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PMID |
Sentence |
1 |
18599524
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Inhibition of phosphatidylinositol 3-kinase/Akt significantly reduced high glucose-induced tuberin phosphorylation and restored OGG1 expression.
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2 |
18599524
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Hyperglycemia in type 1 diabetes and treatment of proximal tubular epithelial cells with high glucose leads to phosphorylation/inactivation of tuberin and downregulation of OGG1 via a redox-dependent activation of Akt in renal tubular epithelial cells.
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3 |
19286253
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The genes TSC1 and TSC2, encoding hamartin and tuberin, respectively, have been shown to be involved in the development of the autosomal dominantly inherited tumor syndrome tuberous sclerosis (TSC).
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4 |
18926585
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Tuberous sclerosis complex (TSC) gene products, TSC1 and TSC2 are tumor suppressors and specifically suppress TORC1 activity.
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5 |
18926585
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Mutation of either TSC1 or TSC2 causes TSC disease, which is characterized by formation of hamartomas in multiple organs.
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6 |
20068142
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Overexpression of ATGL in these cells antagonized the lipogenic effect of TSC2 knockout.
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7 |
21289215
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Induction of diabetes also increased phosphorylation of tuberin in association with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increased cytosolic cytochrome c expression, activation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes.
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8 |
21289215
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In vitro, exposure of PTE cells to HG increased phosphorylation of tuberin and p70S6K, phosphorylation of Bcl-2, expression of cytosolic cytochrome c, and caspase 3 activity.
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9 |
21886784
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We previously found that chronic tuberous sclerosis protein 2 (TSC2) deletion induces activation of mammalian target of rapamycin Complex 1 (mTORC1) and leads to hypertrophy of pancreatic beta cells from pancreatic beta cell-specific TSC2 knockout (?TSC2(-/-)) mice.
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10 |
21886784
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Activation of mTORC1 by TSC2 ablation increases mitochondrial biogenesis and enhances insulin secretion from pancreatic beta cells.
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11 |
21871459
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The myocardium of untreated db/db-/- mice exhibited a marked increase of the phosphorylation of AMPK, ACC, TSC2, expression of p53 and fatty acid translocase (FAT/CD36) membrane expression.
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