Journal ArticleDOI
mTOR complexes in neurodevelopmental and neuropsychiatric disorders
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TLDR
The most recent advances in studies of mTOR signaling in the brain and the possible mechanisms underlying the many different functions of the mTOR complexes in neurological diseases are described and the medical relevance is discussed.Abstract:
The mechanistic target of rapamycin (mTOR) acts as a highly conserved signaling "hub" that integrates neuronal activity and a variety of synaptic inputs. mTOR is found in two functionally distinct complexes, mTORC1 and mTORC2, that crucially control long-term synaptic efficacy and memory storage. Dysregulation of mTOR signaling is associated with neurodevelopmental and neuropsychiatric disorders. In this Review, we describe the most recent advances in studies of mTOR signaling in the brain and the possible mechanisms underlying the many different functions of the mTOR complexes in neurological diseases. In addition, we discuss the medical relevance of these findings.read more
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mTOR in Brain Physiology and Pathologies
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References
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mGluR-Dependent Long-Term Depression Is Associated with Increased Phosphorylation of S6 and Synthesis of Elongation Factor 1A but Remains Expressed in S6K-Deficient Mice
Marcia D. Antion,Lingfei Hou,Lingfei Hou,Helen Wong,Charles A. Hoeffer,Charles A. Hoeffer,Eric Klann,Eric Klann +7 more
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Involvement of the mammalian target of rapamycin signaling in the antidepressant-like effect of group II metabotropic glutamate receptor antagonists.
TL;DR: The present result suggests that the blockade of the mGlu2/3 receptor may activate mTOR signaling, and that the activation of m TOR signaling may contribute to the sustained antidepressant-like effects of mGLU2/ 3 receptor antagonists.
Journal ArticleDOI
TSC2 modulates actin cytoskeleton and focal adhesion through TSC1-binding domain and the Rac1 GTPase
TL;DR: It is found that T SC2 modulates actin dynamics and cell adhesion and the TSC1-binding domain (TSC2-HBD) is essential for this function of TSC2.
Journal ArticleDOI
Dysregulation of synaptic plasticity precedes appearance of morphological defects in a Pten conditional knockout mouse model of autism.
Koichi Takeuchi,Michael Gertner,Jing Zhou,Jing Zhou,Luis F. Parada,Michael V. L. Bennett,R. Suzanne Zukin +6 more
TL;DR: The results reveal that deletion of Pten in dentate granule cells dysregulates synaptic plasticity, a defect that may underlie abnormal social and cognitive behaviors observed in humans with inactivating mutations and potentially other autism spectrum disorders.
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Inhibition of the mammalian target of rapamycin blocks epilepsy progression in NS-Pten conditional knockout mice
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TL;DR: Evaluated the efficacy of an intermittent rapamycin treatment protocol on epilepsy progression using neuron subset‐specific‐Pten (NS‐ Pten) conditional knockout mice.
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