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rs1800849 in UCP3 were significantly associated with prediabetes in a rural Chinese population. Overweight modified the effect of rs660339 of UCP2 on type 2 diabetes. These findings suggested that rs1800849 in UCP3 and rs660339 in UCP2 might play an important role in the incidence and development of type 2 diabetes.
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Data do not support the role of variants in UCP2 as a monogenic cause of hyperinsulinaemic hypoglycaemia.
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Aspergillus protease-mediated mitochondrial Reactive Oxygen Species (ROS) production was associated with downregulation of uncoupling protein (UCP)-2 expression by TGF-beta-SMAD4 signaling, which may play a regulatory role in mitochondrial ROS formation during fungal protease-mediated epithelial inflammation.
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UCP2-866 G/A polymorphism is associated with obesity.
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Dats suggest that UCP2 levels in peripheral blood mononuclear cells of obese women with low REE (resting energy expenditure) are significantly lower compared to obese women with low REE and compared to normal weight women.
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The A/A genotype was found to be an independent marker of good prognosis after adjustment for secondary variables (age, sex, glucose level, NIHSS score at baseline, complete recanalization and early neurological improvement) in a logistic regression analysis. The AA genotype of UCP2-866 may predict a better functional outcome in ischemic stroke after recanalization of proximal MCA occlusion.
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UCP2 inhibits myointimal hyperplasia after vascular injury, probably through suppressing nuclear factor-kappaB-dependent smooth muscle cell proliferation and migration.
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Study shows that the mitochondrial uncoupling protein 2 rs659366 A allele and rs660339 T allele are both related to longer leukocyte telomere in subjects without diabetes, independent of cardiovascular risk factors.
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Evaluated association between nonalcoholic fatty liver disease (NAFLD) and single nucleotide polymorphism 866G of human uncoupling protein 2 (UCP2).
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The present study identified a novel gene, UCP2, that influences the serum urate concentration and the risk of hyperuricemia, and the degree of association varies with gender and BMI levels.
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UCP2 regulates the activity of SIRT3 through sensing the energy level and, in turn, maintaining the mitochondrial steady state, which demonstrates a cytoprotective effect on ischemia-reperfusion injury.
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UCP2 is a key mediator of hypoxia-triggered chemoresistance in non-small cell lung cancer cells via repression of peroxisome proliferator-activated receptor gamma.
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Results here presented suggest that UCP variability has different pleiotropic effects, by affecting both telomere length and glucose homeostasis, likely through an influence on energy metabolism and stress response
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UCP2 expression is associated with weight loss after hypocaloric diet intervention.
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Decreased UCP2 gene expression in mononuclear cells from obese and diabetic patients might contribute to the immunological abnormalities in these metabolic disorders and suggests its role as a candidate gene in future studies of obesity and diabetes.
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UCP2 stimulates hnRNPA2/B1, GLUT1 and PKM2 expression and sensitizes pancreatic cancer cells to glycolysis inhibition.
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The data indicate that in the context of hepatocellular carcinoma, miR-214 acts as a putative tumour suppressor by targeting UCP2 and defines a novel mechanism of regulation of UCP2.
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UCP2 inhibition triggered cellular apoptosis and autophagy.
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The GG genotype of the UCP1-3826 A/G polymorphism appears to contribute to the onset of childhood obesity in Turkish children. The GG genotype of UCP1, together with the del/del genotype of the UCP2 polymorphism, may increase the risk of obesity with synergistic effects. The ins allele of the UCP2 exon 8 del/ins polymorphism may contribute to low HDL cholesterolemia.
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Expression of UCP2 and PLIN1 genes influences the resting metabolic rate in obese individuals and could predict the weight loss after bariatric surgery.
