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Regulation of cell division by ubiquitin-dependent proteolysis and by spindle assembly checkpoint

Regulation of cell division by ubiquitin-dependent proteolysis and by spindle assembly checkpoint
通过泛素依赖性蛋白水解和纺锤体组装检查点调节细胞分裂
批准号:
11480216
负责人:
TODOKORO Kazuo
金额:
$10.11万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B).
财政年份:
1999
资助国家:
日本
项目状态:
已结题
起止时间:
1999 至 2000

项目摘要

项目成果

TODOKORO Kazuo的其他基金

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相关文献

中文摘要
翻译
分析了后期促进复合体(APC)的调控机制。研究发现,APC的活性不仅受其调节因子CDc20和CDH1与APC的结合,而且还受APC自身和CDc20和CDH1的磷酸化的调节。APC10/doc1被鉴定为APC亚基之一。SLK被认为是PLK的上游激酶,调节有丝分裂的不同阶段。鉴定了一种新的动粒蛋白CENP-H。CENP-H在整个细胞周期中仅在活跃的动粒上定位于着丝粒内板,并形成多聚体并与MCAK结合,被认为调节着染色体的分离。CENP-H被发现是基本动粒结构所必需的,因为CENP-H的缺失导致了动粒的关键基本成分之一CENP-C的消除。
英文摘要
Regulatory mechanism of anaphase promoting complex (APC) was analyzed. It was found that APC activity was regulated not only by binding of its regulatory factors Cdc20 and Cdh1 to APC, but also by phosphorylation of APC itself and Cdc20 and Cdh1. APC10/Doc1 was identified as one of the APC subunits. Slk was identified as an upstream kinase of plk, which regulates various stages of mitosis. A novel kinetochore protein CENP-H was identified. The CENP-H was specifically localized in inner kinetochore plate only at active kinetochore throughout the cell cycle, and formed multimer by itself and bound MCAK which was thought to regulate choromosome separation. CENP-H was found to be essential for basic kinetochore structure, since delection of CENP-H resulted in elimination of CENP-C, one of the key basic constituents in kinetochore.
期刊论文(56)
专著(0)
科研奖励(0)
会议论文
Ellinger-Ziegelbauer,H. ら: "Ste20-like kinase (SLK), a regulatory kinase for polo-like kinase(Plk) during the G2/M transition in somatic cells."Genes Cells. 5. 491-498 (2000)
Ellinger-Ziegelbauer, H. 等人:“Ste20 样激酶 (SLK),一​​种体细胞 G2/M 转变期间 polo 样激酶 (Plk) 的调节激酶。”Genes Cells. 5. 491-498 ( 2000)
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通讯作者:
永田由香等: "Activation of hematopoietic progenitor kinase-1 by erythropoietin"Blood. 93. 3347-3354 (1999)
Yuka Nagata 等人:“促红细胞生成素激活造血祖细胞激酶 1”血液 93. 3347-3354 (1999)
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永田由香、戸所一雄: "Requirement of activation of JNK and p38 for environmental stress-induced erythroid differentiation & inactivation of ERK for apoptosis"Blood. 94. 853-863 (1999)
Yuka Nagata,Kazuo Todokoro:“环境应激诱导的红细胞分化所需的 JNK 和 p38 激活以及细胞凋亡中 ERK 的失活”Blood。
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通讯作者:
Sugata,N. ら: "Human CENP-H multimers colocalize with CENP-A and CENP-C at active centromere-kinetochore complexes."Hum.Mol.Genet.. 9. 2919-2926 (2000)
Sugata, N. 等人:“人类 CENP-H 多聚体与 CENP-A 和 CENP-C 在活性着丝粒-动粒复合物上共定位。”Hum.Mol.Genet.. 9. 2919-2926 (2000)
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共 28 条
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    MOLECULAR MECHANISM OF ERYTHROID DIFFERENTIATION
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