Nag Niharika, Tripathi Timir
Molecular and Structural Biophysics Laboratory, Department of Biochemistry, North-Eastern Hill University, Shillong 793022, India.
Regional Director's Office, Indira Gandhi National Open University (IGNOU), Regional Centre Kohima, Kenuozou, Kohima 797001, India.
Brief Funct Genomics. 2023 Apr 13;22(2):161-167. doi: 10.1093/bfgp/elac022.
An emerging pathophysiology associated with the neurodegenerative Alzheimer's disease (AD) is the impairment of nucleocytoplasmic transport (NCT). The impairment can originate from damage to the nuclear pore complex (NPC) or other factors involved in NCT. The phenylalanine-glycine nucleoporins (FG-Nups) form a crucial component of the NPC, which is central to NCT. Recent discoveries have highlighted that the neuropathological protein tau is involved in direct interactions with the FG-Nups and impairment of the NCT process. Targeting such interactions may lead to the identification of novel interaction inhibitors and offer new therapeutic alternatives for the treatment of AD. This review highlights recent findings associated with impaired NCT in AD and the interaction between tau and the FG-Nups.
一种与神经退行性疾病阿尔茨海默病（AD）相关的新兴病理生理学是核质运输（NCT）受损。这种损伤可能源于核孔复合体（NPC）的损伤或参与NCT的其他因素。苯丙氨酸-甘氨酸核孔蛋白（FG-Nups）构成了NPC的关键组成部分，而NPC对NCT至关重要。最近的发现突出表明，神经病理学蛋白tau参与了与FG-Nups的直接相互作用以及NCT过程的损伤。针对这种相互作用可能会导致鉴定出新的相互作用抑制剂，并为AD的治疗提供新的治疗选择。本综述重点介绍了与AD中NCT受损以及tau与FG-Nups之间相互作用相关的最新发现。
