ORGANIZATION AND FUNCTIONS OF THE NUCLEAR LAMINA

核层的组织和功能

• 批准号: 7957746
• 负责人: Larry R. Gerace
• 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/7957746
• 关键词: Biology; C-terminal; Computer Retrieval of Information on Scientific Projects Database; Disease; Excision; Funding; Fungal Genome; Grant; Institution; Lamin Type A; Liver; Molecular; Mus; Mutation; Nuclear Envelope; Nuclear Lamina; Progeria; Proteomics; Research; Research Personnel; Resources; Source; United States National Institutes of Health; base; gain of function; mutant; prevent

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. Hutchinson-Guilford progeria is caused by a mutant form of lamin A that contains an internal deletion in its C-terminal region. This prevents the proteolytic removal of the farnesylated C-terminus of lamin A that normally takes place, and leads to a toxic gain of function. To understand the molecular basis of this disease, we are carrying out proteomic analysis of nuclear envelopes isolated from the livers of mice with mutations that prevent normal removal of the lamin A farnesylated C-terminus.

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