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Validated All-in-One™ qPCR Primer for UCP2(NM_003355.2) Search again
Product ID:
HQP018403
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BMIQ4, SLC25A8, UCPH
Gene Description:
uncoupling protein 2
Target Gene Accession:
NM_003355.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- Glucose induces and leptin decreases expression of uncoupling protein-2 mRNA in human islets.
- microsatellite markers at the UCP2/UCP3 locus on chromosome 11q13 in anorexia nervosa
- evidence for its function as a metabolic regulator (REVIEW)
- hypothesis that recombinant human uncoupling protein-2 (UCP2) ectopically expressed in bacterial inclusion bodies binds nucleotides in a manner identical with the nucleotide-inhibited uncoupling that is observed in kidney mitochondria
- Decreased mitochondrial proton leak and reduced expression in skeletal muscle of obese diet-resistant women
- A functional polymorphism in the promoter enhances obesity risk but reduces type 2 diabetes risk in obese middle-aged humans
- purine nucleotides must be the physiological inhibitors of UCP2-mediated uncoupling in vivo.
- there is a unique, near-uniform distribution of the uncoupling protein 2 insertion/deletion polymorphism in Tonga which may be relevant to the prevalence of obesity and type 2 diabetes
- the common -866G/A polymorphism in the UCP2 gene may contribute to the biological variation of insulin secretion
- UCPs in adipose tissue may play a role in the reduction in 24-h energy expenditure observed in post-obese individuals.
- study of isolation, refolding, transport properties, and regulation of recombinant UCP2
- No evidence for involvement of the promoter polymorphism -866 G/A of the UCP2 gene in childhood-onset obesity in humans
- the recent advancements on the role of UCP2 in the brain and portray this uncoupler as an important player in normal neuronal function as well as a key cell death-suppressing device.
- These data are the first to suggest that polymorphisms in the UCP2 gene may be genetic risk factors of spina bifida.
- Overexpression of human UCP2 attenuates reactive oxygen species generation and prevents mitochondrial Ca2+ overload in cultured neonatal rat cardiomyocytes revealing a novel mechanism of cardioprotection
- Data suggest that uncoupling protein-2 is an inducible protein that is neuroprotective by activating cellular redox signaling or by inducing mild mitochondrial uncoupling that prevents the release of apoptogenic proteins.
- Uncoupling protein-2 variants show significant effects on insulin secretion in interaction with family-specific factors. However, the associated allele and the effects on gene expression are opposite to those reported previously.
- Mitochondrial UCPs precondition neurons by dissociating cellular energy production from that of free radicals to withstand the harmful effects of cellular stress occurring in a variety of neurodegenerative disorders, including epilepsy.
- variation of the uncoupling protein 2 promoter is not associated with obesity or obesity-related intermediary phenotypes in Danish subjects
- Uncoupling protein 2 has a role in neuroprotection [review]
- Juvenile obese subjects who are homozygous for the A variant have an increased ratio (3.6 +/- 1.2) of calories derived from carbohydrates to those from lipids.
- In type 2 diabetes there is a significant gene to gene interaction between the Ala55Val polymorphism in the uncoupling protein 2 gene ( UCP2) and the 161C>T polymorphism in the exon 6 of ppargamma.
- UCP2 promoter polymorphism -866G/A does not affect obesity in Japanese type 2 diabetic patients but affects its transcription in beta-cells.
- UCP2 allelic variants may not have a direct role in the pathogenesis and development of obesity.
- Mitochondrial UCP2 in circulating monocytes may prevent excessive accumulation of monocytes/macrophages in the arterial wall, thereby reducing atherosclerotic plaque formation.
- Polymorphism of uncoupling protein 2 gene is associated with hypertension, and suggests the possibility of uncoupling protein 2 gene as a target molecule for studies on the etiology and treatment of hypertension.
- No association between the different polymorphisms and diabetic nephropathy.
- The -866A/A genotype was associated with diabetes in women, but not in men. The -866A/A genotype of the UCP2 gene may contribute to diabetes susceptibility by affecting insulin sensitivity.
- UCP2 may be part of a novel adaptive response by which oxidative stress is modulated in colon cancer
- UCP2 has a role in hydroperoxy fatty acid cycling
- anion channel structure of UCP2 protein is oligomeric and the second transmembrane domain is essential for the voltage-dependence of this anion channel
- Single nucleotid polymorphism is associated with type 2 diabetes risk in Italy.
- The hypothesis that differences in the UCP-2 genes influence the susceptibility to anorexia nervossa was not supported.
- Our results suggest a role of UCP2 in atherogenesis
- The present results expose the critical importance of UCP2 in normal nigral dopamine cell metabolism.
- UCP-2 can modify atherosclerotic processes inhuman vascular muscle smooth cells in response to high glucose and Angiotensin II.
- reduction of free fatty acids(FFAs) induced by bilio-pancreatic diversion acts in inhibiting FFA transportation to the mitochondria uncoupling protein 2 (UCP-2), contributing to the decreased lipid oxidation inside the adipose tissue
- UCP2 functions as a physiologic regulator of ROS generation in endothelial cells.
- Our results suggest that the LEP and UCP2/UCP3 genes are unlikely to have a substantial effect on variation in obesity phenotypes in this particular US Caucasian population.
- UCP2 promoter polymorphism may contribute to multiple sclerosis susceptibility by regulating the level of UCP2 protein in the central nervous and/or the immune systems.
- neuronal-specific expression of hUCP2 in adult flies decreases cellular oxidative damage and is sufficient to extend life span
- variation in UCP2 may play a role in energy metabolism, but this gene does not contribute significantly to the aetiology of type 2 diabetes and/or obesity in Pima Indians.
- The principal mechanisms regulating UCP2 gene expression are similar in rats and humans, being consistent with a role for UCP2 as a modulator of insulin secretion in humans.
- G-866A polymorphism in the UCP2 gene is associated with a reduced risk of diabetic neuropathy in type 1 diabetes.
- UCP2 promoter gene polymorphism -866 G/A was significantly associated with nerve conduction slowing and vasomotor sympathetic functions suggesting higher UCP2 activity related to A allele has energy-depleting effect on peripheral nerve function in NIDDM
- Functional promoter variants UCP2 and UCP3 increase the prospective risk of type 2 diabetes, and is exacerbated by obesity.
- UCP2 may have a role in dissipating the excess energy of a high-glucose environment
- In conclusion, our results provide correlative evidence for the "PPARgamma-->UCP2-->neuroprotection" cascade in ischemic brain injury.
- These findings suggest that UCP2 and UCP4 have a modest but important involvement in the genetic etiology of schizophrenia.
- UCP2 overexpression can negatively impact proinsulin processing
- UCP2 is very unstable, with a half-life close to 30min, compared to 30h for its homologue UCP1, a difference that may highlight different physiological functions.
- human uncoupling proteins 1 and 2 are activated by polyunsaturated fatty acids in planar lipid bilayers
- High UCP2 transcript levels were detected in reticulocytes and other maturating erythroid cells in mice exposed to hypoxia, and in umbilical cord blood of human neonates and peripheral blood of adults, suggesting involvement of UCP2 in erythropoiesis
- These data suggest that the A55V polymorphism of the UCP2 gene directly affected the levels of leptin but not via an effect on insulin.
- Results show that UCP2 is essential for mitochondrial Ca(2+) sequestration in response to cell stimulation under physiological conditions.
- UCP-2 can possibly modify atherosclerotic processes initiated in vascular cells and agents that increase UCP-2 expression in vascular may prevent atherosclerosis.
- Link between UCP2 single-nucleotide polymorphism and multiple sclerosis and a slight relation with muscle mitochondrial haplotypes.
- UCP2 A55V variant might predispose to obesity and Val55 allele to confer population-attributable risk for 9.5% of obese disorders and increase insulin. V-A-T haplotype within UCP2-UCP3 gene cluster is significantly associated with obesity in Paiwanese.
- 2 SNPs in UCP2, -866G>A and +4787C>T (A55V) that were tightly linked (r(2) = 0.97), were significantly associated with decreased HDL cholesterol levels in Korean women
- UCP2-3 polymorphisms were important genetic factor for the very low calorie diet-induced reduction of body fat mass
- Demonstrate an interaction between the UCP2 -866G>A variant and smoking to increase oxidative stress in diabetics.
- comparison of risk genotype combinations of: UCP2-866GG, mtDNA 10398A and PGC1alpha p.Thr394Thr or p.Gly482Ser for NIDDM
- the association of plasma fatty acids with the -866 G/A polymorphism of uncoupling protein 2 (UCP2) in obese children
- Ala55Val polymorphism on UCP2 gene predicts greater weight loss in morbidly obese patients undergoing gastric banding.
- a single nucleotide polymorphism in the promoter region of the UCP2 gene has a significant association with HDL cholesterol level in Iranian nonobese nondiabetic subjects
- temperature heterogeneity in atherosclerotic plaques is at least in part attributed to UCP2 expression in macrophages. The heat generated might be used to detect unstable, macrophage-rich, atherosclerotic plaques via thermography.
- The brain may respond to neuroprotection through the increased expression of UCP2 under ischemic conditions.
- body fat was reduced significantly less in the ValVal type compared with the other types (p=0.016), whereas the changes in lean body mass, protein, mineral, and water contents were not significantly different according to the Ala55Val polymorphism
- Increased expression of UCP-2 and decreased expression of UCP-3 in humans with chronic hyperglycemia may contribute to impaired glucose-stimulated insulin secretion
- The A allele of the -866G>A variant of UCP2 was associated with reduced risk of coronary artery disease in men with type 2 diabetes in a 6-year prospective study.
- Findings suggest a role of UCP2-UCP3 gene cluster haplotypes in diabetes; in particular, effects of the high-risk haplotypes were more apparent in overweight Caucasian women.
- The -866 A/A genotype may contribute to reduced LDL particle size levels, a significant risk factor for the development of coronary artery disease.
- neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases
- Significant expression of UCP2 and UCP3 was observed also in cultured keratinocytes and fibroblasts.
- Overexpression of UCP2 in HCT116 human colon cancer cells inhibits reactive oxygen species accumulation and apoptosis after exposure to chemotherapeutic agents.
- Subjects with a 45bp insertion allele of UCP2+3474 ins/del might have a higher risk of developing obesity, although the biological effects of this variant are not completely known.
- The Ala55Val polymorphism of UCP2 was not associated with incident T2DM in the Atherosclerosis Risk cohort in Communities (ARIC).
- Microenvironment activation of highly conserved mammalian UCPs may facilitate the Warburg effect in the absence of permanent respiratory impairment.
- The results suggest that the del/del polymorphism of the UCP2 gene is not associated with lower resting energy expenditure in nondialyzed CKD patients
- These results show for the first time a direct association between UCP2 amino acid alteration and human disease and highlight a role for mitochondria in hormone secretion.