Shin'ichi Takeda

Intracellular cell-autonomous association of Notch and its ligands: a novel mechanism of Notch signal modification.

Interleukin 6 induces overexpression of the sarcolemmal utrophin in neonatal mdx skeletal muscle.

Muscle regeneration by reconstitution with bone marrow or fetal liver cells from green fluorescent protein-gene transgenic mice.

Effects of microgravity on myogenic factor expressions during postnatal development of rat skeletal muscle.

Progression of dystrophic features and activation of mitogen-activated protein kinases and calcineurin by physical exercise, in hearts of mdx mice.

Micro-dystrophin cDNA ameliorates dystrophic phenotypes when introduced into mdx mice as a transgene.

Stable micro-dystrophin gene transfer using an integrating adeno-retroviral hybrid vector ameliorates the dystrophic pathology in mdx mouse muscle.

Alpha1-syntrophin-deficient skeletal muscle exhibits hypertrophy and aberrant formation of neuromuscular junctions during regeneration.

Quantitative evaluation of expression of iron-metabolism genes in ceruloplasmin-deficient mice.

Canine X-linked muscular dystrophy in Japan (CXMDJ).

Expression profiling of cytokines and related genes in regenerating skeletal muscle after cardiotoxin injection: a role for osteopontin.

Negamycin restores dystrophin expression in skeletal and cardiac muscles of mdx mice.

Skeletal muscle gene expression in space-flown rats.

Alpha1-syntrophin modulates turnover of ABCA1.

[Gene therapy for muscular dystrophy].

Purification and cell-surface marker characterization of quiescent satellite cells from murine skeletal muscle by a novel monoclonal antibody.

Identification and characterization of epsilon-sarcoglycans in the central nervous system.

Laminin alpha1 chain reduces muscular dystrophy in laminin alpha2 chain deficient mice.

Mac-1(low) early myeloid cells in the bone marrow-derived SP fraction migrate into injured skeletal muscle and participate in muscle regeneration.

Development of a safe oral Abeta vaccine using recombinant adeno-associated virus vector for Alzheimer's disease.

AAV vector-mediated microdystrophin expression in a relatively small percentage of mdx myofibers improved the mdx phenotype.

The utrophin promoter A drives high expression of the transgenic LacZ gene in liver, testis, colon, submandibular gland, and small intestine.

[Current status and perspective of gene therapy on dystrophic animal model].

Epsilon-sarcoglycan compensates for lack of alpha-sarcoglycan in a mouse model of limb-girdle muscular dystrophy.

Coordinate control of axon defasciculation and myelination by laminin-2 and -8.

Participation of bone marrow-derived cells in fibrotic changes in denervated skeletal muscle.

Up-regulation of mitogen activated protein kinases in mdx skeletal muscle following chronic treadmill exercise.

Functional heterogeneity of side population cells in skeletal muscle.

Intracellular localization of dysferlin and its association with the dihydropyridine receptor.

Major clinical and histopathological characteristics of canine X-linked muscular dystrophy in Japan, CXMDJ.

Zeta-sarcoglycan is a functional homologue of gamma-sarcoglycan in the formation of the sarcoglycan complex.

Ubiquitin ligase Cbl-b downregulates bone formation through suppression of IGF-I signaling in osteoblasts during denervation.

Expansion of revertant fibers in dystrophic mdx muscles reflects activity of muscle precursor cells and serves as an index of muscle regeneration.

Identification and characterization of a novel human dysferlin transcript: dysferlin_v1.

Cardiac involvement in Beagle-based canine X-linked muscular dystrophy in Japan (CXMDJ): electrocardiographic, echocardiographic, and morphologic studies.

Cardiac side population cells have a potential to migrate and differentiate into cardiomyocytes in vitro and in vivo.

[Stem cell based cell therapy for muscular dystrophy].

[Therapeutic strategy for muscular dystrophies].

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ).

Molecular signature of quiescent satellite cells in adult skeletal muscle.

Deficiency of Cbl-b gene enhances infiltration and activation of macrophages in adipose tissue and causes peripheral insulin resistance in mice.

Autologous transplantation of SM/C-2.6(+) satellite cells transduced with micro-dystrophin CS1 cDNA by lentiviral vector into mdx mice.

NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS.

Transgenic expression of a myostatin inhibitor derived from follistatin increases skeletal muscle mass and ameliorates dystrophic pathology in mdx mice.

CD90-positive cells, an additional cell population, produce laminin alpha2 upon transplantation to dy(3k)/dy(3k) mice.

Follow-up of three patients with a large in-frame deletion of exons 45-55 in the Duchenne muscular dystrophy (DMD) gene.

Downstream utrophin enhancer is required for expression of utrophin in skeletal muscle.

Selective vacuolar degeneration in dystrophin-deficient canine Purkinje fibers despite preservation of dystrophin-associated proteins with overexpression of Dp71.

The ubiquitin ligase gene (WWP1) is responsible for the chicken muscular dystrophy.

Recombinant adeno-associated virus type 8-mediated extensive therapeutic gene delivery into skeletal muscle of alpha-sarcoglycan-deficient mice.

Muscle CD31(-) CD45(-) side population cells promote muscle regeneration by stimulating proliferation and migration of myoblasts.

Predominant localization of EFA6A, a guanine nucleotide exchange factor for ARF6, at the perisynaptic photoreceptor processes.

Suppression of macrophage functions impairs skeletal muscle regeneration with severe fibrosis.

MicroRNA-206 is highly expressed in newly formed muscle fibers: implications regarding potential for muscle regeneration and maturation in muscular dystrophy.

A deficit of brain dystrophin impairs specific amygdala GABAergic transmission and enhances defensive behaviour in mice.

Transduction efficiency and immune response associated with the administration of AAV8 vector into dog skeletal muscle.

Hepcidin, an antimicrobial peptide is downregulated in ceruloplasmin-deficient mice.

Residual laminin-binding activity and enhanced dystroglycan glycosylation by LARGE in novel model mice to dystroglycanopathy.

Reduced proliferative activity of primary POMGnT1-null myoblasts in vitro.

A renaissance for antisense oligonucleotide drugs in neurology: exon skipping breaks new ground.

Characterization of deletion breakpoints in patients with dystrophinopathy carrying a deletion of exons 45-55 of the Duchenne muscular dystrophy (DMD) gene.

Generation of transplantable, functional satellite-like cells from mouse embryonic stem cells.

Exon-skipping therapy for Duchenne muscular dystrophy.

Scalable purification of adeno-associated virus serotype 1 (AAV1) and AAV8 vectors, using dual ion-exchange adsorptive membranes.

Ubiquitin ligase Cbl-b is a negative regulator for insulin-like growth factor 1 signaling during muscle atrophy caused by unloading.

CCN3 and bone marrow cells.

Evaluation of dystrophic dog pathology by fat-suppressed T2-weighted imaging.

Age-dependent expression of hephaestin in the brain of ceruloplasmin-deficient mice.

[Exon skipping therapy for Duchenne muscular dystrophy by using antisense Morpholino].

Mesenchymal progenitors distinct from satellite cells contribute to ectopic fat cell formation in skeletal muscle.

Efficient gene transfer into neurons in monkey brain by adeno-associated virus 8.

Genetic background affects properties of satellite cells and mdx phenotypes.

Neuronal NOS is dislocated during muscle atrophy in amyotrophic lateral sclerosis.

Gene therapy for muscle disease.

Post-translational maturation of dystroglycan is necessary for pikachurin binding and ribbon synaptic localization.

Progress in muscular dystrophy research with special emphasis on gene therapy.

Six family genes control the proliferation and differentiation of muscle satellite cells.

Antisense PMO found in dystrophic dog model was effective in cells from exon 7-deleted DMD patient.

In-frame dystrophin following exon 51-skipping improves muscle pathology and function in the exon 52-deficient mdx mouse.

[Molecular therapy for muscular dystrophy].

The status of exon skipping as a therapeutic approach to duchenne muscular dystrophy.

Antisense oligo-mediated multiple exon skipping in a dog model of duchenne muscular dystrophy.

SynArfGEF is a guanine nucleotide exchange factor for Arf6 and localizes preferentially at post-synaptic specializations of inhibitory synapses.

Mammalian models of Duchenne Muscular Dystrophy: pathological characteristics and therapeutic applications.

Matrix metalloproteinase-2 ablation in dystrophin-deficient mdx muscles reduces angiogenesis resulting in impaired growth of regenerated muscle fibers.

Synthesis of 2'-O-[2-(N-methylcarbamoyl)ethyl]ribonucleosides using oxa-Michael reaction and chemical and biological properties of oligonucleotide derivatives incorporating these modified ribonucleosides.

Reactive gliosis of astrocytes and Müller glial cells in retina of POMGnT1-deficient mice.

Current status of pharmaceutical and genetic therapeutic approaches to treat DMD.

Identification of muscle-specific microRNAs in serum of muscular dystrophy animal models: promising novel blood-based markers for muscular dystrophy.

Medium-range correlation of Ag ions in superionic melts of Ag2Se and AgI by reverse Monte Carlo structural modelling-connectivity and void distribution.

Comparison of partial structures of melts of superionic AgI and CuI and non-superionic AgCl.

Restoring dystrophin expression in duchenne muscular dystrophy muscle progress in exon skipping and stop codon read through.

Exon-skipping therapy for Duchenne muscular dystrophy.

The structure of molten CuCl, CuI and their mixtures as investigated by using neutron diffraction.

[Derivation of engraftable myogenic precursors from murine ES/iPS cells and generation of disease-specific iPS cells from patients with Duchenne muscular dystrophy (DMD) and other diseases].

Long-term engraftment of multipotent mesenchymal stromal cells that differentiate to form myogenic cells in dogs with Duchenne muscular dystrophy.

Pathogenic exon-trapping by SVA retrotransposon and rescue in Fukuyama muscular dystrophy.

Hesr1 and Hesr3 are essential to generate undifferentiated quiescent satellite cells and to maintain satellite cell numbers.

Fibrosis and adipogenesis originate from a common mesenchymal progenitor in skeletal muscle.

Reprogramming efficiency and quality of induced Pluripotent Stem Cells (iPSCs) generated from muscle-derived fibroblasts of mdx mice at different ages.

Long-term functional adeno-associated virus-microdystrophin expression in the dystrophic CXMDj dog.

[Induced pluripotent stem (iPS) cell-based cell therapy for muscular dystrophy: current progress and future prospects].

[Exon-skipping therapy for Duchenne muscular dystrophy].

Slow-dividing satellite cells retain long-term self-renewal ability in adult muscle.

Protein-anchoring strategy for delivering acetylcholinesterase to the neuromuscular junction.

Calcitonin receptor and Odz4 are differently expressed in Pax7-positive cells during skeletal muscle regeneration.

Laminin regulates postnatal oligodendrocyte production by promoting oligodendrocyte progenitor survival in the subventricular zone.

Bodywide skipping of exons 45-55 in dystrophic mdx52 mice by systemic antisense delivery.

Extensive and prolonged restoration of dystrophin expression with vivo-morpholino-mediated multiple exon skipping in dystrophic dogs.

A conserved regulatory element located far downstream of the gls locus modulates gls expression through chromatin loop formation during myogenesis.

Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy.

Identification of disease specific pathways using in vivo SILAC proteomics in dystrophin deficient mdx mouse.

Imatinib attenuates severe mouse dystrophy and inhibits proliferation and fibrosis-marker expression in muscle mesenchymal progenitors.

Prognostic impact of left ventricular noncompaction in patients with Duchenne/Becker muscular dystrophy--prospective multicenter cohort study.

Translating the genomics revolution: the need for an international gene therapy consortium for monogenic diseases.

Impaired viability of muscle precursor cells in muscular dystrophy with glycosylation defects and amelioration of its severe phenotype by limited gene expression.

Capsaicin mimics mechanical load-induced intracellular signaling events: involvement of TRPV1-mediated calcium signaling in induction of skeletal muscle hypertrophy.

Characteristics of Japanese Duchenne and Becker muscular dystrophy patients in a novel Japanese national registry of muscular dystrophy (Remudy).

Robust Long-term Transduction of Common Marmoset Neuromuscular Tissue With rAAV1 and rAAV9.

Manumycin A corrects aberrant splicing of Clcn1 in myotonic dystrophy type 1 (DM1) mice.

Initial pulmonary respiration causes massive diaphragm damage and hyper-CKemia in Duchenne muscular dystrophy dog.

Highly efficient in vivo delivery of PMO into regenerating myotubes and rescue in laminin-α2 chain-null congenital muscular dystrophy mice.

α1-Syntrophin-deficient mice exhibit impaired muscle force recovery after osmotic shock.

Prednisolone improves walking in Japanese Duchenne muscular dystrophy patients.

Inter-molecular correlations in liquid Se2Br2.

Current Challenges and Future Directions in Recombinant AAV-Mediated Gene Therapy of Duchenne Muscular Dystrophy.

Structural and biochemical characterization of O-mannose-linked human natural killer-1 glycan expressed on phosphacan in developing mouse brains.

Dystrophic mdx mice develop severe cardiac and respiratory dysfunction following genetic ablation of the anti-inflammatory cytokine IL-10.

Discovery of serum protein biomarkers in the mdx mouse model and cross-species comparison to Duchenne muscular dystrophy patients.

Neuromuscular disease. DOK7 gene therapy benefits mouse models of diseases characterized by defects in the neuromuscular junction.

Nationwide patient registry for GNE myopathy in Japan.

Doublecortin marks a new population of transiently amplifying muscle progenitor cells and is required for myofiber maturation during skeletal muscle regeneration.

[Infrastructure for the clinical research of muscular dystrophies: remudy and MDCTN].

Intra-amniotic rAAV-mediated microdystrophin gene transfer improves canine X-linked muscular dystrophy and may induce immune tolerance.

Low intensity training of mdx mice reduces carbonylation and increases expression levels of proteins involved in energy metabolism and muscle contraction.

Fukutin is prerequisite to ameliorate muscular dystrophic phenotype by myofiber-selective LARGE expression.

Doublecortin marks a new population of transiently amplifying muscle progenitor cells and is required for myofiber maturation during skeletal muscle regeneration.

[Exon skipping approach to Duchenne muscular dystorphy].

A muscle-liver-fat signalling axis is essential for central control of adaptive adipose remodelling.

G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy.

Prognostic impact of venous thromboembolism in patients with Duchenne muscular dystrophy: Prospective multicenter 5-year cohort study.

Muscle Satellite Cell Protein Teneurin-4 Regulates Differentiation During Muscle Regeneration.

Erratum: G-CSF supports long-term muscle regeneration in mouse models of muscular dystrophy.

Differential roles of MMP-9 in early and late stages of dystrophic muscles in a mouse model of Duchenne muscular dystrophy.

Nonmechanical Roles of Dystrophin and Associated Proteins in Exercise, Neuromuscular Junctions, and Brains.

Characterization of WWP1 protein expression in skeletal muscle of muscular dystrophy chickens.

Mesoangioblast delivery of miniagrin ameliorates murine model of merosin-deficient congenital muscular dystrophy type 1A.

Calcitonin Receptor Signaling Inhibits Muscle Stem Cells from Escaping the Quiescent State and the Niche.

A Disintegrin and Metalloprotease 10 (ADAM10) Is Indispensable for Maintenance of the Muscle Satellite Cell Pool.

Trends in steroid therapy for Duchenne muscular dystrophy in Japan.

Serum Osteopontin as a Novel Biomarker for Muscle Regeneration in Duchenne Muscular Dystrophy.

Deletion of exons 3-9 encompassing a mutational hot spot in the DMD gene presents an asymptomatic phenotype, indicating a target region for multiexon skipping therapy.

Utility of Cystatin C for Estimating Glomerular Filtration Rate in Patients With Muscular Dystrophy.