Tokyo Institute of Technology · Medicine
Professor Yoshihisa Matsumoto's research lab specializes in molecular and cellular mechanisms underlying genetic disorders and DNA damage response, with a focus on fibrodysplasia ossificans progressiva (FOP) and DNA double-strand break repair. The lab employs patient-specific induced pluripotent stem cells (iPSCs) to model skeletal diseases and study disease mechanisms in vitro, while also investigating the roles of key DNA repair proteins such as DNA-PKcs and XRCC4 in apoptosis and genomic stability. Their work integrates stem cell biology, molecular genetics, and biophysics to develop disease models and explore therapeutic targets for rare genetic conditions and cancer. The lab also examines the biological effects of radiation and DNA-damaging agents, contributing to the development of targeted therapies.
Figures are computed from collected data and may differ slightly.
Our findings establish a FOP disease cell model for in vitro experimentation and provide a proof-of-concept for using human iPS cell models to understand human skeletal disorders.
Successful in vitro disease-recapitulation using patient-specific induced pluripotent stem cells (iPSCs) requires two fundamental technical issues: appropriate control cells and robust differentiation protocols. To investigate fibrodysplasia ossificans progressiva (FOP), a rare genetic disease leading to extraskeletal bone formation through endochondral ossification, gene-corrected (rescued) iPSC clones (resFOP-iPSC) were generated from patient-derived iPSC (FOP-iPSC) as genetically matched cont
We report the p35 and p60 forms of XRCC4 protein, appearing in human leukemia MOLT-4 or U937 cells following X-irradiation or hyperthermia. p35 appeared in conjunction with the cleavage of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and the fragmentation of internucleosomal DNA, and was suppressed by Ac-DEVD-CHO. p35 was also produced in vitro by treating MOLT-4 cell lysate with recombinant caspases, suggesting that p35 was a caspase-cleaved fragment of XRCC4 in apoptotic cell deat
DNA double-strand break (DSB) is considered the most deleterious type of DNA damage, which is generated by ionizing radiation (IR) and a subset of anticancer drugs. DNA-dependent protein kinase (DNA-PK), which is composed of a DNA-PK catalytic subunit (DNA-PKcs) and Ku80-Ku70 heterodimer, acts as the molecular sensor for DSB and plays a pivotal role in DSB repair through non-homologous end joining (NHEJ). Cells deficient for DNA-PKcs show hypersensitivity to IR and several DNA-damaging agents. C
The hybrid liposomes (90mol% DMPC/10mol% C12(EO)8 and 90mol% DMPC/10mol% C12(EO)12) have a highly inhibitory action against the growth of tumor cells. The uniform and stable structure of the hybrid liposomes was revealed on the basis of electron microscopy and dynamic light scattering measurements.
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