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- Table of Contents
Facts about Mitochondrial uncoupling protein 2.
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Human | |
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Gene Name: | UCP2 |
Uniprot: | P55851 |
Entrez: | 7351 |
Belongs to: |
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mitochondrial carrier (TC 2.A.29) family |
mitochondrial uncoupling protein 2; SLC25A8; SLC25A8BMIQ4; Solute carrier family 25 member 8; UCP 2; UCP2; UCPH; uncoupling protein 2 (mitochondrial, proton carrier)
Mass (kDA):
33.229 kDA
Human | |
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Location: | 11q13.4 |
Sequence: | 11; NC_000011.10 (73974671..73982872, complement) |
Widely expressed in adult human tissues, including tissues rich in macrophages. Most expressed in white adipose tissue and skeletal muscle.
Mitochondrion inner membrane; Multi-pass membrane protein.
The UCP2 Marker has many uses, including the regulation of energy metabolism, oxidative stress, and tissue damage. Learn more about this cardioprotective protein from this article. Boster Bio was founded in 1993. Their products include antibodies, ELISAs, and PCR-related molecular biology products. They offer many services to scientists, including free technical resources. They have a 24 hour support line.
The heart is a vital organ, and successful organ preservation is an important goal of clinical heart transplantation. One of the biggest challenges in heart preservation is cardiac mitochondrial dysfunction, which leads to decreased ATP production and increased ischemia-reperfusion injury. In this study, we discovered that UCP2 is upregulated in the left ventricle following chronic hypobaric hypoxia. UCP2 inhibiting drugs prevent cardiac dysfunction by preventing mitochondrial damage and ischemia-induced declines in ATP production.
Autophagy, a key part of the immune response, protects against sepsis, but it is not clear how UCP2 regulates this process. In mice, knockouts of the protein showed an increase in mitochondrial damage, and they also had a higher rate of myocardial damage than control mice. UCP2 also protects against septic cardiomyopathy. It may regulate autophagy through AMPK.
However, overexpression of UCP2 is linked with reduced cardiomyocyte apoptosis and myocardial fibrosis. To determine if UCP2 is associated with a decrease in fibrosis, researchers performed a Masson's trichrome staining of heart tissues. Other studies found that UCP2 was important in protecting against heart failure after MI. Researchers believe that the protein is responsible for a low energy state in the myocardium.
The research in the present study shows that downregulation of UCP2 in vivo activates SIRT1 in humans. This action inhibits oxidative stress and the production of ROS in heart tissue. Nonetheless, it is important to note that this mechanism is dependent on the type of protein being studied. The study was funded by the National Natural Science Foundation of China, Jiaxing Science and Technology Project, and the Zhejiang Province.
It is also known as uncoupling protein-2, and it plays an important role in regulating the mitochondrial membrane potential and reducing the production of ROS. Furthermore, it protects endothelial function and improves coronary vasodilation in diabetic mice. Furthermore, it reduces oxidative stress in human vascular endothelial cells. Hence, UCP2 is an important cardiovascular biomarker.
In humans, the enzyme UCP2 is a regulator of energy metabolism, which may explain the role of this protein in cancer. In eukaryotes, UCPs separate the metabolic process of OXPHOS from ATP synthesis, which occurs in the mitochondria. Both processes result in energy expenditure and balance, but the latter process is called BAT and wastes energy in the form of heat. UCP2 is expressed in many tissues, whereas UCP3 is expressed in skeletal muscle. These markers share a 60% sequence similarity with UCP1, but are independent of one another.
The underlying mechanism for this discovery is unknown, but it is a promising first step towards a more comprehensive understanding of tumor metabolic pathways. The discovery of UCP2 as a tumor biomarker suggests that UCP2 expression is related to the tumor's WHO grade. Further, it may facilitate targeted metabolic therapies, including glycolytic inhibitors. Further research is necessary to further understand the mechanism of UCP2 in cancer cells.
Despite its association with obesity, UCP2 plays an important role in regulating energy metabolism. In addition to controlling energy levels, UCP2 also regulates thermogenesis and prevents adipose tissue accumulation. The mechanism by which UCP2 decreases obesity is shown in Figure 3
Although UCP2 is a mitochondrial enzyme, it can also modulate oxidative stress in cells. Fatty acids oxidized through B-oxidation gain more electrons. These changes in metabolism are linked to a greater OCR/ECAR ratio in differentiated cells when UCP2 is expressed in the IMM. Consequently, ectopic expression of UCP2 inhibits the transition from glycolysis to mitochondria.
The abundant UCP2 expression in hPSCs indicates that UCP2 has a functional role in regulating energy metabolism. In addition, UCP2 has an epigenetic significance in regulating energy metabolism. The expression of UCP2 in hPSCs supports the possibility that it affects gene induction and EB formation in hPSCs. If UCP2 is expressed in hPSCs, it may also regulate ROS levels.
The present study investigated the role of the Boster Bio UCP2 marker in the regulation of oxidative stress, and the effects of rigorous training on the Bcl-2/Bax ratio and ROS production in red gastrocnemius muscle. Furthermore, the authors assessed whether there was a relationship between training and oxidative stress in athletes. However, further research is needed to determine whether overtraining and oxidative stress are related.
The study demonstrated that the UCP2 marker is highly induced by oxidative stress. By blocking the production of ROS, it inhibits the NKA/Src/Erk1/2 pathway. In addition, the three agents inhibited apoptosis and ROS production. Therefore, the Boster Bio UCP2 marker regulates oxidative stress. However, these findings suggest that a protective effect of UCP2 is still needed.
The role of UCP2 in the regulation of oxidative stress has been investigated in various cell systems. The effects of FABP4 on mitochondrial oxidative functions have been investigated in hepatocytes and islets. In both cell systems, UCP2 significantly reduces ATP synthesis and decreases the efficiency of energy metabolism. Moreover, RNA interference reduced the levels of COX2, UCP2, and ACC in adipocytes. Interestingly, overexpression of UCP2 in these cells inhibits apoptosis, cytochrome c release, and mitochondial DNA copy number.
The results showed that the 3S, 3'S-AST inhibits the oxidative stress-related proteins Bax, caspase-3, and Bcl-2. In addition, 3S, 3'S-AST prevented lipid peroxidation and decreased ROS generation. These results are significant for the protection of heart against oxidative stress. The results indicate that Boster Bio UCP2 markers may be valuable in the clinical setting.
The UCP2 marker is known to have an important role in oxidative stress, a process that leads to various inflammatory diseases and metabolism-related disorders. In addition, the protein has been linked to obesity and diabetes, as well as metabolic diseases. Ultimately, understanding the gene can help researchers develop new therapeutic strategies for these conditions. Listed below are some examples of the diseases associated with UCP2 expression.
ROS are produced in many cells, including skin. They remain an important part of inflammation in most cells. Boster Bio's UCP2 marker regulates tissue damage in skin cells. It is implicated in the regulation of skin ROS by the b-adrenergic receptor. Lastly, the skin's UCP2 protein may regulate the production of retinoid-receptor signaling.
In various cell systems, UCP2 modulates oxidative stress. Overexhaustive training increases the production of ROS. UCP2 has been shown to suppress ROS and regulate apoptosis. Apoptosis in cardiomyocytes induced by free fatty acids can be reduced using RNA interference. UCP2 knockdown decreases ROS production and promotes the release of cytochrome c.
Molecular studies have also shown that UCP2 gene polymorphism can impact susceptibility to obesity. The -866G/A polymorphism in the promoter of UCP2 is associated with lower levels of UCP2 and also modulates diabetes. In addition, the GG genotype was found to be the most common in male children and mothers with obesity. These results point to the potential utility of Boster Bio's UCP2 marker in assessing the effects of adiponectin in clinical trials.
PMID: 9180264 by Boss O., et al. Uncoupling protein-3: a new member of the mitochondrial carrier family with tissue-specific expression.
PMID: 9054939 by Fleury C., et al. Uncoupling protein-2: a novel gene linked to obesity and hyperinsulinemia.
*More publications can be found for each product on its corresponding product page