Cell biological study of the RANDAM-2 high positive cells and RANDAM-2 low/negative cells in mouse central nervous system.
Cell biological study of the RANDAM-2 high positive cells and RANDAM-2 low/negative cells in mouse central nervous system.
批准号:
16500252
负责人:
KOTANI Masaharu
金额:
$2.37万
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
项目状态:
已结题
起止时间:
2004 至 2005
中文摘要
RANDAM-2是一种i型跨膜抗原,在小鼠神经发生过程中在兴奋性神经元细胞系上组成性表达,在胚胎第8.5天(E8.5)和E10.5天之间表达量最高。由于这一时期与神经干细胞(NSCs)的增殖阶段重叠,可想而知,RANDAM-2参与了增殖和/或由此产生的神经分化。在本文中,我们证明了通过random -2特异性单克隆抗体的阳性选择,NSCs和npc可以分别作为random -2^<高+>和random -2^<低+/->细胞分离出来。所分离的random -2^<高+>细胞具有高度的自我更新能力和向神经细胞多系分化的潜力。相比之下,几乎所有的RANDAM-2^<低+/->细胞不仅表现出极低的自我再生能力,而且分化能力仅限于神经元。这两个细胞群在与神经分化相关的分子表达水平方面也存在差异。这些发现表明,RANDAM-2可以被视为分离NSCs的有用标记物,并表明其高表达参与了神经细胞作为NSCs的先天特性的保留。
英文摘要
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.
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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:
American Journal of Pathology (in press)
影响因子:
--
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:
Journal cell Science 117
影响因子:
--
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:
American Journal of Pathology 166(4)
影响因子:
--
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:
Journal of Pharmacology and Experimental Therapeutics 308
影响因子:
--
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:
Journal Human Genetics 49
影响因子:
--
作者:
[Sakuraba, H., Matsuzawa, F., Aikawa, S., Doi, Y., Kotani, M., et al.]
通讯作者:
et al.
共 13 条
cDNA cloning of cell membrane surface antigens involved in the neuronal differentiation and identification of the antigen positive cells in mouse cerebrum
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批准号:14580757
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.79万
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财政年份:2002
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负责人:KOTANI Masaharu
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依托单位:
海外基金