M
Mieko Maruyama
Researcher at Niigata University
Publications - 7
Citations - 1194
Mieko Maruyama is an academic researcher from Niigata University. The author has contributed to research in topics: Parkinsonism & Synucleinopathies. The author has an hindex of 7, co-authored 7 publications receiving 1130 citations. Previous affiliations of Mieko Maruyama include RIKEN Brain Science Institute.
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Journal ArticleDOI
A Neurological Disease Caused By an Expanded CAG Trinucleotide Repeat in The TATA-Binding Protein Gene: A New Polyglutamine Disease?
Reiji Koide,Shigeichi Kobayashi,Takayoshi Shimohata,Takeshi Ikeuchi,Mieko Maruyama,Masaaki Saito,Mitsunori Yamada,Hitoshi Takahashi,Shoji Tsuji +8 more
TL;DR: The present study identified a sporadic-onset patient with unique neurologic symptoms consisting of ataxia and intellectual deterioration associated with de novo expansion of the CAG repeat of the TBP gene.
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An autopsy case of autosomal-recessive juvenile parkinsonism with a homozygous exon 4 deletion in the parkin gene.
Shintaro Hayashi,Koichi Wakabayashi,Atsushi Ishikawa,Hiroko Nagai,Masaaki Saito,Mieko Maruyama,Toshiaki Takahashi,Tetsutaro Ozawa,Shoji Tsuji,Hitoshi Takahashi +9 more
TL;DR: Autopsied patient and his siblings had the parkin gene mutation (homozygous exon 4 deletion) that is responsible for the disease; this feature has not been reported previously in AR‐JP.
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Increased expression of p62 in expanded polyglutamine-expressing cells and its association with polyglutamine inclusions.
Utako Nagaoka,Ken Kim,Nihar Ranjan Jana,Hiroshi Doi,Mieko Maruyama,Kenichi Mitsui,Fumitaka Oyama,Nobuyuki Nukina +7 more
TL;DR: The results suggest that p62 may play important roles as a responsive protein to a polyglutamine‐induced stress rather than as a cross‐linker between ubiquitylated proteins.
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α-Synuclein Affects the MAPK Pathway and Accelerates Cell Death
TL;DR: It is concluded that α-synuclein regulates the MAPK pathway by reducing the amount of available active MAPK in cultured cells and thus offers therapeutic insight into synucleinopathies.
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Alpha-synuclein degradation by serine protease neurosin: implication for pathogenesis of synucleinopathies
Atsushi Iwata,Mieko Maruyama,Takumi Akagi,Tsutomu Hashikawa,Ichiro Kanazawa,Shoji Tsuji,Nobuyuki Nukina +6 more
TL;DR: It is found that the serine protease neurosin (kallikrein-6) degrades alpha-synuclein and co-localizes with pathological inclusions such as Lewy bodies and glial cytoplasmic inclusions and also in the pathogenesis of synucleinopathies.