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Related Experiment Video

Updated: May 21, 2026

The Microscopy-Based Assay to Study and Analyze the Recycling Endosomes using SNARE Trafficking

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Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing.

Yonghao Zhao¹, Yunshu Wang, Jiaye Yang

¹Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, College of Medicine, Xiamen University, Xiamen, Fujian 361005, People's Republic of China.

Molecular Neurodegeneration

|June 20, 2012

Summary

Sorting nexin 12 (SNX12) regulates β-site APP cleaving enzyme 1 (BACE1) endocytosis, impacting amyloid-beta (Aβ) production in Alzheimer's disease (AD). Reduced SNX12 in AD brains suggests a role in pathology, offering a new therapeutic target.

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In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

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Published on: July 25, 2019

Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Alzheimer's disease (AD) is linked to β-amyloid (Aβ) production initiated by β-site APP cleaving enzyme 1 (BACE1).
Intracellular trafficking of BACE1 is implicated in Aβ generation and AD pathogenesis.
Sorting nexin 12 (SNX12) is a protein involved in regulating intracellular trafficking.

Purpose of the Study:

To investigate the role of SNX12 in the trafficking of BACE1.
To determine if SNX12 affects BACE1-mediated processing of amyloid precursor protein (APP) and Aβ generation.
To examine SNX12 levels in the brains of Alzheimer's disease patients.

Main Methods:

Investigated SNX12 expression and localization in brain tissues.
Utilized overexpression and downregulation of SNX12 in cellular models.
Assessed levels of APP, BACE1, Aβ, and related fragments.
Measured BACE1 and γ-secretase activities.
Performed co-immunoprecipitation to study SNX12-BACE1 interaction.
Analyzed SNX12 protein levels in human AD brains.

Main Results:

SNX12 is expressed in brain and localized to early endosomes.
SNX12 modulates Aβ, soluble APPβ, and CTFβ levels without affecting secretase activities.
SNX12 interacts with BACE1, regulating its endocytosis and cell surface levels.
SNX12 protein levels are significantly decreased in AD brains compared to controls.

Conclusions:

SNX12 regulates BACE1 endocytosis via interaction, influencing APP β-processing and Aβ production.
Reduced SNX12 levels in AD brains may contribute to disease pathology.
Targeting SNX12 to modulate BACE1 activity presents a potential therapeutic strategy for AD.