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Molecular mechanism of the signaling pathway for execution of spontaneous apoptosis of human B-cell lymphoma

Research Project

Project/Area Number 12670168
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Human pathology
Research InstitutionFukushima Medical University

Principal Investigator

ABE Masafumi  Fukushima Medical University School of Medicine Professor, 医学部, 教授 (00045783)

Co-Investigator(Kenkyū-buntansha) HASHIMOTO Yuko  Fukushima Medical University School of Medicine Instructor, 医学部, 助手 (60305357)
TASAKI Kazuhiro  Fukushima Medical University School of Medicine Instructor, 医学部, 助手 (70244382)
ONO Nobutaka  Fukushima Medical University School of Medicine Instructor, 医学部, 助手 (80233584)
Project Period (FY) 2000 – 2001
Project Status Completed (Fiscal Year 2001)
Budget Amount *help
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
Keywordsapoptosis / caspase / Bcl-2 family / TRAF / NF-kB / B-cell lymphoma / Bcl-2 / Bcl-X_L / 遺伝子導入
Research Abstract

We analyzed bcl-2 family molecules, caspase and TRF molecules using Western blot method and Northern blot method (ribonuclease protection assay) to elucidate the signaling pathway for execution of spontaneous apoptosis of HBL-9 cells. In addition, we examined the NF-kB activity in HBL-9 cells using electrophoretic mobility shift assay (EMSA) to investigate the relationship between NF-kB activation and TRAF molecules or bcl-2 molecules. HBL-9 cells showed the expression of caspase-2, caspase-3, caspase-7 and caspase-8 at the protein and gene (mRNA) levels, and the processing of those caspase molecules was demonstrated. HBL-9 cells displayed the gene expression (mRNA) of bcl-XL, bax, bad and bid and expression of Bax, Bad proteins but no expression of Bcl-2 and Bcl-XL proteins. HBL-9 cells expressed the mRNAs ofTRAF 1, TRAF 2, TRAF 3 and TRAF 4, and showed the expression of TRAF 2 and TRAF 3 proteins but no expression of TRAF 1 and TRAF 4 proteins. NF-kB activity was not detected.
Those data indicate the following on the molecular mechanism for the execution of spontaneous apoptosis of HBL-9 cells ;
1) At least four caspases (caspase-2, caspase-3, caspase-7 and caspase-8) are activated for the spontaneous apoptosis of HBL-9 cells, and an unknown upstream caspase of those caspases might play a role as a key caspase in the caspase cascade.
2) A signaling pathway, bcl-2 family - cytochrome C - Apaf-1 - caspase-9, is not associated with the execution of the spontaneous apoptosis of HBL-9 cells.
3) Disturbance of antiapoptotic mechanism involving lack of Bcl-2 and Bcl-XL molecules and inactivation of NF-kB can cause the induction of the spontaneous apoptosis of HBL-9 cells.

Report

(3 results)
  • 2001 Annual Research Report   Final Research Report Summary
  • 2000 Annual Research Report

URL: 

Published: 2000-04-01   Modified: 2016-04-21  

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