Fatty acid binding site of the mitochondrial uncoupling protein. Demonstration of its existence by EPR spectroscopy of 5-DOXYL-stearic acid
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
8163011
DOI
10.1016/0014-5793(94)80599-7
PII: 0014-5793(94)80599-7
Knihovny.cz E-resources
- MeSH
- Biological Transport MeSH
- Cyclic N-Oxides analysis MeSH
- Electron Spin Resonance Spectroscopy MeSH
- Adipose Tissue, Brown metabolism MeSH
- Ion Channels MeSH
- Cricetinae MeSH
- Mesocricetus MeSH
- Fatty Acids metabolism MeSH
- Membrane Proteins chemistry metabolism MeSH
- Mitochondrial Proteins MeSH
- Mitochondria metabolism MeSH
- Proteolipids metabolism MeSH
- Spin Labels MeSH
- Carrier Proteins chemistry metabolism MeSH
- Uncoupling Protein 1 MeSH
- Binding Sites MeSH
- Hydrogen metabolism MeSH
- Animals MeSH
- Check Tag
- Cricetinae MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 16-nitroxystearic acid MeSH Browser
- 5-doxylstearic acid MeSH Browser
- Cyclic N-Oxides MeSH
- Ion Channels MeSH
- Fatty Acids MeSH
- Membrane Proteins MeSH
- Mitochondrial Proteins MeSH
- Proteolipids MeSH
- proteoliposomes MeSH Browser
- Spin Labels MeSH
- Carrier Proteins MeSH
- Uncoupling Protein 1 MeSH
- Hydrogen MeSH
Fatty acid binding site on isolated mitochondrial uncoupling protein (UcP) is demonstrated using EPR spectroscopy of 5-DOXYL-stearic acid (5-SASL), which also activated H+ transport in proteoliposomes containing UcP. In the presence of UcP the EPR spectrum showed reproducible broadening of the low field peak as well as an increase in h+1I/h+1M ratio, rotational correlation time and in order parameter. The half-height width of the low field peak was even doubled in the presence of another UcP ligand, GDP. Palmitic acid reversed the effect of 5-SASL and non-ionizable 5-DOXYL-decane did not exhibit it.
References provided by Crossref.org
Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling
