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PMID |
Sentence |
1 |
10749987
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Mutations in SCO2 are associated with a distinct form of hypertrophic cardiomyopathy and cytochrome c oxidase deficiency.
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2 |
10749987
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Mutations in SCO2, a cytochrome c oxidase (COX) assembly gene located on chromosome 22, have recently been reported in patients with fatal infantile cardio-encephalomyopathy and severe COX deficiency in heart and skeletal muscle.
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3 |
10749987
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Mutations in SCO2 are associated with a distinct form of hypertrophic cardiomyopathy and cytochrome c oxidase deficiency.
|
4 |
10749987
|
Mutations in SCO2, a cytochrome c oxidase (COX) assembly gene located on chromosome 22, have recently been reported in patients with fatal infantile cardio-encephalomyopathy and severe COX deficiency in heart and skeletal muscle.
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5 |
21185935
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In vitro data indicate that cellular levels of reactive oxygen species depend on the expression and activity of p53, which plays a key role in energy metabolism and as a crucial transcription factor for SCO cytochrome oxidase deficient homolog 2 (SCO2) and tumor p53-induced glycolysis and apoptosis regulator (TIGAR), which regulate mitochondrial respiration and glycolysis in cells.
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6 |
21185935
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Exercise training increased serum adiponectin and decreased serum insulin and levels of glycosylated hemoglobin (P<0.05).
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7 |
21185935
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Exercise training decreased p53 protein levels and TIGAR expression in skeletal muscle (P<0.05), but SCO2 expression was unchanged.
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8 |
21185935
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These data indicate that exercise training can attenuate oxidative stress and increase mitochondrial DNA content in skeletal muscle in rats with T2DM and that exercise-induced suppression of p53 and TIGAR expression may play a role in preventing oxidative stress in insulin resistance.
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9 |
21185935
|
In vitro data indicate that cellular levels of reactive oxygen species depend on the expression and activity of p53, which plays a key role in energy metabolism and as a crucial transcription factor for SCO cytochrome oxidase deficient homolog 2 (SCO2) and tumor p53-induced glycolysis and apoptosis regulator (TIGAR), which regulate mitochondrial respiration and glycolysis in cells.
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10 |
21185935
|
Exercise training increased serum adiponectin and decreased serum insulin and levels of glycosylated hemoglobin (P<0.05).
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11 |
21185935
|
Exercise training decreased p53 protein levels and TIGAR expression in skeletal muscle (P<0.05), but SCO2 expression was unchanged.
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12 |
21185935
|
These data indicate that exercise training can attenuate oxidative stress and increase mitochondrial DNA content in skeletal muscle in rats with T2DM and that exercise-induced suppression of p53 and TIGAR expression may play a role in preventing oxidative stress in insulin resistance.
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