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Data suggest an essential role of hepatic Glrx in regulating SirT1 (zeige SIRT1 Antikörper), which controls protein glutathione adducts in the pathogenesis of hepatic steatosis.
Grx1 deficiency leads to eNOS (zeige NOS3 Antikörper) dysfunction through oxidative modification of S-glutathionylation of eNOS (eNOS (zeige NOS3 Antikörper)-SSG) and inactivation of NO production, enhancing the endothelial TLR4 (zeige TLR4 Antikörper) activation, and ultimately exacerbating necrotizing enterocolitis severity.
Study reports a decrease of Grx expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin (zeige INS Antikörper) secretion, increase of reactive oxygen species (ROS (zeige ROS1 Antikörper)) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx 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 upregulation promotes neuroinflammation and consequent neuronal cell death in vitro, and synergizes with proinflammatory insults to promote DA loss in vivo.
the Glrx1-Protein S-glutathionylation axis plays a pivotal role in house dust mite-induced allergic airways disease.
Glrx ablation stabilizes HIF-1alpha (zeige HIF1A Antikörper) by increasing GSH adducts on Cys (zeige DNAJC5 Antikörper)(520) promoting in vivo HIF-1alpha (zeige HIF1A Antikörper) stabilization, VEGF-A (zeige VEGFA Antikörper) production, and revascularization in the ischemic muscles.
Prx2 (zeige PRRX2 Antikörper) glutathionylation is a favorable reaction that can occur in cells under oxidative stress and may have a role in redox signaling. GSH/Grx1 provide an alternative mechanism to thioredoxin (zeige TXN Antikörper) and thioredoxin reductase (zeige PRDX2 Antikörper) for Prx2 (zeige PRRX2 Antikörper) recycling.
The temporal relationships of Glrx1 with protein S-glutathionylation, glutathione, and cytokines/chemokines were observed as dynamic changes in lungs with allergic airway inflammation
Glutaredoxin 1 plays an important role in controlling epithelial cell responsiveness to IL-17A (zeige IL17A Antikörper)
Up-regulated Glrx inhibits VEGF signaling by increa (zeige FLT1 Antikörper)sed Flt1 causing impaired vascularization.
Overexpression of NOS3 (zeige NANOS3 Antikörper) increased the levels and activities of proteins of the redoxin systems, Trx1 (zeige MLL Antikörper), Grx1, TrxR1 (zeige TXNRD1 Antikörper) and TxnIP (zeige TXNIP Antikörper), and the levels of signaling proteins (Akt1 (zeige AKT1 Antikörper), pAkt1(-)Ser473, MapK (zeige MAPK1 Antikörper), pMapK, Stat3 (zeige STAT3 Antikörper), Fas (zeige FAS Antikörper)).
Reduction potentials of protein disulfides and catalysis of glutathionylation and deglutathionylation by glutaredoxin enzymes
GRX1 overexpression constrains oxidative stress and apoptosis in osteoarthritis chondrocytes by regulating CREB (zeige CREB1 Antikörper)/HO-1 (zeige HMOX1 Antikörper), providing a novel insight into the molecular mechanism and potential treatment of osteoarthritis.
Glutaredoxin 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 (zeige MLL Antikörper) and Grx1 and support the strategy of weakening the thiolic antioxidant defenses when designing new antitumoral therapies.
Prx2 (zeige PRDX2 Antikörper) glutathionylation is a favorable reaction that can occur in cells under oxidative stress and may have a role in redox signaling. GSH/Grx1 provide an alternative mechanism to thioredoxin (zeige TXN Antikörper) and thioredoxin reductase (zeige PRDX5 Antikörper) for Prx2 (zeige PRDX2 Antikörper) recycling.
Glutaredoxin 1 protects human retinal pigment epithelial cells from oxidative damage by preventing AKT (zeige AKT1 Antikörper) glutathionylation.
A new function for GRX1 in neuronal copper homeostasis and in protection from copper-mediated oxidative injury.
Results indicate that the activation of eNOS (zeige NOS3 Antikörper)/NO system is regulated by Grx 1 and coupled with inhibition of JNK (zeige MAPK8 Antikörper) and NF-kappaB (zeige NFKB1 Antikörper) signaling pathway which could alleviate the oxidative stress/apoptosis in coronary arteries endothelial cells induced by HG.
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 1 (thioltransferase)
, glutaredoxin Grx1
, glutaredoxin (grx-1)
, glutaredoxin (thioltransferase)
, hypothetical protein
, thiol disulfide oxidoreductase
, glutaredoxin-1 (Grx1)
, glutaredoxin L homeolog