AN INDUCED-FIT MODEL FOR LANTIBIOTIC AUTOIMMUNITY

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。革兰氏阳性菌L.乳酸乳链菌产生lantibiotic nisin，lantibiotic nisin是靶向其它革兰氏阳性生物体中的脂质II的膜孔形成剂。为了保护自己不受羊毛硫抗生素的腐蚀，L。乳酸链球菌产生一种称为NisI的蛋白质，该蛋白质通过结合和灭活羊毛硫抗生素来保护自身免受成孔剂乳酸链球菌素的影响。我们从以前的研究中知道，NisI是无序的，当不结合到它的同源底物乳酸链球菌素。使用分光光度法，我们希望表明，NisI成为有序后绑定到乳酸链球菌素。

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 gram-positive bacterium L. lactis produces the lantibiotic nisin which is a membrane pore forming agent that targets lipid II in other gram-positive organisms. To protect itself from the caustic nature of this lantibiotic, L. lactis produces a protein called NisI which protects itself from the pore-forming agent nisin by binding and inactivating the lantibiotic. We know from previous studies that NisI is disordered when not bound to its cognate substrate nisin. Using spectropolarimetry, we hope to show that NisI becomes ordered upon binding to nisin.