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抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Grx1 (显示 GRX1 抗体) deficiency leads to eNOS (显示 NOS3 抗体) dysfunction through oxidative modification of S-glutathionylation of eNOS (eNOS (显示 NOS3 抗体)-SSG) and inactivation of NO production, enhancing the endothelial TLR4 (显示 TLR4 抗体) activation, and ultimately exacerbating necrotizing enterocolitis severity.
Study reports a decrease of Grx (显示 GRX1 抗体) expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin (显示 INS 抗体) secretion, increase of reactive oxygen species (ROS (显示 ROS1 抗体)) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx (显示 GRX1 抗体) system for the beta-cell during metabolic stress which may provide a new target for diabetes mellitus type 2 treatment.
Our results indicate that Grx1 (显示 GRX1 抗体) upregulation promotes neuroinflammation and consequent neuronal cell death in vitro, and synergizes with proinflammatory insults to promote DA loss in vivo.
the Glrx1 (显示 GRX1 抗体)-Protein S-glutathionylation axis plays a pivotal role in house dust mite-induced allergic airways disease.
Glrx (显示 GRX1 抗体) ablation stabilizes HIF-1alpha (显示 HIF1A 抗体) by increasing GSH adducts on Cys (显示 DNAJC5 抗体)(520) promoting in vivo HIF-1alpha (显示 HIF1A 抗体) stabilization, VEGF-A (显示 VEGFA 抗体) production, and revascularization in the ischemic muscles.
Prx2 (显示 PRRX2 抗体) glutathionylation is a favorable reaction that can occur in cells under oxidative stress and may have a role in redox signaling. GSH/Grx1 (显示 GRX1 抗体) provide an alternative mechanism to thioredoxin (显示 TXN 抗体) and thioredoxin reductase (显示 PRDX2 抗体) for Prx2 (显示 PRRX2 抗体) recycling.
The temporal relationships of Glrx1 (显示 GRX1 抗体) with protein S-glutathionylation, glutathione, and cytokines/chemokines were observed as dynamic changes in lungs with allergic airway inflammation
Glutaredoxin 1 (显示 GRX1 抗体) plays an important role in controlling epithelial cell responsiveness to IL-17A (显示 IL17A 抗体)
Up-r (显示 GRX1 抗体)egulated Glrx inhibits VEGF signaling by increa (显示 FLT1 抗体)sed Flt1 causing impaired vascularization.
S-glutathionylation of Fas (显示 FAS 抗体) in lung epithelium enhances epithelial apoptosis and clearance of P. aeruginosa. Glutaredoxin-1 (显示 GRX1 抗体) impairs bacterial clearance and increases severity of pneumonia in association with deglutathionylation of Fas (显示 FAS 抗体).
Reduction potentials of protein disulfides and catalysis of glutathionylation and deglutathionylation by glutaredoxin (显示 GRX1 抗体) enzymes
GRX1 (显示 GRX1 抗体) overexpression constrains oxidative stress and apoptosis in osteoarthritis chondrocytes by regulating CREB (显示 CREB1 抗体)/HO-1 (显示 HMOX1 抗体), providing a novel insight into the molecular mechanism and potential treatment of osteoarthritis.
Glutaredoxin (显示 GRX1 抗体) desensitizes lens to oxidative stress by connecting and integrating specific signaling and transcriptional regulation for antioxidant response.
The results demonstrate that the antiproliferative effect of NO is hampered by Trx1 (显示 MLL 抗体) and Grx1 (显示 GRX1 抗体) and support the strategy of weakening the thiolic antioxidant defenses when designing new antitumoral therapies.
Prx2 (显示 PRDX2 抗体) glutathionylation is a favorable reaction that can occur in cells under oxidative stress and may have a role in redox signaling. GSH/Grx1 (显示 GRX1 抗体) provide an alternative mechanism to thioredoxin (显示 TXN 抗体) and thioredoxin reductase (显示 PRDX5 抗体) for Prx2 (显示 PRDX2 抗体) recycling.
Glutaredoxin 1 (显示 GRX1 抗体) protects human retinal pigment epithelial cells from oxidative damage by preventing AKT (显示 AKT1 抗体) glutathionylation.
A new function for GRX1 (显示 GRX1 抗体) in neuronal copper homeostasis and in protection from copper-mediated oxidative injury.
Human Grx1 (显示 GRX1 抗体) can catalyse reduction of Atox1 (显示 ATOX1 抗体) by glutathione but only in the presence of Cu(I).
This gene encodes a member of the glutaredoxin family. The encoded protein is a cytoplasmic enzyme catalyzing the reversible reduction of glutathione-protein mixed disulfides. This enzyme highly contributes to the antioxidant defense system. It is crucial for several signalling pathways by controlling the S-glutathionylation status of signalling mediators. It is involved in beta-amyloid toxicity and Alzheimer's disease. Multiple alternatively spliced transcript variants encoding the same protein have been identified.
, glutaredoxin (thioltransferase)
, glutaredoxin 1 (thioltransferase)