K
Kunikazu Tanji
Researcher at Hirosaki University
Publications - 152
Citations - 10392
Kunikazu Tanji is an academic researcher from Hirosaki University. The author has contributed to research in topics: Dementia with Lewy bodies & Lewy body. The author has an hindex of 38, co-authored 144 publications receiving 9129 citations.
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Journal ArticleDOI
Edaravone and carnosic acid synergistically enhance the expression of nerve growth factor in human astrocytes under hypoxia/reoxygenation.
Hidemi Yoshida,Junsei Mimura,Tadaatsu Imaizumi,Tomoh Matsumiya,Akira Ishikawa,Norifumi Metoki,Kunikazu Tanji,Ken Ota,Ryo Hayakari,Kunio Kosaka,Ken Itoh,Kei Satoh +11 more
TL;DR: The use of edaravone and CA in combination may have therapeutic potential in the treatment of brain damage, particularly ischemia/reperfusion injury.
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Valosin-containing protein immunoreactivity in tauopathies, synucleinopathies, polyglutamine diseases and intranuclear inclusion body disease.
Fumiaki Mori,Kunikazu Tanji,Yasuko Toyoshima,Hidenao Sasaki,Mari Yoshida,Akiyoshi Kakita,Hitoshi Takahashi,Koichi Wakabayashi +7 more
TL;DR: Valosin‐containing protein (VCP) may have common mechanisms in the formation or degradation of cytoplasmic and nuclear inclusions of neurons, but not of glial cells, in several neurodegenerative conditions.
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Ribosome binding protein GCN1 regulates the cell cycle and cell proliferation and is essential for the embryonic development of mice.
Hiromi Yamazaki,Shuya Kasai,Junsei Mimura,Peng Ye,Atsushi Inose-Maruyama,Kunikazu Tanji,Koichi Wakabayashi,Seiya Mizuno,Fumihiro Sugiyama,Satoru Takahashi,Tsubasa Sato,Tsubasa Sato,Taku Ozaki,Douglas R. Cavener,Masayuki Yamamoto,Ken Itoh +15 more
TL;DR: It is demonstrated, for the first time, that GCN1 is essential for both GCN 2-dependent stress response and GCN2-independent cell cycle regulation.
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Interleukin-1 induces tau phosphorylation and morphological changes in cultured human astrocytes.
TL;DR: The early tau phosphorylation induced by IL-1&agr; might create a plastic environment for morphological changes in astrocytes.
Journal ArticleDOI
YOD1 attenuates neurogenic proteotoxicity through its deubiquitinating activity
Kunikazu Tanji,Fumiaki Mori,Yasuo Miki,Jun Utsumi,Hidenao Sasaki,Akiyoshi Kakita,Hitoshi Takahashi,Koichi Wakabayashi +7 more
TL;DR: The data suggest that the deubiquitinase YOD1 contributes to pathogenesis of neurodegenerative disease by decreasing ubiquitination of abnormal proteins and their subsequent degradation.