| Project/Area Number |
22K20964
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund |
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| Review Section |
0906:Surgery related to the biological and sensory functions and related fields
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| Research Institution | Saitama Medical University |
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Principal Investigator |
FUKUDA Eriko 埼玉医科大学, 医学部, 助手 (60740777)
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| Project Period (FY) |
2022-08-31 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2023: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2022: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | BMP / ALK2 / シグナル伝達 / ヒトALK2 / マウスALK2 |
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| Outline of Research at the Start |
ALK2は、Bone Morphogenetic Protein (BMP)の受容体であり、骨格筋に異所性骨化が起こる進行性骨化性線維異形成症 (FOP)、小児の脳腫瘍であるびまん性橋膠腫病 (DIPG)、などの遺伝性疾患の責任分子として知られている。我々は、独自の解析結果から、ヒトALK2とマウスALK2の活性に差があることを見出した。そこで、本研究では、ヒトALK2とマウスALK2で異なるアミノ酸残基に着目し、アミノ酸残基を介したALK2活性制御機構の解明を目的とする。
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| Outline of Final Research Achievements |
ALK2 is a transmembrane kinase receptor for Bone morphogenetic protein (BMP), a member of the TGF-β family. We previously found that between human and mouse ALK2 differ in their activities. In this study, we investigated the molecular mechanism of ALK2 activity is regulated by different amino acid residues in mouse ALK2 and humanALK2. We analyzed the human ALK2 receptor and mutants in which specific amino acid residues were replaced with mouse-type animo acids. We identified a specific amino acid residue that is important for the different activities of mouse ALK2 and human ALK2. It was suggested that the response of ALK2 to BMP ligands may change depending on the identified an amino acid residue.
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| Academic Significance and Societal Importance of the Research Achievements |
動物種の違いに由来する特定の1 アミノ酸残基によって調整されるALK2活性の分子メカニズムの解明により、ALK2の種差による生理的役割の解析や、軟部組織で異所性の骨が形成される難病のFOPや小児脳腫瘍のDIPG等のALK2の遺伝的変異に基づく疾患研究への応用が期待できる。
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