Tuberous sclerosis complex (TSC) tumor suppressors form the TSC1-TSC2 molecular complex. Under poor growth conditions the TSC1-TSC2 complex limits cell growth.[1] A key promoter of cell growth, mTORC1, is inhibited by the tuberous sclerosis complex.[1] Insulin activates mTORC1 and causes dissociation of TSC from the surface of lysosomes.[2]
Resistance to ischemia-reperfusion injury by protein restriction is mediated by activation of the tuberous sclerosis complex.[3]
References
edit- ^ a b Dibble CC, Elis W, Menon S, Qin W, Klekota J, Asara JM, Finan PM, Kwiatkowski DJ, Murphy LO, Manning BD (2012). "TBC1D7 is a third subunit of the TSC1-TSC2 complex upstream of mTORC1". Molecular Cell. 47 (4): 535–546. doi:10.1016/j.molcel.2012.06.009. PMC 3693578. PMID 22795129.
- ^ Menon S, Dibble CC, Talbott G, Hoxhaj G, Valvezan AJ, Takahashi H, Cantley LC, Manning BD (2014). "Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome". Cell. 156 (4): 771–785. doi:10.1016/j.cell.2013.11.049. PMC 403068. PMID 24529379.
- ^ Harputlugil E, Hine C, Vargas D, Robertson L, Manning BD, Mitchell JR (2014). "The TSC complex is required for the benefits of dietary protein restriction on stress resistance in vivo". Cell Reports. 8 (4): 1160–1170. doi:10.1016/j.celrep.2014.07.018. PMC 4260622. PMID 25131199.
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