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Takahiro Miyawaki

Researcher at Yeshiva University

Publications -  17
Citations -  1321

Takahiro Miyawaki is an academic researcher from Yeshiva University. The author has contributed to research in topics: Protein kinase B & AMPA receptor. The author has an hindex of 11, co-authored 17 publications receiving 1239 citations. Previous affiliations of Takahiro Miyawaki include Jichi Medical University & Albert Einstein College of Medicine.

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Journal ArticleDOI

Dysregulation of mTOR Signaling in Fragile X Syndrome

TL;DR: Elevated mTOR signaling may provide a functional link between overactivation of group I mGluRs and aberrant synaptic plasticity in the fragile X mouse, mechanisms relevant to impaired cognition in fragile X syndrome.
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Repressor element-1 silencing transcription factor (REST)-dependent epigenetic remodeling is critical to ischemia-induced neuronal death.

TL;DR: It is shown that neuronal insults trigger activation of REST and CoREST in a clinically relevant model of ischemic stroke and that REST binds a subset of “transcriptionally responsive” genes, of which the AMPA receptor subunit GluA2 is a top hit.
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Ischemic insults promote epigenetic reprogramming of μ opioid receptor expression in hippocampal neurons

TL;DR: These findings implicate MORs in ischemia-induced death of CA1 pyramidal neurons and document epigenetic remodeling of expression of OPRM1 in CA1 inhibitory interneurons.
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Zinc-Dependent Multi-Conductance Channel Activity in Mitochondria Isolated from Ischemic Brain

TL;DR: It is shown that global ischemia promotes alterations in mitochondrial membrane contact points, a rise in intramitochondrial Zn2+, and activation of large, multi-conductance channels in mitochondrial outer membranes by 1 h after insult, and implicate ΔN-BCL-xL and VDAC in the large, Zn 2+-dependent mitochondrial channels observed in post-ischemic hippocampal mitochondria.
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The endogenous inhibitor of Akt, CTMP, is critical to ischemia-induced neuronal death.

TL;DR: It is found that global ischemia in intact rats triggered expression and activation of the Akt inhibitor CTMP (carboxyl-terminal modulator protein) in vulnerable hippocampal neurons and that CTMP bound and extinguished Akt activity and was essential to ischemIA-induced neuronal death.