Endogenous mutations in human uncoupling protein 3 alter its functional properties

被引:21
作者
Brown, AM
Dolan, JW
Willi, SM
Garvey, WT
Argyropoulos, G
机构
[1] Med Univ S Carolina, Dept Med, Div Endocrinol, Charleston, SC 29425 USA
[2] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC 29425 USA
[3] Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA
[4] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA
关键词
mitochondrion; obesity; membrane potential; UCP3;
D O I
10.1016/S0014-5793(99)01708-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Human uncoupling protein 3 (UCP3) is a mitochondrial transmembrane carrier that uncouples oxidative phosphorylation and is a candidate gene for obesity. Expression of native human UCP3 mutations in yeast showed complete loss (R70W), significant reduction (R143X), or no effect (V102I and IVS6+1G>A) on the uncoupling activity of UCP3, It is concluded that certain mutations in UCP3 alter its functional impact on membrane potential (Delta Psi), possibly conferring susceptibility to develop metabolic diseases, (C) 1999 Federation of European Biochemical Societies.
引用
收藏
页码:189 / 193
页数:5
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