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Mitsuyo Maeda

Researcher at Osaka City University

Publications -  31
Citations -  4876

Mitsuyo Maeda is an academic researcher from Osaka City University. The author has contributed to research in topics: Skeletal muscle & Sendai virus. The author has an hindex of 16, co-authored 26 publications receiving 4611 citations. Previous affiliations of Mitsuyo Maeda include Osaka Dental University.

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The Homeoprotein Nanog Is Required for Maintenance of Pluripotency in Mouse Epiblast and ES Cells

TL;DR: Nanog is a critical factor underlying pluripotency in both ICM and ES cells, and it is found that one of them, encoding the homeoprotein Nanog, was capable of maintaining ES cell self-renewal independently of LIF/Stat3.
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mTOR is essential for growth and proliferation in early mouse embryos and embryonic stem cells.

TL;DR: Deletion of the C-terminal six amino acids of mTOR, which are essential for kinase activity, resulted in reduced cell size and proliferation arrest in embryonic stem cells, and showed that mTOR controls both cell Size and proliferation in early mouse embryos and embryonicstem cells.
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Fbx15 is a novel target of Oct3/4 but is dispensable for embryonic stem cell self-renewal and mouse development.

TL;DR: It is found that F-box-containing protein Fbx15 was expressed predominantly in mouse undifferentiated ES cells, and homozygous mutant mice showed no gross developmental defects and were fertile.
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Oligodendrocyte Precursor Cells Support Blood-Brain Barrier Integrity via TGF-β Signaling

TL;DR: It is demonstrated that OPCs increase BBB tightness by upregulating tight junction proteins via TGF-β signaling, which indicates that astrocytes and pericytes are well-known regulators of BBB maturation and maintenance, but also play a pivotal role in promoting BBB integrity.
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Nerve injury-activated microglia engulf myelinated axons in a P2Y12 signaling-dependent manner in the dorsal horn.

TL;DR: Results indicate that engulfment of myelinated axons by activated microglia via P2Y12 signaling in the dorsal horn may be a critical event in the pathogenesis of neuropathic pain.