Sangyeul Han

TL;DR: The results presented here reveal a biological basis for some of the cognitive deficits associated with tuberous sclerosis, and they show that treatment with mTOR antagonists ameliorates cognitive dysfunction in a mouse model of this disorder.

TL;DR: The deregulation of mTORC1 activation underlies the aberrant growth and proliferation of NF2-associated tumors and may restrain the growth of these lesions through negative feedback mechanisms, suggesting that rapamycin in combination with phosphoinositide 3-kinase inhibitors may be therapeutic for NF2.

TL;DR: It is shown that merlin positively regulates the kinase activity of mTORC2, a second functionally distinct mTOR complex, and that downstream phosphorylation of m TORC2 substrates, including Akt, is reduced upon acute merlin deficiency in cells.

TL;DR: A novel mechanism of post-translational inactivation of the TSC2 protein, tuberin, by physiologically inappropriate phosphorylation is demonstrated, which is specific to tuberous sclerosis complex-associated brain lesions and has widespread implications for understanding the tissue specificity of tumor suppressor gene phenotypes.

TL;DR: It is hypothesized that Pam, a protein identified as an interactor of Myc, could regulate the ubiquitination and proteasomal degradation of the tuberin-hamartin complex particularly in the CNS.