Studies on ontogenic significance of PLC signaling systems.
PLC信号系统的本体意义研究。
基本信息
- 批准号:10480172
- 负责人:
- 金额:$ 7.36万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 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
Phospholipase C (PLC) hydrolyzes phosphatidylinositol-4,5-bisphosphate (PIP_2) to generate inositol-1,4,5-trisphosphate (IP_3) and diacylglycerol (DAG), and this catalytic activity is controlled upon receptor activation. It is well understood that these two products, IP_3 and DAG, mediate the calcium release from intracellular stores and protein kinase C activation. Among PLC isoforms, this study focused on biological function of PLC-γ2, Mice with loss of PLC-γ2 function were produced using two different gene knockout strategies. Following results were obtained from this research project.1) Using gene-targeting approach, mice heterogeneously harboring PLC-γ2 gene of which a catalytic X region was replaced by neo, were successfully produced. The homozygous mice, however, were embryonic lethal and died at 〜E8.5.2) The PLC-γ2 gene was inducibly ablated by using IFN-regulated Cre recombinase. Mice with neonatally induced loss of PLC-γ2 function displayed reduced members of mature conventional B cells and peritoneal B l cells and defective responses in vitro to BCR stimulation and in vivo to immunization with thymusindependent type-II Ags. In contrast, T cell development and TCR-mediated proliferation were normal. These results indicate that PLC-γ2 is a critical component of BCR signaling pathways and is required to promote B cell development.
磷脂酶C(PLC)催化磷脂酰肌醇-4,5-二磷酸(PIP_2)生成肌醇-1,4,5-三磷酸(IP_3)和二酰甘油(DAG),这种催化活性受受体激活的控制。众所周知,这两个产物,IP_3和DAG,介导细胞内钙释放和蛋白激酶C的激活。在PLC亚型中,本研究以PLC-γ2的生物学功能为研究重点,采用两种不同的基因敲除策略建立了PLC-γ2功能缺失的小鼠模型。1)利用基因打靶的方法,成功地获得了异源携带pLc-γ-2基因的小鼠,其催化X区被NEO取代。然而,纯合子小鼠是胚胎致死的,并在E8.5岁时死亡。5)用干扰素调节的Cre重组酶诱导PLC-γ2基因被烧毁。新生鼠PLC-γ-2功能丧失后,成熟的常规B细胞和腹膜B-L细胞成员减少,体外对bcr刺激和体内对胸腺非依赖性II型AGS免疫的反应有缺陷。相比之下,T细胞发育和TCR介导的增殖是正常的。这些结果表明,PLC-γ2是bcr信号通路的重要组成部分,是促进B细胞发育所必需的。
项目成果
期刊论文数量(54)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
ITO Taiji, KABUYMA Yukihito, OKAZAKI Satoshi, KAMEDA Takashi, MURAKAMI Masao, IBA Hideo: "Unstable retrovirus mutants with acquired transforming activity: rapid changes in the number of repeats of a specific junD polynucleotide segments"Nucleic Acids Res.
ITO Taiji、KABUYMA Yukihito、OKAZAKI Satoshi、KAMEDA Takashi、MURAKAMI Masao、IBA Hideo:“具有获得性转化活性的不稳定逆转录病毒突变体:特定junD多核苷酸片段重复次数的快速变化”核酸研究。
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Satoh,K., et al.: "Involvement of ErbB-2 in rheumatoid synovial cell growth."Arthritis Rheum.. (in press).
Satoh,K., et al.:“ErbB-2 在类风湿滑膜细胞生长中的参与。”关节炎大黄..(出版中)。
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- 影响因子:0
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Horiguchi,H., et al.: "Cadmium-induced acute hepatic injury is exacerbated in interleukin-8 transgenic mice."Toxicol.Appl.Pharmacol.. 163. 231-239 (2000)
Horiguchi, H., et al.:“镉诱导的急性肝损伤在白细胞介素 8 转基因小鼠中加剧。”Toxicol.Appl.Pharmacol.. 163. 231-239 (2000)
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- 发表时间:
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- 影响因子:0
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- 通讯作者:
A.Hashimoto, et al.: "Essential role of phospholipase C-g2 in B cell development and function"J.Immunol.. 165. 1738-1742 (2000)
A.Hashimoto 等:“磷脂酶 C-g2 在 B 细胞发育和功能中的重要作用”J.Immunol.. 165. 1738-1742 (2000)
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- 影响因子:0
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- 通讯作者:
N.Oyama, et al.: "Different growth properties in response to EGF and IL-6 of primary keratinocytes derived from normal-"J.Dermatol.Sci.. 16. 120-128 (1998)
N.Oyama 等人:“源自正常的原代角质形成细胞对 EGF 和 IL-6 的不同生长特性”J.Dermatol.Sci.. 16. 120-128 (1998)
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HOMMA Yoshimi其他文献
HOMMA Yoshimi的其他文献
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{{ truncateString('HOMMA Yoshimi', 18)}}的其他基金
Studies on molecular basis for regulation of beta-oxidation system
β-氧化系统调控的分子基础研究
- 批准号:
21590314 - 财政年份:2009
- 资助金额:
$ 7.36万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis of DNA methylation pattern of promoter CpG islands in idiopathic pulmonary fibrosis.
特发性肺纤维化启动子CpG岛DNA甲基化模式分析
- 批准号:
15390257 - 财政年份:2003
- 资助金额:
$ 7.36万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Cooperative study on molecular mechanism of GFAP expression.
GFAP表达分子机制合作研究。
- 批准号:
10044307 - 财政年份:1998
- 资助金额:
$ 7.36万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Identification and functional analysis of proteins involved in novel pathway for PLC activation.
PLC 激活新途径中涉及的蛋白质的鉴定和功能分析。
- 批准号:
08458184 - 财政年份:1996
- 资助金额:
$ 7.36万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Trials for development of novel inhibitors for intracellular signaling.
开发新型细胞内信号传导抑制剂的试验。
- 批准号:
06558095 - 财政年份:1994
- 资助金额:
$ 7.36万 - 项目类别:
Grant-in-Aid for Developmental Scientific Research (B)
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6240981 - 财政年份:1996
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07044216 - 财政年份:1995
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Role of tyrosine Kinase in platelet inositol phospholipid metabolism
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- 批准号:
03671182 - 财政年份:1991
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62480303 - 财政年份:1987
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Mechanism and role of inositol phospholipid turnover in yeast morphogenesis
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60560090 - 财政年份:1985
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ROLE OF G-PROTEINS IN THE CONTROL OF INOSITOL PHOSPHOLIPID HYDROLYSIS IN T-CELLS
G 蛋白在控制 T 细胞中肌醇磷脂水解中的作用
- 批准号:
3811105 - 财政年份:
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PIP PHOSPHATASE AND INOSITOL PHOSPHOLIPID HOMEOSTATSIS
PIP 磷酸酶和肌醇磷脂稳态
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5212607 - 财政年份:
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