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1 mics signature in mice overexpressing muscle uncoupling protein 3.
2 ls, as well as a reduction in the content of uncoupling protein 3.
3 d cell death were abrogated by knock down of uncoupling protein 3.
4 ranscription factor 1, citrate synthase, and uncoupling protein-3, although KPF itself is not a direc
5 switches mitochondrial Ca(2+) uptake from an uncoupling protein 3- and mitochondrial calcium uniporte
6 -1, medium-chain acyl-CoA dehydrogenase, and uncoupling protein 3), calcium homeostasis (sarcoplasmic
7 ttenuates anoxia-reoxygenation tolerance but uncoupling protein-3 depletion does not reduce anoxia to
9 a mitochondrial protein known as UCP-3 (for 'uncoupling protein-3') have a diminished thermogenic res
10 ture associated with increased expression of uncoupling protein 3 in brown and white adipose tissues
11 rotein-2 appears to play a greater role than uncoupling protein-3 in modulating ischemia/anoxia toler
12 me proliferator-activated receptor alpha and uncoupling protein 3, increases in mitochondrial protein
14 ith WT mice, along with a marked increase in uncoupling protein 3 mRNA expression in skeletal muscle,
17 ncluding pyruvate-dehydrogenase kinase 4 and uncoupling protein 3, responses that were similar to tho
18 ation of pyruvate-dehydrogenase kinase 4 and uncoupling protein 3, two classical and robustly respons
19 o determine the effect of diabetes on muscle uncoupling protein 3 (UCP-3), a potential regulator of m
20 ibres from the soleus of mice overexpressing uncoupling protein 3 (UCP-3tg) were compared with the pe
22 ity was increased by 25% in O vs YA muscles, uncoupling protein-3 (UCP-3) protein level was upregulat
24 ve stress, and despite a twofold increase in uncoupling protein 3 (UCP3) content, ATP-to-O ratios and
25 gy coupling in skeletal muscle and change in uncoupling protein 3 (UCP3) expression during the transi
28 ers have shown previously that mitochondrial uncoupling protein 3 (UCP3) improves functional recovery
32 tial effects on rates of energy expenditure, uncoupling protein 3 (UCP3) is an obesity candidate gene
35 ion, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing gly
38 tivator of fatty acid oxidizing enzymes, and uncoupling protein 3 (UCP3), a thermogenic mitochondrial
39 lex IV subunit 1 (COX1) was tightly bound to uncoupling protein 3 (UCP3), but this complex was disrup
41 ous system, increasing fatty acid oxidation, uncoupling protein-3 (UCP3) expression, and thus, energy
45 e showed that the glutathionylation state of uncoupling protein-3 (UCP3) modulates the leak of proton
46 f pyruvate dehydrogenase kinase-4 (PDK4) and uncoupling protein-3 (UCP3), genes that are known to be
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