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2016 Fiscal Year Final Research Report

Defining the molecular mechanism of the cell cycle-specific regulation of chromosome end fusion at dysfunctional telomeres

Research Project

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Project/Area Number 25440080
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Cell biology
Research InstitutionGunma University

Principal Investigator

Konishi Akimitsu  群馬大学, 大学院医学系研究科, 講師 (50381877)

Project Period (FY) 2013-04-01 – 2017-03-31
Keywordsテロメア / 染色体不安定化 / DNA損傷反応 / DNA修復 / 細胞周期
Outline of Final Research Achievements

In this study, we aimed to elucidate the molecular mechanism of the cell cycle-specific regulation of chromosome end fusion leading to the cell carcinogenesis. We revealed that chromatin ubiquitination at the end of chromosomes induced by telomere dysfunction was largely diminished in S/G2 cell cycle phase. As a result, the recruitment of 53BP1, which is an essential factor for chromosome end fusion, is suppressed in S/G2 phase. We also elucidated that TRF2, the central factor for telomere protection, directly binds to the chromatin (core histone) to stabilize the chromosome ends.

Free Research Field

細胞生物学

URL: 

Published: 2018-03-22  

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