| Project/Area Number |
25893228
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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 |
TSUKAMOTO SHO 埼玉医科大学, 医学部, 助手 (20707658)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 骨・軟骨代謝学 / シグナル伝達 / 骨系統疾患 / 骨、軟骨代謝学 |
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| Outline of Final Research Achievements |
Smad proteins are transcription factors important for bone formation regulated by BMPs. Smad1, Smad5 and Smad8 (also known as Smad9) are induced phosphorylation by BMP receptors. We have established constitutively active forms of Smad1, Smad5 and Smad8 and found that Smad8 is less active than other Smads. The mRNA levels of Smad8 mRNA were increased by BMP-4 stimulation. RNAi knockdown of Smad8 increased the BMP-induced ALP activity in C2C12 cells. Therefore, Smad8 suppressed BMP activity via a novel molecular mechanism. Smad8 bound to Smad1 with a higher affinity than that of Smad1 homodimer. Taken together, our findings suggest that Smad8 represses intracellular BMP signaling as a dominant negative Smad.
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