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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.1
- 수록면
- 272 - 287 (16page)
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The mechanistic target of rapamycin (mTOR) pathway coordinates the metabolic activity of eukaryotic cells through environmental signals, including nutrients, energy, growth factors, and oxygen. In the nervous system, the mTOR pathway regulates fundamental biological processes associated with neural development and neurodegeneration. Intriguingly, genes that constitute the mTOR pathway have been found to be germline and somatic mutation from patients with various epileptic disorders. Hyperactivation of the mTOR pathway due to said mutations has garnered increasing attention as culprits of these conditions : somatic mutations, in particular, in epileptic foci have recently been identified as a major genetic cause of intractable focal epilepsy, such as focal cortical dysplasia. Meanwhile, epilepsy models with aberrant activation of the mTOR pathway have helped elucidate the role of the mTOR pathway in epileptogenesis, and evidence from epilepsy models of human mutations recapitulating the features of epileptic patients has indicated that mTOR inhibitors may be of use in treating epilepsy associated with mutations in mTOR pathway genes. Here, we review recent advances in the molecular and genetic understanding of mTOR signaling in epileptic disorders. In particular, we focus on the development of and limitations to therapies targeting the mTOR pathway to treat epileptic seizures. We also discuss future perspectives on mTOR inhibition therapies and special diagnostic methods for intractable epilepsies caused by brain somatic mutations.
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참고문헌 (159)
참고문헌 신청
Abu-Remaileh M / 2017 / Lysosomal metabolomics reveals V-ATPase-and mTOR-dependent regulation of amino acid efflux from lysosomes / Science 358:807~813
Alcantara D / 2017 / Mutations of AKT3 are associated with a wide spectrum of developmental disorders including extreme megalencephaly / Brain 140:2610~2622
Alfaiz AA / 2014 / TBC1D7 mutations are associated with intellectual disability, macrocrania, patellar dislocation, and celiac disease / Hum Mutat 35:447~451
Aronica E / 2012 / Malformations of cortical development / Brain Pathol 22:380~401
Avoli M / 1999 / Epileptiform discharges in the human dysplastic neocortex: in vitro physiology and pharmacology / Ann Neurol 46:816~826
Alcantara D / 2017 / Mutations of AKT3 are associated with a wide spectrum of developmental disorders including extreme megalencephaly / Brain 140:2610~2622
Alfaiz AA / 2014 / TBC1D7 mutations are associated with intellectual disability, macrocrania, patellar dislocation, and celiac disease / Hum Mutat 35:447~451
Aronica E / 2012 / Malformations of cortical development / Brain Pathol 22:380~401
Avoli M / 1999 / Epileptiform discharges in the human dysplastic neocortex: in vitro physiology and pharmacology / Ann Neurol 46:816~826
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Modulation of PI3K/PTEN-mTOR signaling pathway in the antibody class switching in activated B cells
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Inhibition of Mast Cell Function and Proliferation by mTOR Activator MHY1485
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