Mutations in genes encoding either hamartin [TSC1 (tuberous sclerosis complex 1)] or tuberin (TSC2) result in a multisystem disorder characterized by the development of benign tumours and hamartomas in several organs. The TSC1 and TSC2 proteins form a complex that lies at the crossroad of many signalling pathways integrating the energy status of the cell with signals induced by nutrients and growth factors. The TSC1/2 complex is a critical negative regulator of mTORC1 [mTOR (mammalian target of rapamycin) complex 1], and by that controls anabolic processes to promote cell growth, proliferation and survival. In the present paper, we review recent evidence highlighting the notion that the TSC1/2 complex simultaneously controls mTOR-dependent and mTOR-independent signals critical for the balancing of cell proliferation and cell death.
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April 2011
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Conference Article|
March 22 2011
The tuberous sclerosis complex: balancing proliferation and survival
Romana Tomasoni;
Romana Tomasoni
*Program in Immunology and Bio-Immuno-Gene Therapy of Cancer (PIBIC), Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, I-20132 Milan, Italy
†Vita-Salute San Raffaele University, San Raffaele Scientific Institute, I-20132 Milan, Italy
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Anna Mondino
Anna Mondino
1
*Program in Immunology and Bio-Immuno-Gene Therapy of Cancer (PIBIC), Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, I-20132 Milan, Italy
1To whom correspondence should be addressed (email anna.mondino@hsr.it).
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Publisher: Portland Press Ltd
Received:
November 11 2010
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (2): 466–471.
Article history
Received:
November 11 2010
Citation
Romana Tomasoni, Anna Mondino; The tuberous sclerosis complex: balancing proliferation and survival. Biochem Soc Trans 1 April 2011; 39 (2): 466–471. doi: https://doi.org/10.1042/BST0390466
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