Werner Syndrome Family Proteins & Telomere Recombination

维尔纳综合征家族蛋白质

• 批准号: 6920690
• 负责人: JULIA Y LEE-SOETY
• 金额: $ 4.99万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-08-01 至 2006-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6920690
• 关键词: Werner' s syndrome; cell senescence; gene mutation; genetic recombination; polymerase chain reaction; postdoctoral investigator; premature aging; protein structure function; telomere; western blottings

DESCRIPTION (provided by applicant): Telomeres shorten with age in many human tissues and such shortening may play a role in the aging process. Werner syndrome (WS) is a recessive genetic disorder characterized by the premature onset of several features of aging. Cells from Werner patients senesce and shorten telomeres at a much faster rate compared to normal cells. Accumulating evidence indicates that the protein deficient in WS, WRN, functions in telomere maintenance. Since cells must preserve proper telomere function for continued survival, and may use homologous recombination to repair shortened telomeres, this proposal attempts to determine whether WRN and its homologues participate in telomere recombination as a way to repair or protect shortened telomeres. Understanding how the Werner syndrome family proteins are involved in telomere maintenance should yield insight into the natural processes of aging.

描述（由申请人提供）：在许多人体组织中，端粒随着年龄的增长而缩短，这种缩短可能在衰老过程中发挥作用。Werner综合征（WS）是一种隐性遗传性疾病，其特征是衰老的几个特征过早发作。与正常细胞相比，沃纳患者的细胞以更快的速度衰老和缩短端粒。越来越多的证据表明，WS缺陷蛋白WRN在端粒维持中起作用。由于细胞必须保持适当的端粒功能，以继续生存，并可能使用同源重组来修复缩短的端粒，这个建议试图确定是否WRN及其同源物参与端粒重组作为一种方式来修复或保护缩短的端粒。了解沃纳综合征家族蛋白质如何参与端粒的维持应该有助于深入了解衰老的自然过程。