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anti-Human TXNIP Antikörper:
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Human Monoclonal TXNIP Primary Antibody für 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
Show all 14 Pubmed References
Human Polyclonal TXNIP Primary Antibody für 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 Polyclonal TXNIP Primary Antibody für WB - ABIN6149733
Zhang, Zhang, Deng, Zhang, Xu: Baicalin protects AML-12 cells from lipotoxicity via the suppression of ER stress and TXNIP/NLRP3 inflammasome activation. in Chemico-biological interactions 2017
Cow (Bovine) Polyclonal TXNIP Primary Antibody für 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 für 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
Thus, CSE inhibits insulin production by upregulating TXNIP via MALAT1-mediated downregulation of miR-17, which provides an understanding of the processes involved in the reduced beta-cells function caused by cigarette smoke
Antioxidant regulation via TXNIP is an important cell death mechanism in human endometrial cancer, and occurs via induction by vitamin D3.
taurine can regulate the function of Caco-2 cells via TXNIP induction
TXNIP functions as a tumor suppressor gene with loss of its expression associated with ductal carcinoma in situ recurrence
Data show that thioredoxin interacting protein (TXNIP) is a tumor suppressor that is downregulated in esophageal adenocarcinoma (EAC).
Age-dependent upregulation of TXNIP results in decreased stress resistance to oxidative challenge in primary human cells.
We show that whereas Ras drives a global increase in protein translation, it suppresses TXNIP protein synthesis by reducing the rate at which ribosomes transit the coding region of TXNIP mRNA. The N terminus of the growing TXNIP polypeptide is the target for Ras-dependent translational repression.
The data suggest that TXNIP plays an important role in fludarabine-induced cytotoxicity and TLR4/NF-kappaB-mediated fludarabine resistance of acute myeloid leukemia cells.
miR-411-5p/3p are required for Non small cell lung carcinoma development by suppressing SPRY4 and TXNIP; thus, the miR-411-SPRY4-AKT axis might act as a promising target for lung cancer therapy clinically.
TXNIP is a key adaptor for c-Myc-driven aerobic glycolysis in prostate cancer
vitamin D and TXNIP were associated with different beta-cell dysfunction markers, indicating their potential abilities to predict the beta-cell status in people with diabetes
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.
TXNIP regulates cellular senescence by inhibiting AKT pathways via a direct interaction under conditions of glucose-derived metabolic stress.
Our study suggests that TXNIP plays a key role in the renal inflammation and fibrosis induced by unilateral ureteral obstruction. The expression of TXNIP was increased in a time-dependent manner in the ligated kidneys.
This study showed that the thioredoxin-interacting protein in brain increase after exposed to chronic stress.
High Txnip expression is associated with renal injury.
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.
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