2011 Fiscal Year Final Research Report
Search for novel myogenic factors and ubiquitination machineries by regulator proteomics
| Project/Area Number |
20570123
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Chiba University |
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Principal Investigator |
TAMURA Takaaki 千葉大学, 大学院・理学研究科, 教授 (30112692)
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| Project Period (FY) |
2008 – 2011
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| Keywords | 筋分化 / ユビキチン化 / TIP120 / SCF / 筋萎縮 / MyoD |
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| Research Abstract |
It was found that myogenin and MyoD were increased by TIP120B overexpression. Moreover, we identified MAFbx as a F-box protein in the SCF1 E3 ligase. Mouse C2C12 cells subjected to the myotube differentiation contained increased amounts of TIP120B and MyoD. Muscle atrophying dexamethasone decreased those proteins. Mouse and human TIP120B promoters, which carry multiple E-box motifs, were potentiated by MyoD. In the human TIP120B, a proximal E-box binds to MyoDinvitroand exhibits MyoD-dependent transcription activation function. Expression of the endogenousTIP120Bgene was correlated with the level of MyoD in different types of muscle-related cells. Furthermore, MyoD binds specifically to a proximal E-box-carrying promoter region in chromatin. Proteasome-sensitive MyoD was increased and decreased by overexpression and knockdown of TIP120B. Moreover, stability of MyoD was increased by TIP120B. Therefore, it is suggested that MyoD an d TIP120B potentiate each other at gene expression and post-translation levels respectively, which may promote myogenesis cooperatively.
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Research Products
(17 results)
