• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2015 Fiscal Year Final Research Report

Exploration of target molecules based on genome analysis and molecular tracing

Planned Research

  • PDF
Project AreaMolecular Science for Nanomedicine
Project/Area Number 23107010
Research Category

Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Allocation TypeSingle-year Grants
Review Section Science and Engineering
Research InstitutionNagoya University

Principal Investigator

Natsume Atsushi  名古屋大学, 医学(系)研究科(研究院), 准教授 (30362255)

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)
Project Period (FY) 2011-04-01 – 2016-03-31
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.

Free Research Field

脳腫瘍学

URL: 

Published: 2017-05-10  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi