Zobrazeno 1 - 8 of 8 pro vyhledávání: '"Sumio Minamiyama"'
1
Akademický článek
Efficacy of oligodendrocyte precursor cells as delivery vehicles for single-chain variable fragment to misfolded SOD1 in ALS rat model
Autor: Sumio Minamiyama, Madoka Sakai, Yuko Yamaguchi, Makiko Kusui, Hideki Wada, Ryota Hikiami, Yoshitaka Tamaki, Megumi Asada-Utsugi, Akemi Shodai, Akiko Makino, Noriko Fujiwara, Takashi Ayaki, Takakuni Maki, Hitoshi Warita, Masashi Aoki, Keizo Tomonaga, Ryosuke Takahashi, Makoto Urushitani
Publikováno v: Molecular Therapy: Methods & Clinical Development, Vol 28, Iss , Pp 312-329 (2023)
Superoxide dismutase1 (SOD 1) mutation is a leading cause of familial amyotrophic lateral sclerosis (ALS). Growing evidence suggests that antibody therapy against misfolded SOD1 protein can be therapeutic. However, the therapeutic effects are limited
Externí odkaz: https://doaj.org/article/125f475f713e45e783a43ac5eb717f6d
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2
Akademický článek
Conformational change of RNA-helicase DHX30 by ALS/FTD-linked FUS induces mitochondrial dysfunction and cytosolic aggregates
Autor: Ryota Hikiami, Toshifumi Morimura, Takashi Ayaki, Tomoyuki Tsukiyama, Naoko Morimura, Makiko Kusui, Hideki Wada, Sumio Minamiyama, Akemi Shodai, Megumi Asada-Utsugi, Shin-ichi Muramatsu, Takatoshi Ueki, Ryosuke Takahashi, Makoto Urushitani
Publikováno v: Scientific Reports, Vol 12, Iss 1, Pp 1-15 (2022)
Abstract Genetic mutations in fused in sarcoma (FUS) cause amyotrophic lateral sclerosis (ALS). Although mitochondrial dysfunction and stress granule have been crucially implicated in FUS proteinopathy, the molecular basis remains unclear. Here, we s
Externí odkaz: https://doaj.org/article/466c0b9b2b744c3492877408d329cf97
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3
Akademický článek
Cellular analysis of SOD1 protein-aggregation propensity and toxicity: a case of ALS with slow progression harboring homozygous SOD1-D92G mutation
Autor: Masanori Sawamura, Keiko Imamura, Rie Hikawa, Takako Enami, Ayako Nagahashi, Hodaka Yamakado, Hidenori Ichijo, Takao Fujisawa, Hirofumi Yamashita, Sumio Minamiyama, Misako Kaido, Hiromi Wada, Makoto Urushitani, Haruhisa Inoue, Naohiro Egawa, Ryosuke Takahashi
Publikováno v: Scientific Reports, Vol 12, Iss 1, Pp 1-10 (2022)
Abstract Mutations within Superoxide dismutase 1 (SOD1) cause amyotrophic lateral sclerosis (ALS), accounting for approximately 20% of familial cases. The pathological feature is a loss of motor neurons with enhanced formation of intracellular misfol
Externí odkaz: https://doaj.org/article/5512a4141a3a461c9c52da902cb141e6
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4
Akademický článek
Failure of DNA double-strand break repair by tau mediates Alzheimer’s disease pathology in vitro
Autor: Megumi Asada-Utsugi, Kengo Uemura, Takashi Ayaki, Maiko T. Uemura, Sumio Minamiyama, Ryota Hikiami, Toshifumi Morimura, Akemi Shodai, Takatoshi Ueki, Ryosuke Takahashi, Ayae Kinoshita, Makoto Urushitani
Publikováno v: Communications Biology, Vol 5, Iss 1, Pp 1-12 (2022)
Phosphorylated microtubule-associated protein tau (p-tau) accumulates at double-strand breaks (DSBs) in neurons. Loss of tau induces failure of DSB repair and excessive DSB accumulation, leading to aberrant p-tau aggregation and apoptotic neurons.
Externí odkaz: https://doaj.org/article/de0adf46df324e2681f7db4538e8e628
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5
In vivo analysis of aggregation propensity of low levels of mislocalized TDP-43 on cytopathological and behavioral phenotype of ALS/FTLD
Autor: Hideki Wada, Ryota Hikiami, Makiko Kusui, Sumio Minamiyama, Megumi Asada-Utsugi, Akemi Shodai, Shin-ichi Muramatsu, Toshifumi Morimura, Makoto Urushitani
Publikováno v: Neuroscience research.
Mislocalization and aggregate formation of TAR DNA-biding protein of 43kD (TDP-43) in the cytoplasm are signatures of amyotrophic lateral sclerosis(ALS) and frontotemporal lobar degeneration (FTLD). However, the role of two cytopathologies in ALS/FTL
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::46a81be33a366c23d9fe4483f373867a
http://hdl.handle.net/10422/00013536
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6
Thigh muscle MRI findings in myopathy associated with anti-mitochondrial antibody
Autor: Sumio Minamiyama, Ran Nakashima, Ryota Fujimoto, Yusuke Sakato, Hirofumi Yamashita, Nobukatsu Sawamoto, Sakiho Ueda, Ryosuke Takahashi, Tsuneyo Mimori, Makoto Urushitani, Hodaka Yamakado, Ichizo Nishino
Publikováno v: MusclenerveREFERENCES. 61(1)
Introduction Myopathy associated with anti-mitochondrial antibody (AMA) has recently been characterized as a distinct type of idiopathic inflammatory myopathy. The purpose of this study is to evaluate the pattern of involvement in thigh muscles in AM
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::34855c6be4d77ec998c33541d190a8f7
https://pubmed.ncbi.nlm.nih.gov/31588577
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7
Elimination of TDP-43 inclusions linked to amyotrophic lateral sclerosis by a misfolding-specific intrabody with dual proteolytic signals
Autor: Toshifumi Morimura, Ryosuke Takahashi, Sumio Minamiyama, Yoshiaki Furukawa, Ryota Hikiami, Ikuo Tooyama, Takashi Ayaki, Yoshitaka Tamaki, Makoto Urushitani, Akemi Shodai
Publikováno v: Scientific Reports, Vol 8, Iss 1, Pp 1-16 (2018)
Scientific Reports
Aggregation of TAR DNA-binding protein of 43 kDa (TDP-43) is implicated in the pathogenesis of sporadic and certain familial forms of amyotrophic lateral sclerosis (ALS), suggesting elimination of TDP-43 aggregates as a possible therapeutic strategy.
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e1fbdf858e031b10fa0d6a66bb4c0e95
http://hdl.handle.net/10422/00012419
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