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Differential mechanism of HDACI induct cell cycle arrest, apoptosis and differentiation between B-precursor and T-lineage leukemia cells

Research Project

Project/Area Number 20790722
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeSingle-year Grants
Research Field Pediatrics
Research InstitutionUniversity of Yamanashi

Principal Investigator

SATO Hiroki  University of Yamanashi, 大学院・医学工学総合研究部, 医学研究員 (70422681)

Project Period (FY) 2008 – 2009
Project Status Completed (Fiscal Year 2009)
Budget Amount *help
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords小児血液学 / シグナル伝達 / アポトーシス / 細胞周期停止 / HDAC inhibitor
Research Abstract

We added TSA which was HDAC inhibitor in Leukemia cell lines. And we analyzed TSA induced apoptosis and cell cycle arrest in Leukemia cell lines. We used B-precursor ALL and T-lineage ALL, and analyzed difference of each other. When apoptosis was induced, Bim was up-regulated in B-precursor ALL and PUMA was up-regulated in T-lineage ALL. About cell cycle arrest, it was suggested p21 associated with G0/G1 arrest in B-precursor ALL, and CDC25C, CDC2, and cyclins contribute G2/M arrest in T-lineage ALL.

Report

(3 results)
  • 2009 Annual Research Report   Final Research Report ( PDF )
  • 2008 Annual Research Report

URL: 

Published: 2008-04-01   Modified: 2016-04-21  

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