轮转周期：APP是AppBp1通路的关键吗？
Cycle on Wheels: Is APP Key to the AppBp1 Pathway?
作者信息
Chen Y, Neve Rn, Zheng H, Griffin Wts, Barger Sw, Mrak Re
机构信息
Department of Geriatrics, University of Arkansas for Medical Sciences, USA.
Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, USA.
出版信息
Austin Alzheimers Parkinsons Dis. 2014;1(2).
Alzheimer's disease (AD) is the gradual loss of the cognitive function due to neuronal death. Currently no therapy is available to slow down, reverse or prevent the disease. Here we analyze the existing data in literature and hypothesize that the physiological function of the Amyloid Precursor Protein (APP) is activating the AppBp1 pathway and this function is gradually lost during the progression of AD pathogenesis. The AppBp1 pathway, also known as the neddylation pathway, activates the small ubiquitin-like protein nedd8, which covalently modifies and switches on Cullin ubiquitin ligases, which are essential in the turnover of cell cycle proteins. Here we discuss how APP may activate the AppBp1 pathway, which downregulates cell cycle markers and protects genome integrity. More investigation of this mechanism-driven hypothesis may provide insights into disease treatment and prevention strategies.
阿尔茨海默病（AD）是由于神经元死亡导致认知功能逐渐丧失的疾病。目前尚无治疗方法可减缓、逆转或预防该疾病。在此，我们分析了文献中的现有数据，并推测淀粉样前体蛋白（APP）的生理功能是激活AppBp1途径，且该功能在AD发病机制进展过程中逐渐丧失。AppBp1途径，也称为NEDDylation途径，可激活小泛素样蛋白Nedd8，后者共价修饰并开启Cullin泛素连接酶，而Cullin泛素连接酶在细胞周期蛋白的周转中至关重要。在此我们讨论APP如何激活AppBp1途径，该途径可下调细胞周期标志物并保护基因组完整性。对这一机制驱动的假说进行更多研究可能会为疾病治疗和预防策略提供见解。
Zotero 插件