MOLECULAR INTERACTIONS OF CRYSTALLINS IN THE EYE

眼睛中晶状体蛋白的分子相互作用

• 批准号: 7953940
• 负责人: Jonathan Mark Petrash
• 金额: $ 0.58万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7953940
• 关键词: Applications Grants; Binding; Cataract; Cell membrane; Computer Retrieval of Information on Scientific Projects Database; Crystallins; Development; Eye; Funding; Grant; Human; Institution; Lipids; Mass Spectrum Analysis; Membrane; Membrane Proteins; Mouse Strains; Post-Translational Protein Processing; Property; Proteins; Research; Research Personnel; Resources; Role; Source; Specificity; Transgenic Mice; United States National Institutes of Health; alpha-Crystallins; biomedical resource; experience; insight; lens; mutant

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. This grant proposal is from a highly experienced investigator to examine whether a mutant form of alphaA-crystallin (R116 C), associated with autosomal dominant cataract in human, has altered property of elevated plasma membrane binding and therefore, causes cataract. Preliminary results shows a change in the property of the mutant alpha-crystallin compared wild type alpha, and according to the P.I., this may be a causative factor in the human autosomal dominant cataract. To investigate this causative factor in the autosomal dominant cataract, three specific aims are proposed. These will determine the specificities of lens membrane proteins and lipids during binding with alpha-crystallin, the effect of post-translational modifications of alpha-crystallin on its membrane-binding capability and finally the role of the mutant protein in cataract development by producing a transgenic mouse strain for lens expression of R116C mutant form of alphaA-crystallin. Together, the studies will provide insight regarding the role of alphaA R116C mutant in potential mechanism of the human autosomal dominant cataract.

这个子项目是众多研究子项目之一