UCP2: Difference between revisions

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| summary_text = 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. Although it was originally thought to play a role in nonshivering thermogenesis, obesity and diabetes, it now appears that the main function of UCP2 is the control of mitochondria-derived reactive oxygen species <ref>Arsenijevic et al Nat Gen 2000. Bai et al J BIol Chem 2005</ref>. Chromosomal order is 5'-UCP3-UCP2-3'.<ref>{{cite web | title = Entrez Gene: UCP2 uncoupling protein 2 (mitochondrial, proton carrier)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7351| accessdate = }}</ref>
| summary_text = 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. Although it was originally thought to play a role in nonshivering thermogenesis, obesity and diabetes, it now appears that the main function of UCP2 is the control of mitochondria-derived reactive oxygen species <ref>Arsenijevic et al Nat Gen 2000. Bai et al J BIol Chem 2005</ref>. Chromosomal order is 5'-UCP3-UCP2-3'.<ref>{{cite web | title = Entrez Gene: UCP2 uncoupling protein 2 (mitochondrial, proton carrier)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7351| accessdate = }}</ref>
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==See also==
* [[Uncoupling protein]]


==References==
==References==

Revision as of 04:05, 6 February 2008

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UCP2
Identifiers
AliasesUCP2, BMIQ4, SLC25A8, UCPH, uncoupling protein 2
External IDsOMIM: 601693; MGI: 109354; HomoloGene: 2516; GeneCards: UCP2; OMA:UCP2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_003355

NM_011671

RefSeq (protein)

NP_035801

Location (UCSC)Chr 11: 73.97 – 73.98 MbChr 7: 100.14 – 100.15 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Uncoupling protein 2 (mitochondrial, proton carrier), also known as UCP2, is a human gene.

Template:PBB Summary

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000175567Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000033685Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

Further reading

Template:PBB Further reading

  • Arsenijevic D, Onuma H; et al. (2000). "Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production". Nature Genetics. 26 (Dec): 435–9. {{cite journal}}: Explicit use of et al. in: |author= (help)
  • Bai Y, Onuma H, Bai X; et al. (2005). "Persistent nuclear factor-KB activation in Ucp2-/- mice leads to enhanced nitric oxide and inflammatory cytokine production". J Biol Chem. 280 (May 13): 19062–9. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.