2000 Fiscal Year Final Research Report Summary
Identification of novel cytoplasmic factors responsible for cell growth and death.
| Project/Area Number |
11557007
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
General medical chemistry
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| Research Institution | Kansai Medical University |
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Principal Investigator |
KUROSAKI Tomohiro Kansai Medical University, Department of Medicine, Professor, 医学部, 教授 (50178125)
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| Co-Investigator(Kenkyū-buntansha) |
OKAWA Katsuya Kirin Brewery Co., LTD., Investigator, 研究員
IWAMATSU Akihiro Kirin Brewery Co., LTD., Principal Investigator, 主任研究員
ISHIAI Masamichi Kansai Medical University, Department of Medicine, Assistant Professor, 医学部, 助手 (90298844)
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| Project Period (FY) |
1999 – 2000
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| Keywords | BCR signaling / Syk / BLNK / BCAP / apoptosis / 遺伝子欠損 / 微量蛋白質精製 |
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| Research Abstract |
The ability of B cells to respond to antigen relies on signals transmitted through the B cell antigen receptor (BCR) complex. Activation of cytoplasmic protein tyrosine kinases (PTKs) is the earliest measurable biochemical response to BCR cross-linking. The initial event leads to the generation of secondary signals including Ras activation, phosphatidylinositol 3-kinase (PI-3K) activation, phospholipase C (PLC)-γ2 activation.
Based upon our previous evidence that Syk, a BCR-associated PTK, is essential for PLC-γ2 activation, we purified tyrosine-phosphorylated proteins mediated by Syk. Among 15 purified proteins, two molecules (BLNK and BCAP) were turned out to play an important role in BCR-mediated apoptosis. In fact, BLNK-deficient B cells abolished apoptosis, whereas this BCR-mediated apoptosis was enhanced by loss of BCAP.
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