LRRK2 与膜转运：帕金森病的关联。
LRRK2 and membrane trafficking: nexus of Parkinson's disease.
机构信息
Department of Neuroscience, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul 08826, Korea.
Department of Neuroscience, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul 08826; Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Seoul 02792, Korea.
出版信息
BMB Rep. 2019 Sep;52(9):533-539. doi: 10.5483/BMBRep.2019.52.9.186.
Recent evidence from genetics, animal model systems and biochemical studies suggests that defects in membrane trafficking play an important part in the pathophysiology of Parkinson's disease (PD). Mutations in leucine-rich repeat kinase 2 (LRRK2) constitute the most frequent genetic cause of both familial and sporadic PD, and LRRK2 has been suggested as a druggable target for PD. Although the precise physiological function of LRRK2 remains largely unknown, mounting evidence suggests that LRRK2 controls membrane trafficking by interacting with key regulators of the endosomal-lysosomal pathway and synaptic recycling. In this review, we discuss the genetic, biochemical and functional links between LRRK2 and membrane trafficking. Understanding the mechanism by which LRRK2 influences such processes may contribute to the development of disease-modifying therapies for PD. [BMB Reports 2019; 52(9): 533-539].
最近的遗传学、动物模型系统和生化研究证据表明，膜转运缺陷在帕金森病（PD）的病理生理学中起着重要作用。富含亮氨酸重复激酶 2（LRRK2）的突变构成了家族性和散发性 PD 最常见的遗传原因，并且 LRRK2 被认为是 PD 的可用药靶。尽管 LRRK2 的精确生理功能在很大程度上仍不清楚，但越来越多的证据表明，LRRK2 通过与内体-溶酶体途径和突触再循环的关键调节剂相互作用来控制膜转运。在这篇综述中，我们讨论了 LRRK2 与膜转运之间的遗传、生化和功能联系。了解 LRRK2 影响这些过程的机制可能有助于开发用于治疗 PD 的疾病修饰疗法。[BMB 报告 2019；52(9):533-539]。
Zotero 插件