Researcher Database

（Last updated : 2022-05-12 13:05:04）

SOEDA SHUHEI

Department / Course College of Pharmaceutical Sciences Department of Pharmacy

Title / Position Assistant Professor

Academic background
1.	2013/09 Degree Acquisition	│ Graduate School of Medical and Pharmaceutical Sciences Doctor of Philosophy (Medicinal Sciences)
2.	～2013/09	Doctoral Program (2nd Semester) │ Graduate School of Medical and Pharmaceutical Sciences │ Graduate School of Chiba University │ Completed
3.	2009/03 Degree Acquisition	│ Graduate School of Pharmaceutical Sciences　of Showa University Master of pharmaceutical sciences degree
4.	～2009/03	Doctoral Program (1st Semester) │ Pharmaceutical Sciences │ Graduate School of Pharmaceutical Sciences │ Graduate School of Showa University │ Completed
5.	～2003/04	Department of Pharmaceutical Sciences │ Faculty of Pharmaceutical Sciences │ Hokuriku University │ Graduated

Business career
1.	2017/04/01 ～	Assistant Professor │ College of Pharmaceutical Sciences, │ Ritsumeikan University

Research activities
1.		The Japanese Biochemical Society
2.		The Pharmaceutical Society of Japan

Qualification and license
1.	2007	License to practice pharmacy

Subject of research
1.	Function analysis of genes related to differentiation and development

Research summary
Analysis of pathogenic mechanism in Prader-Willi syndrome The human necdin gene is located on chromosome 15q11.2-q12, which is deleted in the Prader-Willi syndrome(PWS). PWS is a neurogenetic disorder, and its major symptoms are　short stature due to hypothalamic hormone deficient secretion, mild intellectual impairment, impaired peripheral sensation, obesity, and so on. It is implied that Necdin is involved in the regulation of cell death of nerve cells and cell differentiation. Necdin belongs to the MAGE family and the genes are stored in a wide range of species from plants to higher organisms, it is the only one kind in low organisms.　Recently, it is revealed that a Nse3 of Smc5-Smc6 complexes is a single MADE gene in yeast. The structural maintenance of chromosome (SMC)proteins play roles in sister chromosome cohesion, chromosome condensation and DNA repair. It has known that Nse1, Nse3, and Nse4 form a sub-complex in the Smc5-Smc6 complex. Although it has been known that this complex plays a role in DNA repair, it has not known that each protein’s role. Nse4 belongs to the EID family and it is reported that it is involved in the cell differentiation by depression of transcriptional activity. In addition, although Nse1 has a RING finger structure similar to Ubiquitin ligase, the functions remain to be elucidated. It remains unknown how Nse3 plays a role by itself. Recently, we focus on Sirtuins protein. It has known that Necdin interact with Sirt1, and regulates function by alteration of acetylate level of transcriptional factor Foxo1 involved in energy Metabolic control in hypothalamus. There are seven homologues of sirtuins in mammals, named Sirt1 through Sirt7. By deacetylating histones and other proteins, Sir2 proteins play important roles in various biological processes, including the regulation of longevity, metabolism, and differentiation. We analyse function of the genes related to PWS using cellular slime mold. Sir2 is a NAD-dependent histone deacetylase found in yeasts. D. discoideum encodes encodes at least four Sir2 proteins (Sir2 A-D). Forty one percent of catalytic domains of Sir2C amino acid and fifty percent of Sir2D are correspond with Sirt1.These　facts suggest a possibility that Nse3, which unique MAGE family in D. discoideum, will interact with Sir2, and we analyze Sir2A, C, and D proteins. To analyse Sir2A, C, first, we make Sir2C delated cells, and second, get cDNA clone of Sir2A to make stable Sir2A expressed cells. Finally, we investigate whether finding which got from analysis with D. discoideum is applied to neural stem cell and nerve tissue differentiated from iPS cells getting from Prader-Willi syndrome patient. We think that these works will be possible to help elucidate PWS pathogenic mechanism in PWS nerve system and progress the therapeutic applications.

Present specialized field
Neurochemistry/ Neuropharmacology, Genome biology, Molecular biology, Cell biology, Biological pharmacy (Keyword：Pharmaceutical Sciences, Molecular Cell Biology, Necdin, MAGE family, Prader Willi, Neuron, Differentiation, Development)

Papers
1.	2021/04/26	Abnormal DNA methylation in pluripotent stem cells from a patient with Prader-Willi syndrome results in neuronal differentiation defects │ Stem Cell Research │ 53-102361 (Co-authored)
2.	2021/01/25	Sir2B, A Sirtuin Family Protein, Involves in Cell Adhesion Molecule Expression During Early Dictyostelium Development Upon Starvation │ Cell Biology │ 9 (1),pp.1-6 (Co-authored)
3.	2019/02	Sir2D, a Sirtuin family protein, regulates adenylate cyclase A expression through interaction with the MybB transcription factor early in Dictyostelium development upon starvation │ Heliyon │ 5 (3),pp.e01301 (Co-authored)
4.	2019/03/25	Neuronal differentiation defects in induced pluripotent stem cells derived from a Prader-Willi syndrome patient │ Neuroscience Letters │ 703,pp.162-167 (Co-authored)
5.	2018/08/02	Sirtuin Activator and Inhibitor Affect Early Dictyostelium Development upon Starvation │ Cell Biology │ 6 (1),pp.13-19 (Co-authored)
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Message
1.	Why we study about rare disease Prader-Willi syndrome? Laboratory member said the laboratory which we belong does not attract new students. This reason is we study rear disease and the laboratory inferior to laboratories which study cancer, diabetes, and Alzheimer-type dementia. I accepted this idea and could not say No. Because I took public offering of position of associated researcher,So, I did not know Prader-Willi syndrome(PWS). Then, I thought again whether it has purpose and benefit. In conclusion, the first of this idea, it has a few competition of researcher. For example, it needs much effort, results, and time to be authority of cancer research, but, it has possibility to be authority of PWS with publishing few papers. Second, in fact, there are patients of rear disease PWS. It has problems that there are few researchers for rear disease, and slow progression of the study, so that it is hard to find the therapy. So, we think that we have to approach these problems. Even if there are few patients in the world, they need study of rear diseases.　Someone who is interested in our work, please contact us. It will produce new idea and discovery to collaborate with other fields researchers and other disease studies.