ISOLATION AND CHARACTERIZATION OF CELL CYCLE CHECKPOINT PROTEINS

细胞周期检查点蛋白的分离和表征

• 批准号: 8169795
• 负责人: FRANK PATRICK MCCORMICK
• 金额: $ 0.18万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-09-12 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169795
• 关键词: Apoptosis; Apoptotic; Cell Cycle Checkpoint; Cell division; Chromosomal Instability; Chromosomal Stability; Chromosome Segregation; Clinical; Complex; Computer Retrieval of Information on Scientific Projects Database; Defect; Funding; Grant; Institution; Knowledge; Malignant Neoplasms; Mitosis; Mitotic; Mitotic spindle; Molecular; Paclitaxel; Pharmaceutical Preparations; Proteins; Refractory; Research; Research Personnel; Resources; Signal Transduction; Signal Transduction Pathway; Source; Therapeutic; United States National Institutes of Health; cancer cell; response

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. The mitotic spindle assembly checkpoint (SAC) is the only known checkpoint in mitosis. The SAC is composed of complex multi-signal transduction pathways that promote the proper segregation of chromosomes during cell division. As such, defects in the SAC result in chromosome instability (CIN), a hallmark of cancer. Of clinical importance, apoptosis caused by mitotic catastrophe depends on the activation of SAC. However, our knowledge of SAC signaling is far from complete, and the functional cross-talk between SAC activation and the induction of mitotic apoptosis is poorly understood. This makes it difficult to explain the mechanism by which cancer cells respond or become refractory to anti-mitotic drugs, e.g. taxol, that induced spindle-damage or mitotic catastrophe. Therefore, it is highly important to understand both the molecular mechanism by which SAC (i) controls proper chromosome segregation to maintain chromosome stability during cell division and (ii) elicits an apoptotic response in mitosis to anti-mitotic cancer therapeutic drugs.

这个子项目是众多研究子项目之一