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Tetsuya Imura

Researcher at Kyoto Prefectural University of Medicine

Publications -  39
Citations -  3505

Tetsuya Imura is an academic researcher from Kyoto Prefectural University of Medicine. The author has contributed to research in topics: Stem cell & Neurogenesis. The author has an hindex of 22, co-authored 36 publications receiving 3210 citations. Previous affiliations of Tetsuya Imura include Fukushima Medical University & University of California, Los Angeles.

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GFAP-expressing progenitors are the principal source of constitutive neurogenesis in adult mouse forebrain

TL;DR: These findings identify morphologically distinctive GFAP-expressing progenitor cells as the predominant sources of constitutive adult neurogenesis, and provide new methods for manipulating and investigating these cells.
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STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury

TL;DR: Findings indicate that STAT3 signaling is a critical regulator of certain aspects of reactive astrogliosis and provide additional evidence that scar-forming astrocytes restrict the spread of inflammatory cells after SCI.
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The Predominant Neural Stem Cell Isolated from Postnatal and Adult Forebrain But Not Early Embryonic Forebrain Expresses GFAP

TL;DR: It is demonstrated that the predominant multipotent NSCs isolated from postnatal and adult but not early embryonic GZs express GFAP, and that NSCS exhibit heterogeneous expression of intermediate filaments during developmental maturation.
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Maternal embryonic leucine zipper kinase (MELK) regulates multipotent neural progenitor proliferation

TL;DR: It is shown that MELK serves as a marker for self-renewing multipotent neural progenitors (MNPs) in cultures derived from the developing forebrain and in transgenic mice and is suggested that it regulates the transition from GFAP-expressing progenitor to rapid amplifying progensitors in the postnatal brain.
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Disruption of astrocyte STAT3 signaling decreases mitochondrial function and increases oxidative stress in vitro.

TL;DR: The findings show that the absence of STAT3 signaling in astrocytes leads to increased production of superoxide anion and other reactive oxygen species and decreased level of glutathione, decreased mitochondrial membrane potential and decreased ATP production, and decreased rate of cell proliferation.