Mitochondrial uncoupling protein from mouse brown fat. Molecular cloning, genetic mapping, and mRNA expression
Open accessAbstract
We have identified cDNAs clones for several cold-inducible mRNAs from the brown adipose tissue of mice. pCIN-1, a plasmid with a 900-base pair insert, encoded the mitochondrial uncoupling protein (UCP) as determined by the ability of the cDNA insert to select, by hybridization, an mRNA that could be translated into a 32,000-Da protein immunoprecipitable with anti-UCP antibodies. Nine tissues were analyzed; however, UCP cDNA hybridized to an mRNA species of 1.6 and 2.0 kilobase pairs only in brown adipose tissue. A maximum induction of 10-fold occurred within 6 h of exposure to cold (5 degrees C). A BamHI restriction fragment polymorphism detected by Southern blot analysis of genomic DNA in recombinant inbred mouse strains allowed us to map the UCP gene to Chromosome 8. The analysis of the UCP gene expression in diabetic (db) and obese (ob) mice maintained at 27 degrees C for 3 days followed by cold exposure for 4 h at 5 degrees C indicated that UCP mRNA levels in mutant mice were unaffected at 27 degrees C and only slightly reduced at 5 degrees C. Accordingly, the inability of diabetic and obese mice to thermoregulate is not associated with a lack of UCP mRNA induction.
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UCP-1 is a transmembrane protein localized in the inner mitochondrial membrane that catalyzes proton transport across the mitochondrial membrane and thereby induces mitochondrial uncoupling.
“UCP-1 is a transmembrane protein localized in the inner mitochondrial membrane catalyzing the transport of protons across the mitochondrial membrane and thereby inducing mitochondrial uncoupling [7].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [7]
Strong evidence of mitochondrial uncoupling property is clear for UCP-1 but still heavily debated for other UCPs.
“Importantly, although strong evidence of the mitochondrial uncoupling property is clear for UCP-1 [7,12], it is still heavily debated for the other UCPs [13,14,15].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [7]
In brown adipose tissue, electron transport is greatly accelerated due to tissue-specific expression of the mitochondrial UCP1.
“In this tissue, electron transport is greatly accelerated due to tissue-specific expression of the mitochondrial UCP1.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [154]
UCP1 hinders the establishment of, or dissipates, a proton gradient of sufficient magnitude to sustain the synthetic activity of the mitochondrial ATPase, thus driving continuous accelerated electron transport.
“UCP1 hinders the establishment of, or dissipates, a proton gradient of sufficient magnitude to sustain the synthetic activity of the mitochondrial ATPase (150, 153-155), thus driving continuous accelerated electron transport.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [154]
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- Authors
- Jacobsson, A., Stadler, U., Glotzer, M. A., & Kozak, L. P.
- Affiliations
- Stockholm University (SE)
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1985-12
- Volume
- 260
- Issue
- 30
- Pages
- 16250-16254
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1513078811
- Cited by
- 300
- References
- 36
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 6 · 2021: 10 · 2020: 1 · 2019: 4 · 2018: 8 · 2017: 7 · 2016: 7 · 2015: 1 · 2014: 2 · 2013: 3 · 2012: 3
- FWCI
- 6.62
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- National Institutes of Health
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-08431)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- mitochondrial uncoupling proteins, brown adipose tissue, cold-responsive genes, cDNA cloning, gene mapping, chromosome 8, mRNA expression, cold exposure, thermoregulation, diabetic mice, recombinant inbred mouse strains, restriction fragment polymorphism
- MeSH terms
- Uncoupling Protein 1, Animals, Adipose Tissue, Brown, Carrier Proteins, Cloning, Molecular, Cold Temperature, DNA Transposable Elements, DNA, Mitochondrial, Genes, Ion Channels, Membrane Proteins, Mice, Inbred C57BL, Mice, Mutant Strains, Mitochondria, Molecular Weight, RNA, Messenger, Protein Biosynthesis, Mitochondrial Proteins, Mice
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