2011 Fiscal Year Final Research Report
Pathological features induced by constitutive active mutant of ERK2 : Study focused on premature cellular senescence
| Project/Area Number |
22790281
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Mie University |
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Principal Investigator |
SUGIMURA Kazuto 三重大学, 大学院・医学系研究科, 助教 (90452226)
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| Project Period (FY) |
2010 – 2011
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| Keywords | Erk2 / NCFC症候群 / p53 / 血球・血管内皮 / 細胞老化 |
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| Research Abstract |
Hematopoietic and endothelial cell lineage-specific gain of function mutation of Erk2 in mice resulted in lower rate of birth, lower body weight, and lower body length. The mice had NCFC syndrome-like physical characteristics such as unique facial abnormalities, indicating that constitutive activation of Erk2 was the cause for the part of pathological features in NCFC syndrome. Moreover, p53 was likely to be involved in the phenotype, suggesting that p53-targeted treatment might be effective to the NCFC syndrome-linked pathologies.
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Research Products
(9 results)
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[Journal Article] The Histone Chaperone Facilitates Chromatin Transcription(FACT) Protein Maintains Normal Replication Fork Rates2011
Author(s)
Takuya Abe, Kazuto Sugimura, Yoshifumi Hosono, Yasunari Takami, Motomu Akita, Akari Yoshimura, Shunsuke Tada, Tatsuo Nakayama, Hiromu Murofushi, Katsuzumi Okumura, Shunichi Takeda, Masami Horikoshi, Masayuki Seki, and Takemi Enomoto
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Journal Title
The Journal of Biological Chemistry
Volume: 286
Pages: 30504-30512
Peer Reviewed
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