Misa Shimuta
University of Tokyo
6 Papers
127 Citations
Misa Shimuta is an academic researcher from University of Tokyo. The author has contributed to research in topics: Skeletal muscle & Ryanodine receptor. The author has an hindex of 6, co-authored 6 publications. Previous affiliations of Misa Shimuta include Tokyo Medical and Dental University & Kobe University.
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Papers
Mice deficient in nervous system-specific carbohydrate epitope HNK-1 exhibit impaired synaptic plasticity and spatial learning.
Shoji Yamamoto,Shogo Oka,Mitsuhiro Inoue,Misa Shimuta,Toshiya Manabe,Hideki Takahashi,Masaomi Miyamoto,Masahide Asano,Junko Sakagami,Katsuko Sudo,Yoichiro Iwakura,Katsuhiko Ono,Toshisuke Kawasaki +12 more
TL;DR: It is shown that the loss of a single non-reducing terminal carbohydrate residue attenuates brain higher functions in mice generated with a targeted deletion of the GlcAT-P gene.
146
Mitsugumin29, a novel synaptophysin family member from the triad junction in skeletal muscle.
Hiroshi Takeshima,Misa Shimuta,Shinji Komazaki,Kazuhiro Ohmi,Miyuki Nishi,Masamitsu Iino,Atsuro Miyata,Kenji Kangawa +7 more
TL;DR: The identification using monoclonal antibody and primary structure by cDNA cloning of mitsugumin29, a novel transmembrane protein from the triad junction in skeletal muscle, suggests that mitsUGumin29 is involved in communication between the T-tubular and junctional SR membranes.
103
Structure and expression of mitsugumin29 gene.
Misa Shimuta,Shinji Komazaki,Miyuki Nishi,Masamitsu Iino,Kan-ichi Nakagawara,Hiroshi Takeshima +5 more
TL;DR: Results obtained may suggest that mitsugumin29 is involved in the formation of specialized endoplasmic reticulum systems in skeletal muscle and renal tubule cells.
30
Generation and Characterization of Mutant Mice Lacking Ryanodine Receptor Type 3
Hiroshi Takeshima,Takaaki Ikemoto,Miyuki Nishi,Nobuyoshi Nishiyama,Misa Shimuta,Misa Shimuta,Yoshinobu Sugitani,Junko Kuno,Ichiro Saito,Hiroshi Saito,Makoto Endo,Masamitsu Iino,Tetsuo Noda +12 more
TL;DR: The results indicate that the loss of RyR-3 causes no gross abnormalities and suggest that the lack of Ry R-3-mediated Ca2+ signaling results in abnormalities of certain neurons in the central nervous system.
A region of the ryanodine receptor critical for excitation-contraction coupling in skeletal muscle.
TL;DR: The results indicate that the presence of the D2 region is critical for E-C coupling in skeletal muscle, although the D1 region alone cannot determine the functional difference between RyR-1 and Ry R-2.