| Autor: |
Solanes, Gemma, Vidal-Puig, Antonio, Grujic, Danica, Flier, Jeffrey S., Lowell, Bradford B. |
| Zdroj: |
Journal of Biological Chemistry; October 1997, Vol. 272 Issue: 41 p25433-25436, 4p |
| Abstrakt: |
Uncoupling protein-3 (UCP3) is a recently identified candidate mediator of adaptive thermogenesis in humans. Unlike UCP1and UCP2, UCP3is expressed preferentially and at high levels in human skeletal muscle and exists as short and long form transcripts,UCP3Sand UCP3L.UCP3Sis predicted to encode a protein which lacks the last 37 C-terminal residues of UCP3L. In the present study, we have defined the intron-exon structure for the human UCP3gene and determined that UCP3Sis generated when a cleavage and polyadenylation signal (AATAAA) located in the last intron prematurely terminates message elongation. In addition we have mapped UCP3to the distal segment of human chromosome 11q13 (between framework markers D11S916 and D11S911), adjacent to UCP2. Of note, UCP2and UCP3in both mice and humans colocalize in P1 and BAC genomic clones indicating that these two UCPs are located within 75–150 kilobases of each other and most likely resulted from a gene duplication event. Previous studies have noted that mouse UCP2maps to a region of chromosome 7 which is coincident with three independently mapped quantitative trait loci for obesity. Our study shows that UCP3is also coincident with these quantitative trait loci raising the possibility that abnormalities in UCP3are responsible for obesity in these models. |
| Databáze: |
Supplemental Index |
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