A SCREEN FOR NOVEL MPK1 KINASE DOMAIN BINDING PROTEINS

新型 MPK1 激酶结构域结合蛋白的筛选

• 批准号: 7957700
• 负责人: DAVID E. LEVIN
• 金额: $ 0.7万
• 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/7957700
• 关键词: Area; Binding; Biology; Cell Wall; Computer Retrieval of Information on Scientific Projects Database; Docking; Funding; Fungal Genome; Genes; Grant; Institution; MAP Kinase Gene; Mitogen-Activated Protein Kinases; Mutation; Phosphotransferases; Protein Binding Domain; Proteins; Research; Research Personnel; Resources; Screening procedure; Source; Surface; Transcriptional Activation; United States National Institutes of Health; genetic regulatory protein; novel

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. The MAP kinase Mpk1 is a key regulatory protein controlling activation of transcription (via Rlm1) of cell wall genes. Our lab has previously shown Mpk1 has both a kinase dependent and a kinase independent mechanism of transcriptional activation. Here we try to not only identify novel binding partners of Mpk1 kinase domain, but we also wish to identify surfaces of interaction of the protein by screening an Mpk1 bait that contains surface mutations on 2 major MAPK binding areas-the substrate binding domain and the docking domain.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 MAP激酶Mpk1是控制细胞壁基因转录激活(通过Rlm1)的关键调节蛋白。我们的实验室先前已经证明，Mpk1既有依赖于激酶的转录激活机制，也有不依赖于激酶的转录激活机制。在这里，我们不仅试图确定新的Mpk1激酶域的结合伙伴，而且我们还希望通过筛选在两个主要MAPK结合区-底物结合域和对接结构域-包含表面突变的Mpk1诱饵来识别蛋白质的相互作用表面。