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Gene Information
Gene symbol: GPX1
Gene name: glutathione peroxidase 1
HGNC ID: 4553
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | ABL1 | 1 hits |
| 2 | AKT1 | 1 hits |
| 3 | ALB | 1 hits |
| 4 | CASP3 | 1 hits |
| 5 | CAT | 1 hits |
| 6 | INS | 1 hits |
| 7 | MAFA | 1 hits |
| 8 | MGEA5 | 1 hits |
| 9 | MMP9 | 1 hits |
| 10 | OGT | 1 hits |
| 11 | PAX3 | 1 hits |
| 12 | SOD1 | 1 hits |
| 13 | TP53 | 1 hits |
| 14 | VEGFA | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 15827346 | Compared with normal mice, diabetic Gpx1+/+ and -/- mice had a two- to threefold increase in urine albumin excretion at 2 and 4 mo of diabetes. |
| 2 | 17066087 | Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysed erythrocytes. |
| 3 | 17275003 | Multivariate logistic regression analysis with adjustment for the prevalence of diabetes mellitus revealed that the 1615G-->A polymorphism of BCHE, the 7,067,365C-->A polymorphism of INSR, the C-->T polymorphism of GPX1, the G-->A polymorphism of ROS1, and the G-->A polymorphism of MMP9 were associated (P<0.05) with in-stent restenosis. |
| 4 | 18387670 | Moreover, we found that maternal diabetes causes decreased expression of genes involved in the oxidative stress defense system (CuZnSOD in non-malformed D11 embryos, MnSOD at all gestational time points, ECSOD and Gpx-1 at GD11-GD15, CAT and Gpx-2 at GD15), decreased expression of Pax-3 at GD11, and increased expression of Vegf-A at all gestational time points. |
| 5 | 18728230 | In MDm embryos, we detected increased activated caspase-3 immunostaining in the first visceral arch and cardiac area and decreased Gpx-1 immunostaining in the cardiac tissue; both findings differed from the caspase/Gpx-1 immunostaining of the MDn and N embryos. |
| 6 | 19808019 | The increased insulin sensitivity in Gpx1(-/-) mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the antioxidant N-acetylcysteine. |
| 7 | 19819955 | Importantly, the loss of intranuclear musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) that was observed in nontransgenic db/db mice was prevented by GPx-1 overexpression, making this a likely mechanism for the improved glycemic control. |
| 8 | 19944066 | Here, we report that hyperglycemia-induced protein glycosylation by O-linked N-acetylglucosamine (O-GlcNAc) is crucial for activation of GPX1 and for its binding to c-Abl and Arg kinases. |
| 9 | 19944066 | GPX1 itself is modified with O-GlcNAc on its C-terminus. |
| 10 | 19944066 | We also demonstrate that pharmacological injection of the O-GlcNAcase inhibitor NTZ induces GPX1 activation in the mouse liver. |
| 11 | 20586612 | Null of SOD1 and GPX1 elevated respective islet superoxide and hydroperoxide production, and upregulated p53 phosphorylation. |
| 12 | 20618069 | Although knockouts of Gpx1 and Sod1 each alone or together decreased pancreatic ? cell mass and plasma insulin concentrations, these knockouts improved body insulin sensitivity to different extents. |
| 13 | 20618069 | Phenotypes resulted from altering GPX1 and/or SOD1 were partly mediated through these factors, along with protein kinase B and c-jun terminal kinase. |