Abstract
In this issue of Molecular Cell, Ozcan et al. (2008) show that the loss of the tuberous sclerosis tumor suppressor complex induces endoplasmic reticulum stress, leading to attenuation of insulin receptor signaling activity via the unfolded protein response.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Comment
MeSH terms
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Animals
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Endoplasmic Reticulum / metabolism
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Humans
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Mechanistic Target of Rapamycin Complex 1
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Mice
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Multiprotein Complexes
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Neoplasms / metabolism
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Oxidative Stress*
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Proteins
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Receptor, Insulin / metabolism
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Signal Transduction / physiology*
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TOR Serine-Threonine Kinases
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism
Substances
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Multiprotein Complexes
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Proteins
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Transcription Factors
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Tumor Suppressor Proteins
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Receptor, Insulin
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Mechanistic Target of Rapamycin Complex 1
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TOR Serine-Threonine Kinases