Kiichiro Matsumura

Tokyo, Japan

Last Updated: 09/26/2026

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Found 9 publications

Antioxidants restore store-operated Ca2+ entry in patient-iPSC-derived myotubes with tubular aggregate myopathy-associated Ile484ArgfsX21 STIM1 mutation via upregulation of binding immunoglobulin protein.

Antioxidants restore store-operated Ca2+ entry in patient-iPSC-derived myotubes with tubular aggregate myopathy-associated Ile484ArgfsX21 STIM1 mutation via upregulation of binding immunoglobulin protein.

Journal: FASEB bioAdvances
Published: July 19, 2023

N-terminal domain on dystroglycan enables LARGE1 to extend matriglycan on α-dystroglycan and prevents muscular dystrophy.

N-terminal domain on dystroglycan enables LARGE1 to extend matriglycan on α-dystroglycan and prevents muscular dystrophy.

Journal: eLife
Published: August 25, 2022

Unexpected Mutations by CRISPR-Cas9 CTG Repeat Excision in Myotonic Dystrophy and Use of CRISPR Interference as an Alternative Approach.

Unexpected Mutations by CRISPR-Cas9 CTG Repeat Excision in Myotonic Dystrophy and Use of CRISPR Interference as an Alternative Approach.

Journal: Molecular therapy. Methods & clinical development
Published: May 12, 2020

Protective role for the N-terminal domain of α-dystroglycan in Influenza A virus proliferation.

Protective role for the N-terminal domain of α-dystroglycan in Influenza A virus proliferation.

Journal: Proceedings of the National Academy of Sciences of the United States of America
Published: May 18, 2019

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.

Journal: Proceedings of the National Academy of Sciences of the United States of America
Published: September 15, 2016

Tubular aggregate myopathy caused by a novel mutation in the cytoplasmic domain of STIM1.

Tubular aggregate myopathy caused by a novel mutation in the cytoplasmic domain of STIM1.

Journal: Neurology. Genetics
Published: March 17, 2015

Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice.

Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice.

Journal: Human molecular genetics
Published: April 12, 2014

LARGE glycans on dystroglycan function as a tunable matrix scaffold to prevent dystrophy.

LARGE glycans on dystroglycan function as a tunable matrix scaffold to prevent dystrophy.

Journal: Nature
Published: January 24, 2013

Histone deacetylase inhibitor trichostatin A enhances myogenesis by coordinating muscle regulatory factors and myogenic repressors.

Histone deacetylase inhibitor trichostatin A enhances myogenesis by coordinating muscle regulatory factors and myogenic repressors.

Journal: Biochemical and biophysical research communications
Published: September 26, 2011
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Last Updated: 09/26/2026