HUMAN MITOTIC CHECKPOINT GENE--HSMAD2

人类有丝分裂检查点基因--HSMAD2

• 批准号: 2023464
• 负责人: ROBERT I BENEZRA
• 金额: $ 17.31万
• 依托单位: SLOAN-KETTERING INST CAN RESEARCH
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-05-01 至 2000-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2023464
• 关键词: HeLa cells; SDS polyacrylamide gel electrophoresis; Xenopus oocyte; alleles; cell cycle; cell growth regulation; embryonic stem cell; flow cytometry; gene mutation; immunoprecipitation; laboratory mouse; mitotic spindle apparatus; neoplasm /cancer genetics; neoplastic process; phenotype; polymerase chain reaction; site directed mutagenesis; western blottings

The aims of this proposal are to define how human MAD2 (hsMAD2) functions as a mitotic checkpoint gene and to determine if disruption of hsMAD2 contributes to the generation of neoplasia in mouse models. hsMAD2 is the human homolog of a mitotic checkpoint gene first identified in budding yeast (scMAD2). The investigator proposes to test the hypothesis is that the biochemical mechanism underlying human MAD2 checkpoint function is its ability to inhibit the APC through its interactions with Cdc16 and Cdc27. In addition, MAD2 will be disrupted in both ES cells and mice to determine the contribution made by MAD2 to mitotic checkpoint control in mammalian cells.

该提案的目的是定义人类 MAD2 (hsMAD2) 的功能 作为有丝分裂检查点基因并确定 hsMAD2 是否受到破坏 有助于小鼠模型中肿瘤的产生。 hsMAD2 是 有丝分裂检查点基因的人类同源物首次在出芽中发现 酵母（scMAD2）。 研究者提议检验的假设是 人类 MAD2 检查点功能的生化机制是 通过与 Cdc16 和 Cdc27 相互作用抑制 APC 的能力。 此外，ES细胞和小鼠中的MAD2都将被破坏，以确定 MAD2 对哺乳动物有丝分裂检查点控制的贡献 细胞。