Zobrazeno 1 - 10
of 94
pro vyhledávání: '"Megumi Asada"'
Autor:
Megumi Asada-Utsugi, Makoto Urushitani
Publikováno v:
International Journal of Molecular Sciences, Vol 25, Iss 14, p 7906 (2024)
Neurons in the brain are continuously exposed to various sources of DNA damage. Although the mechanisms of DNA damage repair in mitotic cells have been extensively characterized, the repair pathways in post-mitotic neurons are still largely elusive.
Externí odkaz:
https://doaj.org/article/ebb39be2c8bb4570b5c2aeafa9ae5ebf
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
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
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
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
Publikováno v:
IEICE Transactions on Communications.
Publikováno v:
2021 IEEE 94th Vehicular Technology Conference (VTC2021-Fall).
Autor:
Masato Maesako, Maiko Uemura, Yoshitaka Tashiro, Kazuki Sasaki, Kiwamu Watanabe, Yasuha Noda, Karin Ueda, Megumi Asada-Utsugi, Masakazu Kubota, Katsuya Okawa, Masafumi Ihara, Shun Shimohama, Kengo Uemura, Ayae Kinoshita
Publikováno v:
PLoS ONE, Vol 10, Iss 9, p e0131199 (2015)
Obesity and type 2 diabetes are risk factors of Alzheimer's disease (AD). We reported that a high fat diet (HFD) promotes amyloid precursor protein (APP) cleavage by β-site APP cleaving enzyme 1 (BACE1) without increasing BACE1 levels in APP transge
Externí odkaz:
https://doaj.org/article/d3c1b127c225412f90873488877015f6
Autor:
Y. Tashiro, Ryosuke Takahashi, Tsuyoshi Miyakawa, Makoto Kinoshita, Hodaka Yamakado, Ayae Kinoshita, Megumi Asada-Utsugi, Satoko Hattori, Makoto Urushitani, Katsunori Kobayashi, T. M. Uemura, Kengo Uemura, Yasuha Noda, Natsumi Ageta-Ishihara, Masakazu Kubota
Publikováno v:
Molecular Brain, Vol 14, Iss 1, Pp 1-16 (2021)
Molecular Brain
Molecular Brain
N-cadherin is a homophilic cell adhesion molecule that stabilizes excitatory synapses, by connecting pre- and post-synaptic termini. Upon NMDA receptor (NMDAR) activation by glutamate, membrane-proximal domains of N-cadherin are cleaved serially by a
Autor:
Megumi Asada-Utsugi, Kengo Uemura, Masakazu Kubota, Yasuha Noda, Yasutaka Tashiro, Maiko T Uemura, Hodaka Yamakado, Makoto Urushitani, Ryosuke Takahashi, Satoko Hattori, Tsuyoshi Miyakawa, Natsumi Ageta-Ishihara, Katsunori Kobayashi, Makoto Kinoshita, Ayae Kinoshita
N-cadherin is a homophilic cell adhesion molecule that stabilizes excitatory synapses, by connecting pre- and post-synaptic termini. Upon NMDA receptor (NMDAR) activation by glutamate, membrane-proximal domains of N-cadherin are cleaved serially by a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::74d3efa8b281679b5c9f1aad4fb1fc54
https://doi.org/10.21203/rs.3.rs-64344/v3
https://doi.org/10.21203/rs.3.rs-64344/v3