2015 Fiscal Year Final Research Report
Exploration of target molecules based on genome analysis and molecular tracing
Project Area | Molecular Science for Nanomedicine |
Project/Area Number |
23107010
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Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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Allocation Type | Single-year Grants |
Review Section |
Science and Engineering
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Research Institution | Nagoya University |
Principal Investigator |
Natsume Atsushi 名古屋大学, 医学(系)研究科(研究院), 准教授 (30362255)
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Co-Investigator(Kenkyū-buntansha) |
SENGA Takeshi 名古屋大学, 医学系研究科, 准教授 (80419431)
URISU Tsuneo 名古屋大学, 工学研究科, 客員教授 (50249950)
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Project Period (FY) |
2011-04-01 – 2016-03-31
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Keywords | 脳腫瘍 / がん / ゲノム |
Outline of Final Research Achievements |
Various serine/threonine kinases are activated in cells upon numerous extracellular stresses, such as heat, hypoxia and oxidation. These stresses activate four different types of kinases, EIF2AK1, EIF2AK2, EIF2AK3, EIF2AK4, which consequently promote phosphorylation of eIF2α at Ser51. Our proteomics analysis of SG components revealed UBAP2L is a critical component of SG. UBAP2L contains ubiquitin-associated domain and RGG motif. UBAP2L is localized to SGs when cells are treated with heat, arsenite, hydrogen peroxide, and sorbitol. Fluorescence recovery after photobleaching (FRAP) analysis revealed that UBAP2L localization to the SG is dynamic. UBAP2L depletion by siRNA transfection showed that UBAP2L was critical for the organization of SG. Formation of SG is associated with cell survival in the presence of extracellular stresses. Further analysis of UBAP2L and UBAP2 functions in RNA processing and SG formation may give insight for the pathogenesis of neurodegenerative diseases.
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Free Research Field |
脳腫瘍学
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