IDENTIFYING MEIOSIS-SPECIFIC SUBSTRATES OF CLB5-CDK1

鉴定 CLB5-CDK1 减数分裂特异性底物

• 批准号: 7957827
• 负责人: DAVID I. STUART
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957827
• 关键词: Animals; Biochemical; Biological Models; Biology; Cell Division Process; Cell division; Cells; Chromosomes; Complex; Computer Retrieval of Information on Scientific Projects Database; Congenital Abnormality; Cyclins; Defect; Down Syndrome; Female; Funding; Fungal Genome; Genetic; Grant; Human; Infertility; Institution; Lead; Malignant neoplasm of ovary; Meiosis; Property; Proteins; Regulation; Reproduction; Research; Research Personnel; Resources; Source; Therapeutic; Time; United States National Institutes of Health; cell type; design; egg; male; protein complex; sperm cell

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. Cells that make up an animal or human normally divide a specific number of times before they stop and take on properties that allow them to perform specific functions. One particular cell type ultimately forms sperm in males and egg cells in females; these cells are essential for reproduction. A protein complex referred to as Cyclin/Cdk is responsible for controlling cell division and this complex is a key regulator of cells as they progress to become sperm or eggs. Cyclin/Cdk functions by modifying the activity of a specific set of other proteins at just the right time during the process of cell division. Loss of Cyclin/Cdk activity leads to infertility, and improper regulation of the complex can lead to chromosome damage resulting in birth defects such as Downs Syndrome. Additionally, elevated Cyclin/Cdk activity is associated with aggressive testicular and ovarian cancers. We are using a model system to understand how Cyclin/Cdk activity is controlled, and what influences cause defects in its activity. In the present study we are applying a combination of genetic and biochemical analysis to identify the spectrum of proteins that are controlled by Cyclin/Cdk. By discovering the details of how this complex functions, and what other proteins it regulates we hope to be able to design rational strategies to overcome some types of infertility and develop new and specific therapeutic approaches to testicular and ovarian cancers.

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