Abstract
Recent studies show that hyperactivated mTOR, the 'target of rapamycin' that senses nutrient availability in eukaryotic cells, inhibits signaling by insulin receptor substrates. This crosstalk reveals how hyperactivated mTOR may suppress metastasis locally, while causing systemic insulin resistance that can progress to diabetes.
MeSH terms
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Animals
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Enzyme Activation / physiology*
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GTPase-Activating Proteins / metabolism
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Humans
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Insulin Resistance / physiology
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Models, Biological
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Mutation / genetics
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Neoplasm Metastasis / physiopathology*
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Protein Kinases / metabolism*
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Proteins / genetics
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Receptor, Insulin / antagonists & inhibitors*
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Signal Transduction / physiology*
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TOR Serine-Threonine Kinases
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Tuberous Sclerosis / metabolism*
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Tuberous Sclerosis / physiopathology
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Tuberous Sclerosis Complex 1 Protein
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Tumor Suppressor Proteins
Substances
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GTPase-Activating Proteins
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Proteins
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Tuberous Sclerosis Complex 1 Protein
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Tumor Suppressor Proteins
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Protein Kinases
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MTOR protein, human
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Receptor, Insulin
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TOR Serine-Threonine Kinases