一种从G85R突变蛋白组装体的挫折分析中推导得出的SOD1错误折叠传播机制。
A mechanism for propagated SOD1 misfolding from frustration analysis of a G85R mutant protein assembly.
作者信息
Healy Eamonn F
机构信息
Department of Chemistry, St. Edward's University, Austin, TX 78704, USA.
出版信息
Biochem Biophys Res Commun. 2016 Sep 30;478(4):1634-9. doi: 10.1016/j.bbrc.2016.08.172. Epub 2016 Aug 31.
Abstract
Application of landscape theory and the dehydron hypothesis to a crystal structure of a G85R mutant superoxide dismutase (SOD1) tetrameric complex allows for the description of a prion-like hypothesis that serves to explain propagated SOD1 misfolding. We have developed two conformational-change scenarios, one local to the ESL at the complex interface, and a second displacement at the ESL of the otherdimeric subunit. When taken together these provide for a prion-like mechanism that can serve to explain the observed conversion of wtSOD1 to a misfolded form by the G85R mutant.
摘要
将景观理论和脱氢子假说应用于G85R突变超氧化物歧化酶（SOD1）四聚体复合物的晶体结构，有助于描述一种类朊病毒假说，该假说用于解释SOD1错误折叠的传播。我们已经开发了两种构象变化情景，一种是复合物界面处ESL的局部变化，另一种是另一个二聚体亚基ESL的位移。综合起来，这些情景提供了一种类朊病毒机制，可用于解释观察到的野生型SOD1被G85R突变体转化为错误折叠形式的现象。
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