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PHOSPHORYLATION OF MAD1 BY TTK

PHOSPHORYLATION OF MAD1 BY TTK
TTK 磷酸化 MAD1
批准号:
8171354
负责人:
Don W Cleveland
金额:
$0.24万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-09-01 至 2011-08-31

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项目成果

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中文摘要
翻译
这个子项目是众多研究子项目之一
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Progression through the cell cycle is regulated at multiple checkpoints. For example, the spindle checkpoint monitors the fidelity of chromosome segregation. This checkpoint inhibits cells from progressing into anaphase until all sister chromatids are properly attached to the mitotic spindle and aligned at the metaphase plate. A number of proteins have been shown to be important in this process including MAD1, MAD2, TTK, Bub1, BubR1 and BubR2. To further understand the molecular mechanism by which these protein regulated the spindle checkpoint a mass spectrometry analysis was performed to identify phosphorylation sites on Mad1 by the TTK kinase.
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会议论文
In vivo modelling and therapy development for stathmin-2 loss in TDP-43 proteinopathies
  • 批准号:
    10317404
  • 项目类别:
  • 资助金额:
    $250.73万
  • 财政年份:
    2021
  • 负责人:
    Don W Cleveland
  • 依托单位:
Determining stathmin-2 function and potential as a therapeutic target in ALS/FTD
Determining stathmin-2 function and potential as a therapeutic target in ALS/FTD
Mechanisms of chromosome segregation, aneuploidy, and tumorigenesis
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