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anti-Human TXNIP Antibodies:
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Mouse (Murine) Polyclonal TXNIP Primary Antibody for WB - ABIN1881961
Martin: [Growing old]. in Revue médicale suisse 2010
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Human Polyclonal TXNIP Primary Antibody for WB - ABIN1881962
Zhuo, Niu, Chen, Xin, Guo, Mao: Vitamin D3 up-regulated protein 1(VDUP1) is regulated by FOXO3A and miR-17-5p at the transcriptional and post-transcriptional levels, respectively, in senescent fibroblasts. in The Journal of biological chemistry 2010
Show all 4 Pubmed References
Human Polyclonal TXNIP Primary Antibody for IF (p), IHC (p) - ABIN750808
Li, Shen, Sun, Li, Sun, Liu, Zhang, Huang, Meng, Li: MicroRNA-20a negatively regulates expression of NLRP3-inflammasome by targeting TXNIP in adjuvant-induced arthritis fibroblast-like synoviocytes. in Joint, bone, spine : revue du rhumatisme 2016
Show all 2 Pubmed References
Human Monoclonal TXNIP Primary Antibody for IHC (p), IP - ABIN5080370
Zaragoza-Campillo, Morán: Reactive Oxygen Species Evoked by Potassium Deprivation and Staurosporine Inactivate Akt and Induce the Expression of TXNIP in Cerebellar Granule Neurons. in Oxidative medicine and cellular longevity 2017
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Cow (Bovine) Polyclonal TXNIP Primary Antibody for WB - ABIN2784817
Stoltzman, Peterson, Breen, Muoio, Billin, Ayer: Glucose sensing by MondoA:Mlx complexes: a role for hexokinases and direct regulation of thioredoxin-interacting protein expression. in Proceedings of the National Academy of Sciences of the United States of America 2008
Human Polyclonal TXNIP Primary Antibody for WB - ABIN4250210
Lee, Lee, Bae, Kang, Kim: Genome-wide identification of target genes for miR-204 and miR-211 identifies their proliferation stimulatory role in breast cancer cells. in Scientific reports 2016
Using oxygen-glucose deprivation and reoxygenation (OGD/R) to create a cell model of hepatic I/R injury, we found that the mRNA and protein expression levels of TXNIP were upregulated in HL7702cells exposed to OGD/R.
Expression of TXNIP2 isoform, not TXNIP1, is upregulated in leukocytes of patients with acute myocardial infarction.
Thioredoxin-interacting protein (TXNIP) is highly induced in retinal vascular endothelial cells under diabetic conditions. Data (including data from studies using knockout mice) suggest that TXNIP in retinal vascular endothelial cells plays role in diabetic retinal angiogenesis via VEGF/VEGFR2 and Akt/mTOR signaling. (VEGFR2 = vascular endothelial growth factor receptor-2)
miR-20a could negatively regulate TLR4 and NLRP3 signaling to protect human aortic endothelial cells from inflammatory injuries.
Results found the mRNA level of TRX-1 was significantly decreased (p<0.005), while the mRNA levels of TBP-2, COX-2, and TNF-alpha were significantly increased in the placentas in preeclampsia when compared to the normal group.
Consistent with its enhanced expression in Laron syndrome, we provide evidence that TXNIP gene expression is negatively regulated by IGF1.
TXNIP contributes to the dysregulation of tubular autophagy and mitophagy in diabetic nephropathy through activation of the mTOR signaling pathway.
This study thus characterizes ERK-mediated suppression of TXNIP as a presently unreported mechanism by which ap junctions regulate cell behaviors.
Results indicate an internal ribosome entry sites (IRESes) within the thioredoxin-interacting protein (TXNIP) protein; 5' untranslated region (5'UTR), and regulatory IRES trans-acting factors.
The data of this study suggested that TXNIP blocked autophagic flux and induced alpha-synuclein accumulation through inhibition of ATP13A2.
Compared with normal tissues, TXNIP expression was significantly decreased in human breast cancer tissues and canine mammary tumors, along with tumor progression.
This finding suggested statistically significant role of interaction of TXNIP and AF1q polymorphisms (TXNIP-rs2236566, TXNIP-rs7211, and AF1q-rs2769605) in schizophrenia susceptibility.
summarize the current state of our understanding of TXNIP biology, highlight its role in metabolic regulation and raise critical questions that could help future research to exploit TXNIP as a therapeutic target
intracellular TXNIP protein is a critical regulator of activation of the fructose-induced NLRP3 inflammasome
This study provides insight into the molecular mechanisms of TXNIP overexpression in liver cancer cell survival and apoptosis and indicated that TXNIP may be a novel promising agent for liver cancer treatment.
Study showed that the expression of TXNIP was significantly increased in RNF2 knockdown prostate tumor cells and that TXNIP is an important downstream target of RNF2.
Depletion of glycolytic intermediates led to a consistent decrease in TXNIP expression in response to 1,25(OH)2D3, an effect that coincided with the activation of AMPK signaling and a reduction in c-MYC expression.
We found no evidence of decreased TXNIP DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT TXNIP DNA methylation and gene expression changes in O-GDM subjects
the association of TXNIP (thioredoxin-interacting protein) with NLRP3 induced by ROS promoted NLRP3 inflammasome activation in senescent HUVEC endothelial cells
histone acetylation serves as a key regulator of glucose-induced increase in TXNIP gene expression
findings demonstrate a key role for endothelial TXNIP in arterial impairments induced by metabolic stress, making endothelial TXNIP a potential therapeutic target.
SIRT6 suppresses Txnip expression in beta cells via deacetylation of histone H3 and plays a critical role in maintaining beta cell function and viability
TXNIP facilitates the oxidative stress response in glomerular mesangial cells partially through AMPK pathway.
Study in transgenic mice finds that T-cell activation is linked to a drastic downregulation of Txnip and an increase in Txn1/Txnrd1 expression, which is absolutely required for synthesis of 2'-deoxyribonucleotides during T-cell metabolic reprogramming. These results uncover a pivotal function of the Trx1 system in metabolic reprogramming of thymic and peripheral T cells.
Thioredoxin-interacting protein (Txnip) is highly induced in retinal vascular endothelial cells under diabetic conditions. Data (including data from studies using knockout mice) suggest that Txnip in retinal vascular endothelial cells plays role in diabetic retinal angiogenesis via Vegf/Vegfr2 and Akt/mTOR signaling. (Vegfr2 = vascular endothelial growth factor receptor-2)
These results suggest that mitochondrial ROS-TXNIP/NLRP3/IL-1beta axis activation is responsible for tubular oxidative injury, which can be ameliorated by MitoQ via the inhibition of mtROS overproduction
crucial role in haematopoietic stem cell aging by inhibiting p38 activity via direct interaction
Data show that p38MAPK phosphorylation significantly increased in lentivirus vector thioredoxin interacting protein (LV-GFP-TXNIP) cells.
Endogenous hydrogen sulfide-mediated MAPK inhibition preserves endothelial function through TXNIP signaling.
NLR family, pyrin domain containing 3 protein (NLRP3)-/- mice exhibited less severe non-alcoholic steatohepatitis (NASH) than WT mice, whereas thioredoxin-interacting protein (TXNIP) deficiency enhanced NLRP3 inflammasome.
TXNIP is a direct substrate of protein kinase B (AKT) and is responsible for mediating AKT-dependent acute glucose influx after growth factor stimulation.
Our data indicate for the first time that the inflammasome is involved in the inflammatory response and cell death in hypoxia-induced beta cells through the ROS-TXNIP-NLRP3 axis in vitro. This provides new insight into the relationship between hypoxia and inflammation in T2D.
Here the authors demonstrate that thioredoxin-interacting protein (Txnip), which regulates glucose homeostasis in mammals, binds to fructose transporters and promotes fructose absorption by the small intestine.
thioredoxin-interacting protein deficiency alleviates diabetic renal lipid accumulation through regulation of Akt/mTOR pathway
All-trans retinoic acid plays a key role in inhibition of hepatic stellate cell activation via suppressing TXNIP expression, which reduces oxidative stress levels.
TXNIP-NFYA-SREBP2/miR-33a-AMPKalpha/CROT/CPT1/HADHB pathway is conserved in mouse, rat, and human cardiomyocytes and regulates myocardial beta-oxidation.
results suggest that melatonin confers protection against Cd-induced liver inflammation and hepatocyte death via inhibition of the TXNIP-NLRP3 inflammasome pathway.
proteomic and functional analyses demonstrated that Txnip inhibits glucose transport through direct binding to glucose transporter 1 (GLUT1). An ex vivo analysis of perfused hearts further demonstrated that the enhanced functional reserve afforded by deletion of Txnip was associated with myocardial glucose utilization during beta-adrenergic stimulation.
Thrombin activates reactive oxygen species (ROS)/thioredoxin binding protein (TXNIP)/NLRP3 signaling in BV2 microglia cells, which may indicate a mechanism that pro-inflammatory and pro-apoptotic contributes to the development of intracerebral hemorrhage (ICH).
TxNIP appears to be an important factor in FFA-induced ROS generation and insulin resistance in skeletal muscle cells
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 in Vascular endothelial cells, leading to increased TXNIP expression and consequently to senescence.
regulates thioredoxin to play an important role in the preservation of cellular viability
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
, thioredoxin interacting protein
, Thioredoxin-interacting protein
, thioredoxin interacting protein a