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Facts about Mitochondrial brown fat uncoupling protein 1.
However, LCFAs remaining associated with the transporter via their hydrophobic tails, it results in an apparent transport of protons triggered by LCFAs. Thereby, dissipates the mitochondrial proton gradient and converts the energy of substrate oxydation into heat rather than ATP.
Human | |
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Gene Name: | UCP1 |
Uniprot: | P25874 |
Entrez: | 7350 |
Belongs to: |
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mitochondrial carrier (TC 2.A.29) family |
SLC25A7; SLC25A7mitochondrial brown fat uncoupling protein 1; Solute carrier family 25 member 7; Thermogenin; UCP 1; UCP; UCP1; uncoupling protein 1 (mitochondrial, proton carrier)
Mass (kDA):
33.005 kDA
Human | |
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Location: | 4q31.1 |
Sequence: | 4; NC_000004.12 (140555770..140568961, complement) |
Brown adipose tissue.
Mitochondrion inner membrane; Multi-pass membrane protein.
This article will help you learn the best ways to use UCP1 markers. This article will discuss flow cytometry applications in a variety different disciplines. There are many topics to be covered, including high-connectivity DEPs (high-connectivity), hypoxia, soft tissue sarcomas, cell count analysis, and hypoxia. Continue reading to learn more about these topics.
In this study, we tested whether mice expressing UCP1 had increased levels of iBAT protein by using an antibody specific for this peptide. Mice without the transgene were referred as the WT group and mice with the UCP1+DTR transgene to be called the DTR+DT. All mice received b-3 adrenergic receptor antagonists (CL316, 243) at each end of each 24 hour period. Tissue samples from the mice were taken 24 hours following the last CL injection. Western blot analysis confirmed the presence of UCP1 within iBAT, ingWAT.
The antibody was then diluted in PBS, and incubated for 1h. Next, adipocytes where fixed in 4% Paraformaldehyde were left for 20 min. After that, the cells were permeated with 0.1% Triton X100 in 1x PBS. The cells were then washed with PBS three more times. PBS containing 1.1% BSA was then added to the cells.
The results of this study revealed that brown adipocytes that express UCP1 do not influence the levels of adiponectin, insulin, or leptin in the plasma. In addition, mice with the UCP1-DTR gene were not affected by DT treatment. In addition, the mice were fed a standard diet for 6 weeks. Both groups had similar levels, but HFD-fed mice had greater body weight gain. The DT treatment had no effect on the body weight of UCP1-DTR mice.
These results were consistent with previous reports. The UCP1 gene has been associated with a significant increase in brite/beige cells. Both UCP1 and Pgc1a levels decreased significantly after DT treatment in the DTR-DT group. These results indicate that tumor cells with increased UCP1 expression have the anti-UCP1 gene. Therefore, it is important to ensure the accuracy of these data before making a decision about the type of treatment for your research.
UCP1-deficient mice displayed similar EE at RT to WT, but their response to b3AR agonist treatment was slowed. Interestingly, the UCP1-DTR model showed that mice with a reduced UCP1 cell count had no change in oxygen consumption. UCP1beige cells make up only 10% of the BAT's thermogenic capacity and are not responsible to weight gain.
Steven Boster founded the company in 1993. He was known as "the man who converted science in the lavatory" for his success in developing high-connectivity DEPs. As his business grew, he introduced various products for immunohistochemistry and developed hundreds of primary antibodies. By the late nineties, Boster had grown to be the largest catalog antibody company in China. PicoKine(tm), a platform for high-sensitivity ELISA kits, was developed by Boster.
The gene expression pattern of hypoxia-related genes is influenced by the level of UCP1 in the BAT of the naked mole rat. The UCP1ox plants had a significantly higher expression level than the WT controls. Other genes, however, showed no significant changes. Many other factors regulate hypoxia-related gene transcription, including oxidative stresses.
HIF1a expression is also significantly lower in the mitochondria of cold-exposed mice. Hypoxia-induced UCP1 transcription in iBAT cellular cells is associated by a reduction of thermogenesis, mitochondrial biogenesis, and thermogenesis. Both the HIF1a, UCP1 gene levels and levels of the complex proteins in mitochondrial DNA are altered. Hypoxia-induced UCP1 expression results in a reduction in thermogenic proteins (iWAT) of HIF1a/deficient mice. However UCP3's expression level remains unchanged.
Uncoupling Protein-1 (UCP1) is a primary regulator that regulates thermogenesis in small mammals. This protein decouples mitochondrial respiration (ATP-synthesis) from the electron transport chain, resulting in futile cycling. Naked mole rats have functional brown fat tissue. However, no studies have been done to examine their hypoxia-related adaptations. Hypoxia is a high metabolic expense for a small naked rodent. Therefore, low thermoregulation is necessary to survive.
Hypoxia results in decreased expression of UCP1 in both social and solitary mole-rat species. However, hypoxia did not consistently modify the level of the ETC proteins in these three species. The UCP1 gene, which is a key component of the ETC, is closely linked with hypoxia. It may also play a part in the regulation GIPDH.
In addition to hypoxia, oxidative stress and living at high altitudes have protective effects on humans. However, there is ongoing debate regarding the role oxygen delivery systems play in humans. This makes it imperative to have precise in vivo methods that can determine the role for oxygen delivery systems in humans. The use of novel in vitro models may be essential in dispelling this controversy. They could also be used to identify therapeutic targets.
The clinical application of UCP1 in soft tissue tumours is very limited due to the small number patients who have been affected by soft tissue Sarcomas. These cancers share many common molecular features, which could be helpful in the development of practical biomarkers. Further research is needed to assess the value of biomarker candidates. In addition, specific antibodies and protein inhibitors may be useful in clinical trials.
The UCP1 marker was originally found in tumours of adipose differentiation, which is a large subtype of soft tissue cancers. These tumours include lipoma, liposarcoma, and liposarcoma. UCP1 is a rare protein found in soft tissue tumors, but it is present in many types.
To identify the UCP1 marker during soft tissue amplification (soft tissue amplification), the cells from the second and third passages of soft tissue were immunostained for BMP2. The fourth-passage tumours had mixed populations, so they were not positive to UCP1 expression. This type of analysis can be useful in assessing the prognosis patients with soft-tissue sarcomas.
The identification of UCP1-positive tumors cells was also possible through clinical observations. These results have been confirmed by proteomic studies. Proteomic studies showed that UCP1+ tumor cells were significantly higher on days two-four than those of control cells. To confirm the association between UCP1 and the prognosis, further research is required.
The diagnosis of soft tissue cancers requires the biopsy of a tumor sample. A biopsy involves removing a small amount from the tumor and examining it under a microscope. The pathologist must then interpret the tissue samples to make a definite diagnosis. A biopsy is not a definitive diagnosis. It may be necessary to perform additional surgery to remove the tumor.
PMID: 2380264 by Cassard A.M., et al. Human uncoupling protein gene: structure, comparison with rat gene, and assignment to the long arm of chromosome 4.
PMID: 3165741 by Bouillaud F., et al. Detection of brown adipose tissue uncoupling protein mRNA in adult patients by a human genomic probe.