Genes & development · 2004
Regulation of the TSC pathway by LKB1: evidence of a molecular link between tuberous sclerosis complex and Peutz-Jeghers syndrome.
СтатьяПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Corradetti Michael N, Inoki Ken, Bardeesy Nabeel, DePinho Ronald A, Guan Kun-Liang
Аннотация
Tuberous sclerosis complex (TSC) and Peutz-Jeghers syndrome (PJS) are dominantly inherited benign tumor syndromes that share striking histopathological similarities. Here we show that LKB1, the gene mutated in PJS, acts as a tumor suppressor by activating TSC2, the gene mutated in TSC. Like TSC2, LKB1 inhibits the phosphorylation of the key translational regulators S6K and 4EBP1. Furthermore, we show that LKB1 activates TSC2 through the AMP-dependent protein kinase (AMPK), indicating that LKB1 plays a role in cell growth regulation in response to cellular energy levels. Our results suggest that PJS and other benign tumor syndromes could be caused by dysregulation of the TSC2/mTOR pathway.
Предметные рубрики MeSH
AMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Cycle ProteinsCells, CulturedDeoxyglucoseEukaryotic Initiation FactorsFibroblastsGenes, Tumor SuppressorHeLa CellsHumansMiceMultienzyme ComplexesMutationPeutz-Jeghers SyndromePhosphoproteinsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesRNA InterferenceRepressor ProteinsRibosomal Protein S6 KinasesSignal TransductionTOR Serine-Threonine KinasesTuberous SclerosisTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins