Mechanisms involved in GPI-anchored-protein signaling dimer formation
GPI 锚定蛋白信号二聚体形成涉及的机制
基本信息
- 批准号:10672190
- 负责人:
- 金额:$ 2.11万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1998
- 资助国家:日本
- 起止时间:1998 至 2000
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Various cell surface proteins are anchored to cell membranes via a glycosyl-phosphatidylinositol (GPI) anchor. Although these proteins function as signaling molecules, mechanisms involved in the signaling are largely unknown. In this study we focused on a GPI-anchored complement regulatory protein, CD59, as a model for elucidating the mechanisms involved in the GPI-anchored protein mediating signaling.We identified a CD59-associating protein by cross-linking surface proteins by chemical cross-linker and revealed that the protein is CD59 molecule itself. We also developed the method for direct measurement of CD59 signaling by means of a C9 peptide as a ligand. By ligation with the C9 peptide, specific increase in intracellular Ca2+ was detected. These findings enable the direct assessment of CD59 signaling rather than by activation with Ab cross-linking.GPI-anchored proteins are distributed on membrane domains designated "rafts". Caveolin, a main protein on one type of rafts (caveolae), functions as a key molecule in various types of signaling. To know whether caveolin is involved in CD59 signaling, we tested caveolin expression in blood and blood cell lines in which CD59 signaling is identified. To our surprise none of them expressed caveolin. Only sub line of adult T cell leukemia (ATL) cell lines in a ctivated states expressed caveolin. We are now on the way to elucidate the function of caveolin in CD59 signaling using these positive cells.
各种细胞表面蛋白通过糖基磷脂酰肌醇(GPI)锚定在细胞膜上。虽然这些蛋白质作为信号分子发挥作用,但参与信号传递的机制在很大程度上是未知的。在本研究中,我们以GPI锚定的补体调节蛋白CD59为模型,通过化学交联剂对表面蛋白进行交联化,确定了CD59结合蛋白,揭示了该蛋白本身就是CD59分子。我们还建立了以C9多肽为配体直接测定CD59信号的方法。通过与C9多肽的结合,检测到细胞内钙离子的特异性增加。这些发现使得对CD59信号的直接评估成为可能,而不是通过抗体的交联性激活。GPI锚定的蛋白分布在被称为“筏”的膜域上。小窝蛋白是一种木筏(小窝)上的主要蛋白质,在各种类型的信号传递中起着关键分子的作用。为了了解小窝蛋白是否参与CD59信号转导,我们测试了小窝蛋白在血液和CD59信号转导的血细胞系中的表达。令我们惊讶的是,他们中没有一个人表达了洞察力。只有处于激活状态的成人T细胞白血病(ATL)细胞亚系表达小窝蛋白。我们现在正在利用这些阳性细胞来阐明小窝蛋白在CD59信号转导中的作用。
项目成果
期刊论文数量(31)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Hatanaka, M., T.Maeda, T.Ikemoto, H.Mori, T.Seya, and A.Shimizu.: "Expression of caveolin-1 in human T cell leukemia cell lines."Biophis.Biochem.Res.Comm.. 253. 382-387 (1998)
Hatanaka, M.、T.Maeda、T.Ikemoto、H.Mori、T.Seya 和 A.Shimizu.:“caveolin-1 在人 T 细胞白血病细胞系中的表达。”Biophis.Biochem.Res.Comm。
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- 影响因子:0
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- 通讯作者:
畑中道代ら: "Expression of caveolin-1 in human T cell lleukemia cell lines"Biochem.Biophys.Res.Comm.. 253. 382-387 (1998)
Michiyo Hatanaka 等:“人 T 细胞白血病细胞系中 Caveolin-1 的表达”Biochem.Biophys.Res.Comm.. 253. 382-387 (1998)
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畑中道代 ら: "Caveolae構造とcaveolin(1)caveolinとシグナル伝達"神戸常盤短期大学紀要. 22. 31-39 (2000)
Michiyo Hatanaka 等:“Caveolae 结构和 Caveolin(1) Caveolin 和信号转导”神户常盘短期大学报 22. 31-39 (2000)。
- DOI:
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畑中道代 ら: "Cellular distribution of a GPI-anchored complement regulatory protein CD59 : homodimerization on the surface on the HeLa and CD59-transfected CHO cel"J.Biochem.. 123. 579-586 (1998)
Michiyo Hatanaka 等人:“GPI 锚定补体调节蛋白 CD59 的细胞分布:HeLa 和 CD59 转染的 CHO 细胞表面上的同二聚化” J.Biochem.. 123. 579-586 (1998)
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Ikemoto, T., T.Nakagawa, M.Hatanaka, M.Hasegawa, T.Kageyama, M.Hirano, and A.Shimizu.: "My-4+/LeuM3- molecules and CD19 antigen down-modulated by low affinity Fc gamma receptor II (CD32) stimulation on CD56-positive B lymphoma cells."Leukemia Lymphoma. 39
Ikemoto, T.、T.Nakakawa、M.Hatanaka、M.Hasekawa、T.Kageyama、M.Hirano 和 A.Shimizu.:“My-4 /LeuM3- 分子和 CD19 抗原被低亲和力 Fc gamma 下调
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HATANAKA Michiyo其他文献
HATANAKA Michiyo的其他文献
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{{ truncateString('HATANAKA Michiyo', 18)}}的其他基金
The Signal Transduction Mechanisms of a GPI-anchored Complement Regulatory Protein, CD59.
GPI 锚定补体调节蛋白 CD59 的信号转导机制。
- 批准号:
08672654 - 财政年份:1996
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Mechanisms involved in loss of PI-anchored proteins (DAF and CD59) in human leukemia cell lines.
人类白血病细胞系中 PI 锚定蛋白(DAF 和 CD59)丢失的机制。
- 批准号:
05671933 - 财政年份:1993
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Studies on the mechanisms of C9 activation and of C9 inactivation by the regulatory protein(MACIF)
调节蛋白(MACIF)激活C9和失活C9机制的研究
- 批准号:
03671118 - 财政年份:1991
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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