A Mouse Model of Tuberous Sclerosis: Neuronal Loss of Tsc1 Causes Dysplastic and Ectopic Neurons, Reduced Myelination, Seizure Activity, and Limited Survival
Lynsey M. Meikle(Brigham and Women's Hospital), David J. Kwiatkowski(Brigham and Women's Hospital)
Cited by 460
Related Papers
Response of a Neuronal Model of Tuberous Sclerosis to Mammalian Target of Rapamycin (mTOR) Inhibitors: Effects on mTORC1 and Akt Signaling Lead to Improved Survival and Function
|Journal of Neuroscience|2008|502
Loss of Tsc1/Tsc2 activates mTOR and disrupts PI3K-Akt signaling through downregulation of PDGFR
|Journal of Clinical Investigation|2003|479
PDGFRs are critical for PI3K/Akt activation and negatively regulated by mTOR
|Journal of Clinical Investigation|2007|381
Regulable neural progenitor-specific <i>Tsc1</i> loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex
|Proceedings of the National Academy of Sciences|2011|178