Cell biological study of the RANDAM-2 high positive cells and RANDAM-2 low/negative cells in mouse central nervous system.
小鼠中枢神经系统 RANDAM-2 高阳性细胞和 RANDAM-2 低/阴性细胞的细胞生物学研究。
基本信息
- 批准号:16500252
- 负责人:
- 金额:$ 2.37万
- 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:2004
- 资助国家:日本
- 起止时间:2004 至 2005
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
RANDAM-2, a type-I transmembrane antigen constitutively expressed on the excitatory neuronal cell lineage during mouse neurogenesis, shows the highest expression level between embryonic day 8.5 (E8.5) and E10.5. As the period well overlaps with the proliferating stages of neural stem cells (NSCs), it is conceivable that RANDAM-2 is involved in the proliferation and/or the resulting neural differentiation. In this paper, we show that NSCs and NPCs can be isolated as RANDAM-2^<high+> and RANDAM-2^<low+/-> cells, respectively, by positive selection with a monoclonal antibody specific to RANDAM-2. The isolated RANDAM-2^<high+> cells had the characteristics as the highly self-renewal capability and potential for multilineage differentiation into neural cells. In contrast, almost all of the RANDAM-2^<low+/-> cells exhibited not only the extremely low self-renewability but the differentiation capability restricted to neurons. These two cell populations also differed from each other in terms of the expression level of molecules associated with neural differentiation. These findings demonstrate that RANDAM-2 can be regarded as a useful marker for isolation of the NSCs, and suggest that its high expression takes part in the retention of the neural cells within the innate properties as NSCs.
RANDAM-2是一种在小鼠神经发生期间在兴奋性神经元细胞谱系上组成性表达的I型跨膜抗原,在胚胎第8.5天(E8.5)和E10.5之间显示出最高表达水平。由于该时期与神经干细胞(NSC)的增殖阶段完全重叠,因此可以想象RANDAM-2参与增殖和/或导致的神经分化。在本文中,我们表明,神经干细胞和NPC可以分离为RANDAM-2^<高+>和RANDAM-2^<低+/->细胞,分别通过阳性选择与RANDAM-2特异性的单克隆抗体。RANDAM-2^<high+>细胞具有高度的自我更新能力和向神经细胞多向分化的潜能。相反,几乎所有的RANDAM-2^<low+/->细胞不仅表现出极低的自我更新能力,而且表现出仅限于神经元的分化能力。这两个细胞群体在与神经分化相关的分子的表达水平方面也彼此不同。这些发现表明,RANDAM-2可以被认为是一个有用的标记物,用于分离的神经干细胞,并表明其高表达参与保留神经细胞的先天属性作为神经干细胞。
项目成果
期刊论文数量(38)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Distal myopathy with rimmed vacuoles : Impaired O-glycan formation in saroolemmal glycoproteins.
伴有边缘空泡的远端肌病:肌膜糖蛋白中的 O-聚糖形成受损。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Tajima;Y.;Uyama;E.;Go;S.;Sato;C.;Tao;N.;Kotani;M.;et al.
- 通讯作者:et al.
ALK receptor tyrosine kinase promotes cell growth and neurite outgrowth as revealed by an agonist anti-ALK monoclonal antibody.
激动剂抗 ALK 单克隆抗体显示,ALK 受体酪氨酸激酶可促进细胞生长和神经突生长。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Motegi;A.;Fujimoto;J.;Kotani;M.;et al.
- 通讯作者:et al.
Distal myopathy with rimmed vacuoles : Impaired O-glycan formation in sarcolemmal glycoproteins.
伴有边缘空泡的远端肌病:肌膜糖蛋白中的 O-聚糖形成受损。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Tajima;Y;Uyama;E.;Go;S.;Sato;C.;Tao;N.;Kotani;M.;et al.
- 通讯作者:et al.
Reversibility versus persistence of GPIIb/IIIa blocker-induced conformational change of GP_IIb/III_a (aIIbβ3,CD41/CD61)
GPIIb/IIIa 阻滞剂诱导的 GP_IIb/III_a (aIIbβ3、CD41/CD61) 构象变化的可逆性与持久性
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Schwarz;M.;Katagiri;Y.;Kotani;M.et al.
- 通讯作者:M.et al.
Structure and immunocytochemical studies on α-N-acetylgalactosaminidase deficiency (shindler/Kanzaki desease).
α-N-乙酰氨基半乳糖苷酶缺乏症(shindler/Kanzaki 病)的结构和免疫细胞化学研究。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Sakuraba;H.;Matsuzawa;F.;Aikawa;S.;Doi;Y.;Kotani;M.;et al.
- 通讯作者:et al.
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KOTANI Masaharu其他文献
KOTANI Masaharu的其他文献
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{{ truncateString('KOTANI Masaharu', 18)}}的其他基金
cDNA cloning of cell membrane surface antigens involved in the neuronal differentiation and identification of the antigen positive cells in mouse cerebrum
小鼠大脑神经元分化相关细胞膜表面抗原的cDNA克隆及抗原阳性细胞的鉴定
- 批准号:
14580757 - 财政年份:2002
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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