A missense variant in DEPDC5 resulted in abnormal morphology and increased seizure susceptibility and mortality through regulating mTOR signaling.

 0 Người đánh giá. Xếp hạng trung bình 0

Tác giả: Rui Huang, Patrick Kwan, Jie Liu, Yuanlin Ma, Fenglin Tang

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: United States : Neurobiology of disease , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 717299

 Dishevelled, Egl-10 and Pleckstrin domain-containing 5 (DEPDC5), a key inhibitor of the mammalian/mechanistic target of rapamycin (mTOR) pathway, is frequently associated with epilepsy. However, the functional consequences of most DEPDC5 variants rely on in silico predictions and have not been experimentally confirmed.This study aimed to determine the functional consequences of a DEPDC5 variant identified in patients with epilepsy across multiple generations in a Chinese family. We identified a missense heterozygous variant (c. 2055C >
  A
  p. Phe685Leu) in DEPDC5 in Chinese family affected by epilepsy across three generations. This variant has not been previously reported in the Chinese population. Primary neuron cultures transfected with the mutant plasmid exhibited altered subcellular localization. To explore the mechanisms of epilepsy linked to this variant, we created nervous system-specific conditional human DEPDC5 knock-in mouse using Cre-recombination under the Nestin promotor (hDEPDC5
Tạo bộ sưu tập với mã QR

THƯ VIỆN - TRƯỜNG ĐẠI HỌC CÔNG NGHỆ TP.HCM

ĐT: (028) 36225755 | Email: tt.thuvien@hutech.edu.vn

Copyright @2024 THƯ VIỆN HUTECH