTCH1 | 1 hits |
| 4 | ZC3H12A | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 27913625 | Absence of miR-146a in Podocytes Increases Risk of Diabetic Glomerulopathy via Up-regulation of ErbB4 and Notch-1. |
| 2 | 27913625 | The miR-146a targets, Notch-1 and ErbB4, were also significantly up-regulated in the glomeruli of diabetic patients and mice, suggesting induction of the downstream TGFβ signaling. |
| 3 | 27913625 | Treatment of podocytes in vitro with TGF-β1 resulted in increased expression of Notch-1, ErbB4, pErbB4, and pEGFR, the heterodimerization partner of ErbB4, suggesting increased ErbB4/EGFR signaling. |
| 4 | 27913625 | TGF-β1 also increased levels of inflammatory cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppressor of miR-146a, suggesting an autocrine loop. |
| 5 | 27913625 | Inhibition of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this signaling. |
| 6 | 27913625 | They also point to ErbB4/EGFR as a novel, druggable target for therapeutic intervention, especially because several pan-ErbB inhibitors are clinically available. |
| 7 | 27913625 | Absence of miR-146a in Podocytes Increases Risk of Diabetic Glomerulopathy via Up-regulation of ErbB4 and Notch-1. |
| 8 | 27913625 | The miR-146a targets, Notch-1 and ErbB4, were also significantly up-regulated in the glomeruli of diabetic patients and mice, suggesting induction of the downstream TGFβ signaling. |
| 9 | 27913625 | Treatment of podocytes in vitro with TGF-β1 resulted in increased expression of Notch-1, ErbB4, pErbB4, and pEGFR, the heterodimerization partner of ErbB4, suggesting increased ErbB4/EGFR signaling. |
| 10 | 27913625 | TGF-β1 also increased levels of inflammatory cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppressor of miR-146a, suggesting an autocrine loop. |
| 11 | 27913625 | Inhibition of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this signaling. |
| 12 | 27913625 | They also point to ErbB4/EGFR as a novel, druggable target for therapeutic intervention, especially because several pan-ErbB inhibitors are clinically available. |
| 13 | 27913625 | Absence of miR-146a in Podocytes Increases Risk of Diabetic Glomerulopathy via Up-regulation of ErbB4 and Notch-1. |
| 14 | 27913625 | The miR-146a targets, Notch-1 and ErbB4, were also significantly up-regulated in the glomeruli of diabetic patients and mice, suggesting induction of the downstream TGFβ signaling. |
| 15 | 27913625 | Treatment of podocytes in vitro with TGF-β1 resulted in increased expression of Notch-1, ErbB4, pErbB4, and pEGFR, the heterodimerization partner of ErbB4, suggesting increased ErbB4/EGFR signaling. |
| 16 | 27913625 | TGF-β1 also increased levels of inflammatory cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 induced protein-1 (MCPIP1), a suppressor of miR-146a, suggesting an autocrine loop. |
| 17 | 27913625 | Inhibition of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this signaling. |
| 18 | 27913625 | They also point to ErbB4/EGFR as a novel, druggable target for therapeutic intervention, especially because several pan-ErbB inhibitors are clinically available. |