Home
Resources
Publications
Cleavage of Potassium Channel Kv2.1 by BACE2 Reduces Neuronal Apoptosis

Cleavage of Potassium Channel Kv2.1 by BACE2 Reduces Neuronal Apoptosis

Fuchen Liu, Yun Zhang, Zonglai Liang, Qianwen Sun, Heng Liu, Juan Zhao, Jingwen Xu, Jinfan Zheng, Yan Yun, Xiao Yu, Weihong Song, Xiulian Sun

Mol Psychiatry. 2018 Jul;23(7):1542-1554.

PMID: 29703946

Abstract:

Potassium channel Kv2.1 regulates potassium current in cortical neurons and potassium efflux is necessary for cell apoptosis. As a major component of delayed rectifier current potassium channels, Kv2.1 forms clusters in the membrane of hippocampal neurons. BACE2 is an aspartyl protease to cleave APP to prevent the generation of Aβ, a central component of neuritic plaques in Alzheimer's brain. We now identified Kv2.1 as a novel substrate of BACE2. We found that BACE2 cleaved Kv2.1 at Thr376, Ala717, and Ser769 sites and disrupted Kv2.1 clustering on cell membrane, resulting in decreased Ik of Kv2.1 and a hyperpolarizing shift in primary neurons. Furthermore, we discovered that the BACE2-cleaved Kv2.1 forms, Kv2.1-1-375, Kv2.1-1-716, and Kv2.1-1-768, depressed the delayed rectifier Ik surge and reduced neuronal apoptosis. Our study suggests that BACE2 plays a neuroprotective role by cleavage of Kv2.1 to prevent the outward potassium currents, a potential new target for Alzheimer's treatment.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
LS7931506	Potassium 1,3-dimethoxy-6-benzyloxymethyltrifluoroborate			Price

As a specialist in analytical chemical Products, Alfa Chemistry offers consumers a wealth of raw materials and a full range of technologies and services.

QUICK LINKS

HEADQUARTERS

Tel:

Fax:

Email: