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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Thioredoxin interacting protein

TXNIP, VDUP1, Thioredoxin-interacting protein, TRF3
regulates thioredoxin to play an important role in the preservation of cellular viability [RGD, Feb 2006] (from NCBI)
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Top mentioned proteins: Thioredoxin, V1a, Ros, Insulin, CAN
Papers using TXNIP antibodies
Purinergic regulation of high-glucose-induced caspase-1 activation in the rat retinal Müller cell line rMC-1
Singh Lalit P. et al., In Experimental Diabetes Research, 2010
... Predesigned TXNIP siRNAs were purchased from Qiagen (SABiociences) ...
Suppression of fatty acid synthase, differentiation and lipid accumulation in adipocytes by curcumin.
Schneider-Stock Regine, In PLoS ONE, 2010
... Thioredoxin-interacting protein (TxNIP) antibody was obtained from MBL International Corporation (Woburn, MA) ...
Evaluation of the adeno-associated virus mediated long-term expression of channelrhodopsin-2 in the mouse retina
Singh L P et al., In Cell Death & Disease, 2008
... Antibody for TXNIP was purchased from MBL Biotechnology (Woburn, MA, USA), ...
Papers on TXNIP
Mitochondria-targeted peptide SS-31 attenuates renal injury via an antioxidant effect in diabetic nephropathy.
Shi et al., China. In Am J Physiol Renal Physiol, Jan 2016
Furthermore, SS-31 inhibited expression of TGF-β1, Nox4 and thioredoxin interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
Response of esophageal cancer cells to epigenetic inhibitors is mediated via altered thioredoxin activity.
Lassmann et al., Freiburg, Germany. In Lab Invest, Jan 2016
For this, we first analyzed human tissue specimens of 37 esophageal cancer patients by immunohistochemistry for Trx, Trx-interacting protein (TXNIP) and Trx reductase (TXNRD).
MiR-17 down-regulation by high glucose stabilizes Thioredoxin-interacting protein and removes thioredoxin inhibition on ASK1 leading to apoptosis.
Yang et al., Baltimore, United States. In Toxicol Sci, Jan 2016
High glucose suppressed miR-17 expression, which led to an increase in its target gene Txnip (Thioredoxin-interacting protein).
Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis.
Ayer et al., Salt Lake City, United States. In Br J Cancer, Jan 2016
More recently, the c-Myc-related transcription factor MondoA has been shown to restrict glucose uptake and aerobic glycolysis via its induction of thioredoxin-interacting protein (TXNIP).
Single nucleotide polymorphisms in the Trx2/TXNIP and TrxR2 genes of the mitochondrial thioredoxin antioxidant system and the risk of diabetic retinopathy in patients with Type 2 diabetes mellitus.
Petrovic et al., Ljubljana, Slovenia. In J Diabetes Complications, Dec 2015
The aim of this study was to examine the possible association between seven single nucleotide polymorphisms (SNPs) of the Trx2/TXNIP and TrxR2 genes encoding proteins involved in the thioredoxin antioxidant defence system and the risk of diabetic retinopthy (DR).
Endoplasmic reticulum stress is involved in the connection between inflammation and autophagy in type 2 diabetes.
Li et al., Harbin, China. In Gen Comp Endocrinol, 2015
In this process, thioredoxin-interacting protein (TXNIP) is induced by endoplasmic reticulum (ER) stress, which further demonstrates a potential role for ER stress in innate immunity via activation of the NOD-like receptor (NLRP) 3/caspase1 inflammasome and in diabetes pathogenesis via the release of cytokines.
Timosaponin B-II ameliorates diabetic nephropathy via TXNIP, mTOR, and NF-κB signaling pathways in alloxan-induced mice.
Li et al., Nanjing, China. In Drug Des Devel Ther, 2014
The expression of mammalian target of rapamycin (mTOR), thioredoxin-interacting protein (TXNIP), and nuclear transcription factor-κB (NF-κB) signaling pathways was also measured using Western blot analysis.
NLRP3 inflammasome: from a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases.
Rouis et al., Paris, France. In Redox Biol, 2014
In addition, we have reviewed the functional link between NLRP3 inflammasome, the regulator of cellular redox status Trx/TXNIP complex, endoplasmic reticulum stress and the pathogenesis of diseases such as type 2 diabetes.
Thioredoxin-interacting protein: pathophysiology and emerging pharmacotherapeutics in cardiovascular disease and diabetes.
Horowitz et al., Adelaide, Australia. In Cardiovasc Drugs Ther, 2014
Thioredoxin-interacting protein (TXNIP), also known as vitamin D-upregulated protein or thioredoxin-binding-protein-2, functions as a physiological inhibitor of Trx, and pathological suppression of Trx by TXNIP has been demonstrated in diabetes and cardiovascular diseases.
Minireview: Thioredoxin-interacting protein: regulation and function in the pancreatic β-cell.
Shalev, Birmingham, United States. In Mol Endocrinol, 2014
Discovered as the top glucose-induced gene in a human islet microarray study 12 years ago, thioredoxin-interacting protein (TXNIP) has now emerged as such a key player in pancreatic β-cell biology.
Thioredoxin-interacting protein regulates insulin transcription through microRNA-204.
Shalev et al., Birmingham, United States. In Nat Med, 2013
We identified thioredoxin-interacting protein (TXNIP), a cellular redox regulator, as a crucial factor in beta-cell biology and show that beta-cell TXNIP is upregulated in diabetes, whereas TXNIP deficiency protects against diabetes by preventing beta-cell apoptosis.
TXNIP maintains the hematopoietic cell pool by switching the function of p53 under oxidative stress.
Choi et al., Taejŏn, South Korea. In Cell Metab, 2013
Thioredoxin-interacting protein (TXNIP), which is induced by oxidative stress, is a known regulator of intracellular ROS.
Thioredoxin-interacting protein mediates ER stress-induced β cell death through initiation of the inflammasome.
Urano et al., Worcester, United States. In Cell Metab, 2012
Here we report that thioredoxin-interacting protein (TXNIP) is a critical signaling node that links ER stress and inflammation.
TXNIP switches tracks toward a terminal UPR.
Wek et al., New Brunswick, United States. In Cell Metab, 2012
(2012) discover that thioredoxin-interacting protein (TXNIP) is a regulatory switch connecting the terminal unfolded protein response (UPR) and NLRP3 inflammasome to mediate β cell death.
IRE1α induces thioredoxin-interacting protein to activate the NLRP3 inflammasome and promote programmed cell death under irremediable ER stress.
Papa et al., San Francisco, United States. In Cell Metab, 2012
We discovered that thioredoxin-interacting protein (TXNIP) is a critical node in this "terminal UPR." TXNIP becomes rapidly induced by IRE1α, an ER bifunctional kinase/endoribonuclease (RNase).
TXNIP in Agrp neurons regulates adiposity, energy expenditure, and central leptin sensitivity.
Schwartz et al., New York City, United States. In J Neurosci, 2012
these results identify a critical role for TXNIP in Agrp neurons in mediating diet-induced obesity through the regulation of energy expenditure and adipose tissue metabolism, independently of food intake.
TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover.
Bollerslev et al., Oslo, Norway. In Eur J Endocrinol, 2012
Data indicate that TXNIP may mediate some of the detrimental effects of glucocorticoids on osteoblast (OB) function as well as modulate OB-mediated osteoclastogenesis by regulating the OPG/RANKL ratio.
Thioredoxin interacting protein genetic variation is associated with diabetes and hypertension in the Brazilian general population.
Pereira et al., São Paulo, Brazil. In Atherosclerosis, 2012
Suggest that genetic variation in the TXNIP gene may act as a "common ground" modulator of diabetes and hypertension.
Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.
Berk et al., Rochester, United States. In Circ Res, 2012
Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.
TXNIP links innate host defense mechanisms to oxidative stress and inflammation in retinal Muller glia under chronic hyperglycemia: implications for diabetic retinopathy.
Singh et al., Detroit, United States. In Exp Diabetes Res, 2011
hyperglycemia sustains TXNIP up-regulation in Muller glia and evokes a program of cellular defense/survival mechanisms that ultimately lead to oxidative stress, ER stress/inflammation, autophagy and apoptosis.
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