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Taken together, our results firstly reveal that TMAO induces inflammation and endothelial dysfunction via activating ROS (show ROS1 Proteins)-TXNIP-NLRP3 (show NLRP3 Proteins) inflammasome, suggest a likely mechanism for TMAO-dependent enhancement in atherosclerosis and cardiovascular risks.
results suggest that TXNIP is required early in the apoptotic-inducing pathway resulting from r-Moj-DM binding to the alphav integrin (show ITGAV Proteins) subunit
Hypoxia suppresses thioredoxin binding protein-2 gene expression, which may ultimately alter placental development.
Heme oxygenase (show HMOX1 Proteins) rs2071749 polymorphism was positively associated with obesity in Mexicans.
These data identify novel Txnip protein interactions.
Glucose exerts strong stimulatory effects on activation histone marks while having inhibitory effects on repression marks in the promoter of the TXNIP gene, and this was associated with a marked increase in expression of the proinflammatory gene in kidney.
No evidence that SNPS in TXNIP has effect, but the rs4485648 polymorphism of the TrxR2 (show TXNRD2 Proteins) gene might exert an independent effect on the development of Diabetic retinopathy.
An association has been found between the TXNIP gene methylation pattern and type 2 diabetes mellitus in ischemic stroke patients through epigenetic mechanisms, related to sustained hyperglycemia levels with HbA1c >/= 7%.
These findings thereby provide new mechanistic insight into the regulation of TXNIP and beta-cell biology and reveal novel links between proinflammatory cytokines, carbohydrate response element binding protein (show MLXIPL Proteins)-mediated transcription, and microRNA signaling.
The crystal structure of the complex between a phosphorylated PPxY motif of TXNIP and the SH2 domain of Vav2 reveals a conserved recognition mechanism.
The molecular characterization of porcine TXNIP gene, is described.
single-marker and haplotype analyses revealed significant effects of TXNIP on hot carcass weight, test daily gain, and lifetime daily gain
Foam cell-released 4-hydroxnonenal activates PPARdelta (show PPARD Proteins) in Vascular endothelial cells, leading to increased TXNIP expression and consequently to senescence.
Diabetes induces TXNIP expressions at mRNA levels, but shows the opposite effect on GS.
ITCH targets TXNIP for ubiquitin-proteasome degradation in cardiomyocytes and ameliorates reactive oxygen species-induced cardiotoxicity through the thioredoxin (show TXN Proteins) system.
Txnip plays an important role in oxidative inflammatory response and atherosclerotic lesion development in ApoE (show APOE Proteins) knockout mice.
The results indicate that a lack of TxNIP protects against diabetic nephropathy (DN) and support in vitro data that upregulation of TxNIP by glucose is a key mediator of early oxidative stress and a trigger for the development and progression of DN.
Reactive oxygen species regulation through REDD1 (show DDIT4 Proteins)/TXNIP is physiological rheostat controlling stress-induced autophagy.
These findings suggest that TXNIP is required for endothelial cell survival and homeostasis especially under stress conditions including hyperoxia.
HG-induced NADPH oxidase (show NOX1 Proteins) activation is driven by TXNIP which subsequently triggers NALP3 (show NLRP3 Proteins) inflammasome activation in podocytes and ultimately led to podocyte injury
Data indicate that thioredoxin-interacting protein (TXNIP)levels are induced in erythroid differentiation.
regulates thioredoxin to play an important role in the preservation of cellular viability
thioredoxin interacting protein
, Thioredoxin-interacting protein
, thioredoxin binding protein 2
, thioredoxin-binding protein 2
, thioredoxin-interacting protein
, upregulated by 1,25-dihydroxyvitamin D-3
, vitamin D3 up-regulated protein 1
, hyperlipidemia 1
, thioredoxin binding protein-2