Tuberous sclerosis complex (TSC) is a genetic disorder characterized by seizures, mental disability, renal dysfunction and dermatological abnormalities. The disease is caused by inactivation of either hamartin or tuberin, the products of the TSC1 and TSC2 tumour-suppressor genes. Hamartin and tuberin form a complex and antagonise phosphoinositide 3-kinase/protein kinase B/target of rapamycin signal transduction by inhibiting p70 S6 kinase, an activator of translation, and activating 4E-binding protein 1, an inhibitor of translation initiation. Phosphorylation-dependent binding between tuberin and members of the 14-3-3 protein family indicates how the tuberin–hamartin complex may interact with upstream and downstream effectors, and suggests how phosphorylation-dependent regulation of the complex may be controlled.
Skip Nav Destination
Conference Article| June 01 2003
Regulation of tuberous sclerosis complex (TSC) function by 14-3-3 proteins
Biochem Soc Trans (2003) 31 (3): 587–591.
- Views Icon Views
- Share Icon Share
M. Nellist, M.A. Goedbloed, D.J.J. Halley; Regulation of tuberous sclerosis complex (TSC) function by 14-3-3 proteins. Biochem Soc Trans 1 June 2003; 31 (3): 587–591. doi: https://doi.org/10.1042/bst0310587
Download citation file:
Don't already have an account? Register
Get Access To This Article
Buy This Article