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Gene Information
Gene symbol: CSE
Gene name: choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)
HGNC ID: 2430
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | CBS | 1 hits |
| 2 | JUP | 1 hits |
| 3 | NPHS1 | 1 hits |
| 4 | SIRT1 | 1 hits |
| 5 | TJP2 | 1 hits |
| 6 | TP53 | 1 hits |
| 7 | TRPC6 | 1 hits |
| 8 | TXN | 1 hits |
| 9 | TXNIP | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 26261567 | Then, ZO-2, nephrin, β-catenin, and cystathionine γ-lyase (CSE) protein expression levels were determined by western blot. |
| 2 | 26261567 | We found that high glucose significantly reduced nephrin, ZO-2, and CSE expression levels (P<0.05), and overtly elevated β-catenin amounts (P<0.05), in a time-dependent manner. |
| 3 | 26261567 | Likewise, PPG at different concentrations in normal glucose resulted in significantly lower CSE, ZO-2, and nephrin levels (P<0.05), and increased β-catenin amounts (P<0.05). |
| 4 | 26261567 | Interestingly, significantly increased ZO-2 and nephrin levels, and overtly reduced β-catenin amounts were observed in the HG + NaHS group compared with HG treated cells (P<0.01). |
| 5 | 26261567 | Compared with NG treated cells, decreased ZO-2 and nephrin levels and higher β-catenin amounts were obtained in the HG + NaHS group. |
| 6 | 26261567 | In conclusion,CSE downregulation contributes to hyperglycemia induced podocyte injury, which is alleviated by exogenous H2S possibly through ZO-2 upregulation and the subsequent suppression of Wnt/β-catenin pathway. |
| 7 | 30639567 | Given that Trx/ASK1/P38 signaling pathway mediates many oxidative cell responses, we tested whether and how H2S affected this pathway. |
| 8 | 30639567 | Further analysis revealed that H2S did not affect the protein level of TXNIP and Trx, two pivotal regulators of ASK1/P38 activation, but it promoted the dissociation of Trx from TXNIP. |
| 9 | 30639567 | In HepG2 cells, inhibition of H2S-producing enzyme cystathionine γ-lyase (CSE) increased Trx oxidation, promoted Trx binding to TXNIP and exaggerated cell injury caused by Trx inhibition. |
| 10 | 30639567 | Collectively, our results indicate that H2S exerted its antioxidative effects through the regulation of the redox state of Trx and interference with Trx/ASK1/P38 signaling pathway. |
| 11 | 31865328 | Taurine Supplementation Reverses Diabetes-Induced Podocytes Injury via Modulation of the CSE/TRPC6 Axis and Improvement of Mitochondrial Function. |
| 12 | 34396581 | Exercise training ameliorates early diabetic kidney injury by regulating the H2 S/SIRT1/p53 pathway. |
| 13 | 34396581 | Exercise training enhanced renal sirtuin 1 (SIRT1) expression in diabetic mice, accompanied by an inhibition of the p53-#ediated pro-apoptotic pathway. |
| 14 | 34396581 | NaHS treatment restored SIRT1 expression, inhibited the p53-mediated pro-apoptotic pathway and attenuated diabetes-associated apoptosis and renal injury. |
| 15 | 34396581 | In high glucose-treated MPC5 podocytes, NaHS treatment inhibited the p53-mediated pro-apoptotic pathway and podocyte apoptosis in a SIRT1-dependent manner. |
| 16 | 34396581 | Collectively, exercise training upregulated CBS/CSE expression and enhanced the endogenous H2 S production in renal tissues, thereby contributing to the modulation of the SIRT1/p53 apoptosis pathway and improvement of diabetic nephropathy. |