FBXL16: a new regulator of neuroinflammation and cognition in Alzheimer's disease through the ubiquitination-dependent degradation of amyloid precursor protein.

ABSTRACT:

Background

Activating the ubiquitin-proteasome system to dismantle disease- related proteins such as tau, β-amyloid, APP, and α-synuclein is an important focus in the research of neurodegenerative proteinopathy. By analyzing the serum RNA extracted from wild-type and Alzheimer's disease (AD) transgenic mice at different ages (4, 8, and 12 months), this study revealed a new protective role of FBXL16 in AD, primarily through facilitating the degradation of disease-related proteins via the ubiquitin proteasome system.

Methods

Proteomic analysis were conducted using protein lysates from HEK293 cells overexpressing FBXL16 to identify potential interacting proteins that interact with FBXL16. Subsequent experiments demonstrated that FBXL16 promotes the proteasomal degradation of th

SUBMITTER: Qu L 

PROVIDER: S-EPMC11580471 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature