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anti-Rat (Rattus) Glutaredoxin 1 Anticorps:
anti-Mouse (Murine) Glutaredoxin 1 Anticorps:
anti-Human Glutaredoxin 1 Anticorps:
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Data suggest an essential role of hepatic Glrx in regulating SirT1 (Montrer SIRT1 Anticorps), which controls protein glutathione adducts in the pathogenesis of hepatic steatosis.
Grx1 deficiency leads to eNOS (Montrer NOS3 Anticorps) dysfunction through oxidative modification of S-glutathionylation of eNOS (eNOS (Montrer NOS3 Anticorps)-SSG) and inactivation of NO production, enhancing the endothelial TLR4 (Montrer TLR4 Anticorps) 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 (Montrer INS Anticorps) secretion, increase of reactive oxygen species (ROS (Montrer ROS1 Anticorps)) 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 (Montrer HIF1A Anticorps) by increasing GSH adducts on Cys (Montrer DNAJC5 Anticorps)(520) promoting in vivo HIF-1alpha (Montrer HIF1A Anticorps) stabilization, VEGF-A (Montrer VEGFA Anticorps) production, and revascularization in the ischemic muscles.
Prx2 (Montrer PRRX2 Anticorps) 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 (Montrer TXN Anticorps) and thioredoxin reductase (Montrer PRDX2 Anticorps) for Prx2 (Montrer PRRX2 Anticorps) 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 (Montrer IL17A Anticorps)
Up-regulated Glrx inhibits VEGF signaling by increa (Montrer FLT1 Anticorps)sed Flt1 causing impaired vascularization.
Glutaredoxin-1 silencing induces cell senescence via p53/p21/p16 signaling axis.
Overexpression of NOS3 (Montrer NANOS3 Anticorps) increased the levels and activities of proteins of the redoxin systems, Trx1 (Montrer MLL Anticorps), Grx1, TrxR1 (Montrer TXNRD1 Anticorps) and TxnIP (Montrer TXNIP Anticorps), and the levels of signaling proteins (Akt1 (Montrer AKT1 Anticorps), pAkt1(-)Ser473, MapK (Montrer MAPK1 Anticorps), pMapK, Stat3 (Montrer STAT3 Anticorps), Fas (Montrer FAS Anticorps)).
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 (Montrer CREB1 Anticorps)/HO-1 (Montrer HMOX1 Anticorps), 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 (Montrer MLL Anticorps) and Grx1 and support the strategy of weakening the thiolic antioxidant defenses when designing new antitumoral therapies.
Prx2 (Montrer PRDX2 Anticorps) 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 (Montrer TXN Anticorps) and thioredoxin reductase (Montrer PRDX5 Anticorps) for Prx2 (Montrer PRDX2 Anticorps) recycling.
Glutaredoxin 1 protects human retinal pigment epithelial cells from oxidative damage by preventing AKT (Montrer AKT1 Anticorps) glutathionylation.
Results indicate that the activation of eNOS (Montrer NOS3 Anticorps)/NO system is regulated by Grx 1 and coupled with inhibition of JNK (Montrer MAPK8 Anticorps) and NF-kappaB (Montrer NFKB1 Anticorps) 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