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UCP2 Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P |
|---|---|
| Primary Accession | P55851 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 33229 Da |
| Gene ID | 7351 |
|---|---|
| Other Names | UCP2; SLC25A8; Mitochondrial uncoupling protein 2; UCP 2; Solute carrier family 25 member 8; UCPH |
| Dilution | IHC~~Immunohistochemistry: 1/100 - 1/300. ELISA: 1/10000. Not yet tested in other applications. |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| Name | UCP2 |
|---|---|
| Synonyms | SLC25A8 {ECO:0000303|PubMed:33798544} |
| Function | Antiporter that exports dicarboxylate intermediates of the Krebs cycle in exchange for phosphate plus a proton across the inner membrane of mitochondria, a process driven by mitochondrial motive force with an overall impact on glycolysis, glutaminolysis and glutathione-dependent redox balance. Continuous export of oxaloacetate and related four-carbon dicarboxylates from mitochondrial matrix into the cytosol negatively regulates the oxidation of acetyl-CoA substrates via the Krebs cycle, lowering the ATP/ADP ratio and reactive oxygen species (ROS) production (PubMed:24395786). Proton transporter activity is debated, but if it occurs it may mediate inducible proton re-entry into the mitochondrial matrix affecting ATP turnover as a protection mechanism against oxidative stress. Proton re-entry may be coupled to metabolite transport to allow for proton flux switching and optimal ATP turnover (PubMed:11171965, PubMed:33373220, PubMed:11278935, PubMed:22524567, PubMed:26182433) (By similarity). Regulates the use of glucose as a source of energy. Required for glucose-induced DRP1- dependent mitochondrial fission and neuron activation in the ventromedial nucleus of the hypothalamus (VMH). This mitochondrial adaptation mechanism modulates the VMH pool of glucose-excited neurons with an impact on systemic glucose homeostasis (By similarity). Regulates ROS levels and metabolic reprogramming of macrophages during the resolution phase of inflammation. Attenuates ROS production in response to IL33 to preserve the integrity of the Krebs cycle required for persistent production of itaconate and subsequent GATA3-dependent differentiation of inflammation-resolving alternatively activated macrophages (By similarity). Can unidirectionally transport anions including L-malate, L-aspartate, phosphate and chloride ions (PubMed:24395786, PubMed:22524567, PubMed:26182433). Does not mediate adaptive thermogenesis (By similarity). |
| Cellular Location | Mitochondrion inner membrane {ECO:0000250|UniProtKB:P70406}; Multi-pass membrane protein |
| Tissue Location | Widely expressed in adult human tissues, including tissues rich in macrophages. Most expressed in white adipose tissue and skeletal muscle. |
Citations (0)
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Application Protocols
Provided below are standard protocols that you may find useful for product applications.
Background
UCP are mitochondrial transporter proteins that create proton leaks across the inner mitochondrial membrane, thus uncoupling oxidative phosphorylation from ATP synthesis. As a result, energy is dissipated in the form of heat.
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$ 350.00
Cat# AP72996
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