| Project/Area Number |
15H06568
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Saitama Medical University |
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Principal Investigator |
OHTE Satoshi 埼玉医科大学, 医学部, 助教 (00547979)
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| Research Collaborator |
KATAGIRI Takenobu 埼玉医科大学, 医学部, 教授
TSUKAMOTO Sho 埼玉医科大学, 医学部, 助手
KURATANI Mai 埼玉医科大学, 医学部, 研究員
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 骨形成因子 / PAH / BMP / シグナル伝達 / FOP |
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| Outline of Final Research Achievements |
Bone morphogenetic proteins (BMPs) are cytokines, which important for bone development. Intracellular BMP signaling is activated by type I and type II BMP receptors. These receptors contain intracellular kinase domain, which consist of about 300 amino acids. A long form (LF) of BMPR-II has a unique 500 amino acid tail domain at the C-termini. Several mutations in the tail domain of BMPR-II have been identified in patients with pulmonary arterial hypertension, suggesting that the tail domain has a novel function in BMP signaling. In this study, we analyzed a function of the BMPR-II tail domain. Western blot analysis revealed that protein level of BMPR-II LF was lower than that of BMPR-II short form (SF), but mRNA level seemed comparable. BMPR-II SF induced higher ALP activity than that of BMPR-II LF in C2C12 cells co-expressed with a BMP type I receptor. These findings suggest that BMPR-II LF is suppressed the activity by the tail domain through a reduction of protein stability.
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