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anti-Human UCP2 Antikörper:
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Mouse (Murine) Polyclonal UCP2 Primary Antibody für ELISA, ICC - ABIN5629187
Vázquez-Medina, Popovich, Thorwald, Viscarra, Rodriguez, Sonanez-Organis, Lam, Peti-Peterdi, Nakano, Nishiyama, Ortiz: Angiotensin receptor-mediated oxidative stress is associated with impaired cardiac redox signaling and mitochondrial function in insulin-resistant rats. in American journal of physiology. Heart and circulatory physiology 2013
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Human Polyclonal UCP2 Primary Antibody für IF (p), IHC (p) - ABIN675428
Chuang, Lin, Huang, Chang, Liou, Chen, Chang, Chan et al.: Peroxisome proliferator-activated receptors ?/mitochondrial uncoupling protein 2 signaling protects against seizure-induced neuronal cell death in the hippocampus following experimental status ... in Journal of neuroinflammation 2012
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Dog (Canine) Polyclonal UCP2 Primary Antibody für ELISA, WB - ABIN5553326
Liu, Shim, Nguyen, Gibbons, Mitchell, Poirier: Tempol protects cardiomyocytes from nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity. in Toxicological sciences : an official journal of the Society of Toxicology 2014
Dog (Canine) Polyclonal UCP2 Primary Antibody für ELISA, WB - ABIN547885
Dando, Fiorini, Pozza, Padroni, Costanzo, Palmieri, Donadelli: UCP2 inhibition triggers ROS-dependent nuclear translocation of GAPDH and autophagic cell death in pancreatic adenocarcinoma cells. in Biochimica et biophysica acta 2013
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Human Polyclonal UCP2 Primary Antibody für WB - ABIN5518965
Liu, He, Li: Exhaustive training increases uncoupling protein 2 expression and decreases Bcl-2/Bax ratio in rat skeletal muscle. in Oxidative medicine and cellular longevity 2013
except for reduced lipid peroxidation, we did not observe any significant reactive oxygen species reduction associated with increased Ucp2 activation in cold-exposed group.
AtUCP1 and AtUCP2 are the first reported mitochondrial carriers in Arabidopsis to transport aspartate and glutamate
Studied energy expenditure as well as expression of uncoupling protein 2 (UCP2) in skeletal muscle of obese subjects participating in caloric restriction studies.
PEDF was demonstrated to increase UCP2 gene expression in ARPE19 cells.
UCP2 (G-866A) polymorphism may play a crucial role in the pathogenesis of insulin secretion thus leads to the development of type 2 diabetes.
UCP2 is mainly localized in proximal convoluted tubule cells, which may explain their relative propensity to damage in pathological conditions including the hypertensive disease.
tests variants in the UCP2 gene and diabetic retinopathy (DR) in Han Chinese with Type 2 Diabetes. Logistic regression analysis showed that the AA and GA genotypes of rs659366 were significantly associated with an increased risk for nonproliferative DR. Patients harboring the II and DI genotypes had a higher risk for proliferative DR in the codominant model and the DI genotype showed a higher risk for Non Proliferative DR
Polymorphism of Ala55Val UCP2 genotype in the male group showed that TT genotype and T allele significantly lowers the risk of obesity. Insertion/deletion of 45 bp UCP2 gene in the male group showed that II genotype and I allele significantly increase the risk of obesity whereas for women it showed that the DI genotype and I allele lower the risk of obesity.
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.
Data do not support the role of variants in UCP2 as a monogenic cause of hyperinsulinaemic hypoglycaemia.
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.
UCP2-866 G/A polymorphism is associated with obesity.
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.
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.
UCP2 inhibits myointimal hyperplasia after vascular injury, probably through suppressing nuclear factor-kappaB-dependent smooth muscle cell proliferation and migration.
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.
Evaluated association between nonalcoholic fatty liver disease (NAFLD) and single nucleotide polymorphism 866G of human uncoupling protein 2 (UCP2).
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.
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.
UCP2 is a key mediator of hypoxia-triggered chemoresistance in non-small cell lung cancer cells via repression of peroxisome proliferator-activated receptor gamma.
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
UCP2 expression is associated with weight loss after hypocaloric diet intervention.
Study data indicate that UCP2 induction in melanoma cells blocks the immunosuppressive feature of the tumor microenvironment by shifting the cytokine milieu in an interferon regulatory factor 5-dependent manner, leading to engagement of the conventional type 1 dendritic cell- and CD8+ T cell-dependent anti-tumor immune cycle, and prolonged survival in mouse B16 melanoma model.
UCP2 expression correlates with the extent of lymphocytes invasion in spinal cord and is antigen-independent. The maximum of UCP2 expression coincides with the peak of the active experimental autoimmune encephalomyelitis.
Here, the authors report that mice deficient in the mitochondrial uncoupling protein 2 gene (Ucp2(-/-)) spontaneously developed Polycystic liver diseases when they were over 12 months old.
UCP2 regulates daily rhythms of insulin secretion in MIN6 cells and isolated islets from male mice.
Study provides evidence that UCP2 plays a protecting role against LPS by regulating the balance between autophagy and apoptosis of cardiomyocytes, and by which mechanisms, it may contribute to homeostasis of cardiac function and cardiomyocytes activity.
Upregulation of UCP2 conferred protective effects to the stressed beta-cell through mechanisms not directly associated with superoxide production.
UCP2-dependent modulations have a major impact on cardiac electrophysiology.
UCP2 regulates embryonic neurogenesis through reactive oxygen species-mediated Yap alternation, thus shedding new sight on mitochondrial metabolism involved in embryonic neurogenesis.
Data demonstrate that UCP2 controls pancreas development through the ROS-AKT signaling pathway.
UCP2 has two glycine-rich motifs, motif 1: EGIRGLWKG (170-178) and a Walker A-like motif 2: EGPRAFYKG (264-272). These motifs seem to be important for the function of UCP2. UCP2/K177E- or UCP2/G174L-expressed cells did not induce enlarged cell shapes. UCP2/K177E and UCP2/G174L produced functional incompetence of the glycine-rich motif 1. Senescent-like cells significantly decreased the mitochondrial membrane potentials.
our findings reveal that UCP2 regulates inflammation responses in astrocytes and plays an important role in the pathogenesis of depression and that UCP2 may be a promising therapeutic target for depression.
These results suggest that Leishmania exploits A20 and UCP2 to impair inflammasome activation for disease propagation
attenuates renal ischemia-reperfusion injury, probably by reducing cell apoptosis through protection of autophagy
UCP-2 prevents angiotensin-II-induced abdominal aortic aneurysm in apolipoprotein E-knockout mice via antioxidant and antiapoptotic activities.
This study demonstrating a FABP4-UCP2 axis with the potential to modulate the microglial inflammatory response.
The miR-133a-UCP2 pathway participates in inflammatory bowel disease (IBD) by altering downstream inflammation, oxidative stress and markers of energy metabolism, which provides novel clues and potential therapeutic targets for IBD.
PPARgamma inhibited PDGF-BB-induced ROS in VSMCs by upregulating UCP2 expression.
these data offer a novel pathway whereby FABP4/aP2 regulates macrophage redox signaling and inflammasome activation via control of UCP2 expression.
Ucp2 affects glutathione metabolism by regulating hepatic efflux of glutathione. Nrf2 deficiency may not aggravate oxidative stress in Ucp2-deficient mice.
Despite patent grafts, revascularized hibernating myocardium demonstrates a submaximal response to dobutamine infusion and increased mitochondrial UCP-2 expression.
Seven deletion polymorphisms were covered in introns of linkage genes of UCP2 and UCP3, showing that UCPs have conservation and genetic reliability.
The in vivo data indicate that beta-adrenergic agonists may function in regulating UCP2 and UCP3 expression in selected muscles.
UCPs do have uncoupling properties when expressed in mitochondria but that uncoupling by UCP1 or UCP2 does not prevent acute substrate-driven endothelial cell superoxide as effluxed from mitochondria respiring in vitro.
A study evaluating the relationships of uncoupling protein 2 and 3 expression, SNP of mitochondrial DNA, and residual feed intake (RFI) in Angus steers selected to have high or low RFI is presented.
The effect of single nucleotide polymorphisms in 6 genes and their associations with production factors in beef cattle are reported.
These results suggest that UCP2 play an important role of lipid and energy metabolism in mammary epithelial cells.
Mitochondrial uncoupling proteins (UCP) are members of the larger family of mitochondrial anion carrier proteins (MACP). UCPs separate oxidative phosphorylation from ATP synthesis with energy dissipated as heat, also referred to as the mitochondrial proton leak. UCPs facilitate the transfer of anions from the inner to the outer mitochondrial membrane and the return transfer of protons from the outer to the inner mitochondrial membrane. They also reduce the mitochondrial membrane potential in mammalian cells. Tissue specificity occurs for the different UCPs and the exact methods of how UCPs transfer H+/OH- are not known. UCPs contain the three homologous protein domains of MACPs. This gene is expressed in many tissues, with the greatest expression in skeletal muscle. It is thought to play a role in nonshivering thermogenesis, obesity and diabetes. Chromosomal order is 5'-UCP3-UCP2-3'.
mitochondrial uncoupling protein 2
, uncoupling protein 2 (mitochondrial, proton carrier)
, Mitochondrial uncoupling protein 2
, uncoupling protein 2
, UCP 2
, solute carrier family 25 member 8
, uncoupling protein 2, mitochondrial
, uncoupling protein homolog
, Uncoupling protein 2, mitochondrial