ArticleCurrent Alzheimer research2013
BRI2 interacts with BACE1 and regulates its cellular levels by promoting its degradation and reducing its mRNA levels.
Article in Current Alzheimer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Assessing Co-Localization of ITM2B With Alzheimer's Disease and Limbic-Predominant Age-Related TDP-43 Encephalopathy Neuropathologic Changes.Neuropathology : official journal of the Japanese Society of Neuropathology · 2025Article
- The role of the integral type II transmembrane protein BRI2 in health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Identification and characterization of the BRI2 interactome in the brain.Scientific reports · 2018Article
- The Bri2 and Bri3 BRICHOS Domains Interact Differently with AβJournal of Alzheimer's disease reports · 2018Article
- Transthyretin and BRICHOS: The Paradox of Amyloidogenic Proteins with Anti-Amyloidogenic Activity for Aβ in the Central Nervous System.Frontiers in neuroscience · 2017Review
- BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells.Cellular and molecular life sciences : CMLS · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BRI2, a protein mutated in Familial British and Familial Danish Dementias, interacts with Amyloid Precursor Protein (APP) and reduces the levels of secreted APPβ (sAPPβ), which derives from APP cleavage by β-secretase (BACE1). Exploring the mechanisms of this effect, we obtained data that BRI2 decreases the cellular levels of BACE1 thus reducing the β-cleavage of APP. Deletion of N-terminal cytoplasmic or C-terminal extracellular sequences of BRI2 neither affected its interaction with BACE1 or APP (Fotinopoulou et al., 2005) nor the reduction in the levels of BACE1 and sAPPβ. These results suggest that BRI2 may prevent access of BACE1 to APP and the BRI2/BACE1 interaction may mediate the reduction in BACE1 levels. In support, BRI2 expression induced lysosomal but not proteasomal degradation of BACE1. In parallel, BRI2 expression was also found to reduce BACE1 mRNA levels by 50%. This study adds novel information regarding the mechanism by which BRI2 affects APP processing and BACE1 levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.