Abstract
Yin-and-Yang of mTORC1/C2 in Angelman syndrome mice.
Highlights
The mammalian/mechanistic target of rapamycin exists in two complexes, mTORC1 and mTORC2
We found that while mTORC1 activity is increased in the cerebellum of Angelman syndrome (AS) mice, mTORC2 activation is reduced
We found that S6K1-mediated inhibitory phosphorylation of rictor was increased in AS mice [2]
Summary
The mammalian/mechanistic target of rapamycin (mTOR) exists in two complexes, mTORC1 and mTORC2. Our recent studies have revealed that mTOR signaling is abnormal in the cerebellum of the mouse model for Angelman syndrome (AS) [2]. The AS mice have maternal Ube3A deficiency and display the major phenotypes of AS, including memory and motor deficits, and impairment in synaptic plasticity [4, 5].
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