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Uncoupling protein 2

UCP2, uncoupling protein 2
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'. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Insulin, UCP1, ACID, Ros, CAN
Papers using UCP2 antibodies
cdc25A is necessary but not sufficient for optimal c-myc-induced apoptosis and cell proliferation of vascular smooth muscle cells.
Kleinschnitz Christoph, In PLoS ONE, 1998
... UCP2/3 transgenic overexpressing mice were generated ...
Interaction of carbohydrate and fat fuels in human skeletal muscle: impact of obesity and NIDDM
Thorens Bernard et al., In Diabetes, 1995
... Studies of UCP2 transgenic and knockout mice reveal ...
Papers on UCP2
Loss of Fatty Acid Binding Protein 4/aP2 Reduces Macrophage Inflammation Through Activation of SIRT3.
Bernlohr et al., Minneapolis, United States. In Mol Endocrinol, Feb 2016
Prior work using high-fat fed mice has shown that ablation of the adipocyte fatty acid binding protein (FABP4/aP2) in macrophages leads to an anti-inflammatory state both in situ and in vivo and the mechanism is linked, in part, to increased intracellular monounsaturated fatty acids and the up-regulation of UCP2.
A PGC-1α-Mediated Transcriptional Network Maintains Mitochondrial Redox and Bioenergetic Homeostasis against Doxorubicin-Induced Toxicity in Human Cardiomyocytes: Implementation of TT21C.
Peng et al., Beijing, China. In Toxicol Sci, Feb 2016
Our in vitro study revealed a well-defined POD concentration of DOX below which adaptive induction of PGC-1α-mediated mitochondrial genes, including NRF-1, MnSOD, UCP2, and COX1, concurred with negligible changes in mitochondrial superoxide and cytotoxicity.
Aspalathin, a dihydrochalcone C-glucoside, protects H9c2 cardiomyocytes against high glucose-induced shifts in substrate preference and apoptosis.
Louw et al., Cape Town, South Africa. In Mol Nutr Food Res, Feb 2016
Aspalathin inhibited high glucose-induced loss of membrane potential in H9c2 cells as observed by an increase in JC-1 ratio (orange\red fluorescence) and decreased apoptosis by reducing intracellular ROS and DNA nick formation, while increasing glutathione, superoxide dismutase, UCP2 and Bcl-2\Bax ratio.
Mitochondria controlled by UCP2 determine hypoxia-induced synaptic remodeling in the cortex and hippocampus.
Horvath et al., New Haven, United States. In Neurobiol Dis, Feb 2016
We identified that the changing oxygen tension triggered mitochondrial uncoupling protein 2 (UCP2) expression and showed that UCP2 is crucial for these adaptive mitochondrial responses.
Overexpression of uncoupling protein-2 in cancer: metabolic and heat changes, inhibition and effects on drug resistance.
Pitt, Paraparaumu, New Zealand. In Inflammopharmacology, Dec 2015
This paper deals with the role of uncoupling protein-2 (UCP2) in cancer.
Methylglyoxal Impairs Insulin Secretion of Pancreatic β-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs.
Meng et al., Wenzhou, China. In J Diabetes Res, Dec 2015
Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.
Mitochondrial mechanisms of endothelial dysfunction.
Zablocki et al., Warsaw, Poland. In Pharmacol Rep, Aug 2015
Uncoupling protein 2 (UCP2) is a regulator of mitochondrial ROS generation and can antagonise oxidative stress-induced endothelial dysfunction.
The Diagnosis and Management of Hyperinsulinaemic Hypoglycaemia.
Hussain et al., London, United Kingdom. In J Clin Res Pediatr Endocrinol, Jun 2015
Recent advances in genetics have linked CHI to mutations in 9 genes that play a key role in regulating insulin secretion (ABCC8, KCNJ11, GLUD1, GCK, HADH, SLC16A1, UCP2, HNF4A and HNF1A).
Crystal structures of the human adiponectin receptors.
Yokoyama et al., Yokohama, Japan. In Nature, May 2015
The zinc-binding structure may have a role in the adiponectin-stimulated AMPK phosphorylation and UCP2 upregulation.
The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.
Dixit et al., New Haven, United States. In Nat Med, Mar 2015
BHB blocks the NLRP3 inflammasome without undergoing oxidation in the TCA cycle, and independently of uncoupling protein-2 (UCP2), sirtuin-2 (SIRT2), the G protein-coupled receptor GPR109A or hydrocaboxylic acid receptor 2 (HCAR2).
Capsaicin may have important potential for promoting vascular and metabolic health.
O'Keefe et al., Encinitas, United States. In Open Heart, 2014
TRPV1 activation induces calcium influx, and in certain tissues this is associated with increased activation or expression of key proteins such as endothelial nitric oxide synthase (eNOS), uncoupling protein 2 (UCP2), KLF2, PPARdelta, PPARgamma, and LXRα.
Fatty acid flippase activity of UCP2 is essential for its proton transport in mitochondria.
Chou et al., Boston, United States. In Cell Metab, 2014
We find, by nuclear magnetic resonance and functional mutagenesis, that UCP2 can bind FAs laterally through its peripheral site, and this intramembrane molecular recognition is essential for UCP2-catalyzed FA flipping across the membrane, which in turn is essential for proton translocation.
New Prophylactic and Therapeutic Strategies for Spinal Cord Injury.
Hong et al., South Korea. In J Lifestyle Med, 2013
Physical activity has been shown to increase the gene expression of several brain neurotrophins (brain-derived neurotrophic factor [BDNF], nerve growth factor, and galanin) and the production of mitochondrial uncoupling protein 2, which promotes neuronal survival, differentiation, and growth.
Metabolic regulation by the mitochondrial phosphatase PTPMT1 is required for hematopoietic stem cell differentiation.
Qu et al., Cleveland, United States. In Cell Stem Cell, 2013
Further analyses demonstrated that PTPMT1 deficiency altered mitochondrial metabolism and that phosphatidylinositol phosphate substrates of PTPMT1 directly enhanced fatty-acid-induced activation of mitochondrial uncoupling protein 2. Intriguingly, depletion of PTPMT1 from myeloid, T lymphoid, or B lymphoid progenitors did not cause any defects in lineage-specific knockout mice.
Marked over expression of uncoupling protein-2 in beta cells exerts minor effects on mitochondrial metabolism.
Grill et al., Trondheim, Norway. In Biochem Biophys Res Commun, 2012
These findings question an impact of moderately elevated UCP-2 levels in beta cells as seen in diabetes.
Toward understanding the mechanism of ion transport activity of neuronal uncoupling proteins UCP2, UCP4, and UCP5.
Jelokhani-Niaraki et al., Waterloo, Canada. In Biochemistry, 2012
Neuronal UCP2 exhibits transmembrane chloride transport activity.
Uncoupling protein-2 expression and effects on mitochondrial membrane potential and oxidant stress in heart tissue.
McFalls et al., Minneapolis, United States. In Transl Res, 2012
chronic PPARgamma stimulation leads to depolarization of the inner membrane and reduced superoxide of isolated heart mitochondria, which was critically dependent on increased expression of UCP-2
Uncoupling protein-2 protects endothelial function in diet-induced obese mice.
Huang et al., Hong Kong, Hong Kong. In Circ Res, 2012
UCP2 preserves endothelial function through increasing nitric oxide bioavailability secondary to the inhibition of ROS production in the endothelium of obese diabetic mice.
Acute knockdown of uncoupling protein-2 increases uncoupling via the adenine nucleotide transporter and decreases oxidative stress in diabetic kidneys.
Palm et al., Uppsala, Sweden. In Plos One, 2011
blockade of the diabetes-induced upregulation of UCP- 2 results in excessive uncoupling and reduced oxidative stress in the kidney via activation of ANT.
Mitochondrial uncoupling protein 2 structure determined by NMR molecular fragment searching.
Chou et al., Boston, United States. In Nature, 2011
a solution-NMR method for structural characterization of UCP2
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