M.D., Ph.D. Professor Hirohide Takebayashi
Our research focuses on the development, plasticity, and age-related changes in the nervous system, a complex and delicate organ. Specifically, we aim to elucidate the pathogenesis of neurological diseases and develop treatments, focusing on the involvement of glial cells. In medical school education, we lead courses on human systemic anatomy at the Center for Anatomical Studies and oversee clinical anatomy training conducted at the Clinical Anatomy Laboratory (CAL).
Research and Education
The brain is an organ that is the source of intelligence and behavior unique to humans. Our primary research interest lies in understanding the mechanisms underlying the development, plasticity, and age-related transformations of the nervous system. We have a particular focus on oligodendrocytes because our group is one of the groups that identified Olig transcription factors essential for oligodendrocyte development. We are also investigating to clarify the molecular and cellular mechanisms of neurological diseases with glial cell abnormality and neurological diseases that exhibit involuntary movements for developing treatments. In addition to our research activities, we provide systematic anatomy education at the medical school and support the implementation of clinical anatomy at CAL. Through surgical training programs, we will help young surgeons improve their skills and contribute to improving the quality of medical care.
Ddx20-mediated regulation of oligodendrocyte development and differentiation.
Center for Anatomical Studies, Kyoto University.
Recent Publications
- Sensory-motor circuit is a therapeutic target for dystonia musculorum mice, a model of hereditary sensory and autonomic neuropathy 6. Yoshioka N, Kurose M, Sano H, Tran DM, Chiken S, Tainaka K, Yamamura K, Kobayashi K, Nambu A, Takebayashi H. Sci Adv 10: eadj9335, 2024. doi: 10.1126/sciadv.adj9335.
- Ddx20, an Olig2 binding factor, governs the survival of neural and oligodendrocyte progenitor cells via proper Mdm2 splicing and p53 suppression. Bizen N, Bepari AK, Zhou L, Abe M, Sakimura K, Ono K, Takebayashi H. Cell Death Differ 29: 1028-1041, 2022. doi: 10.1038/s41418-021-00915-8.
- Isoform-specific mutation in Dystonin-b gene causes late-onset protein aggregate myopathy and cardiomyopathy. Yoshioka N, Kurose M, Yano M, Tran DM, Okuda S, Mori-Ochiai Y, Horie M, Nagai T, Nishino I, Shibata S, Takebayashi H. eLife 11: e78419, 2022. doi: 10.7554/eLife.78419.
- Ddx20, DEAD box helicase 20, is essential for the differentiation of oligodendrocyte and maintenance of myelin gene expression. Simankova A, Bizen N, Saitoh S, Shibata S, Ohno N, Abe M, Sakimura K, Takebayashi H. Glia 69: 2559-2574, 2021. doi: 10.1002/glia.24058.
- Oligodendrocyte generation during mouse development. Takebayashi H, Ikenaka K. Glia 63:1350-1356, 2015. doi: 10.1002/glia.22863.
Laboratory
Hirohide Takebayashi M.D., Ph.D. Professor