T
Takashi Matsuwaki
Researcher at University of Tokyo
Publications - 63
Citations - 2018
Takashi Matsuwaki is an academic researcher from University of Tokyo. The author has contributed to research in topics: Skeletal muscle & Neurogenesis. The author has an hindex of 22, co-authored 60 publications receiving 1731 citations. Previous affiliations of Takashi Matsuwaki include Linköping University.
Papers
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Journal ArticleDOI
Granulin Is a Soluble Cofactor for Toll-like Receptor 9 Signaling
Boyoun Park,Ludovico Buti,Ludovico Buti,Sungwook Lee,Takashi Matsuwaki,Eric Spooner,Melanie M. Brinkmann,Masugi Nishihara,Hidde L. Ploegh +8 more
TL;DR: In this paper, the authors investigated the presence of an analagous soluble cofactor that might assist in the recruitment of CpG oligonucleotides (CpG-ODNs) to TLR9.
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Alteration of behavioural phenotype in mice by targeted disruption of the progranulin gene.
Yuko Kayasuga,Shuichi Chiba,Masatoshi Suzuki,Takefumi Kikusui,Takashi Matsuwaki,Keitaro Yamanouchi,Hayato Kotaki,Reiko Horai,Yoichiro Iwakura,Masugi Nishihara +9 more
TL;DR: The results suggest that PGRN gene plays a role in establishing sexual dimorphic behaviours at least partially by modulating the brain serotonergic system.
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Proteolytic processing of TAR DNA binding protein‐43 by caspases produces C‐terminal fragments with disease defining properties independent of progranulin
Dorothee Dormann,Anja Capell,Aaron Carlson,Sunita S. Shankaran,Ramona Rodde,Manuela Neumann,Elisabeth Kremmer,Takashi Matsuwaki,Keitaro Yamanouchi,Masugi Nishihara,Christian Haass +10 more
TL;DR: It is shown that caspase‐mediated processing generates CTFs of similar biochemical properties as those occurring in nuclear and cytoplasmic deposits of FTLD‐U patients independent of PGRN levels, and phosphorylation at S409/410 apparently occurs late during the conversion of soluble to insoluble TDP‐43.
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Possible involvement of lysosomal dysfunction in pathological changes of the brain in aged progranulin-deficient mice
Yoshinori Tanaka,Yoshinori Tanaka,James K. Chambers,Takashi Matsuwaki,Keitaro Yamanouchi,Masugi Nishihara +5 more
TL;DR: The present study shows that aged PGRN-deficient mice present with NCL-like pathology as well as TDP-43 aggregates in the VPM/VPL, where a particular vulnerability has been reported in NCL model mice, and suggests that these pathological changes of the brain are likely a result of lysosomal dysfunction.
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Progranulin regulates lysosomal function and biogenesis through acidification of lysosomes.
Yoshinori Tanaka,Genjiro Suzuki,Takashi Matsuwaki,Masato Hosokawa,Geidy E. Serrano,Thomas G. Beach,Keitaro Yamanouchi,Masato Hasegawa,Masugi Nishihara +8 more
TL;DR: It is shown PGRN is a secretory lysosomal protein that regulates lysOSomal function and biogenesis by controlling the acidification of lYSosomes and the change of P GRN levels led to a cell‐type‐specific increase of insoluble TDP‐43.