ArticleThe Journal of biological chemistry2009
BRI3 inhibits amyloid precursor protein processing in a mechanistically distinct manner from its homologue dementia gene BRI2.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The Emerging Roles of E3 Ligases and DUBs in Neurodegenerative Diseases.Molecular neurobiology · 2023Pooled it
- The emerging roles of ITM2A: At the molecular crossroads of development and pathogenesis.iScience · 2026Review
- Comprehensive High-Depth Proteomic Analysis of Plasma Extracellular Vesicles Containing Preparations in Rett Syndrome.Biomedicines · 2024Article
- Exploratory Mass Spectrometry of Cerebrospinal Fluid from Persons with Autopsy-Confirmed LATE-NC.Journal of molecular neuroscience : MN · 2024Article
- Proteomic changes in the human cerebrovasculature in Alzheimer's disease and related tauopathies linked to peripheral biomarkers in plasma and cerebrospinal fluid.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Proteomic Changes in the Human Cerebrovasculature in Alzheimer's Disease and Related Tauopathies Linked to Peripheral Biomarkers in Plasma and Cerebrospinal Fluid.medRxiv : the preprint server for health sciences · 2024Article
- Updates on Aβ Processing by Hsp90, BRICHOS, and Newly Reported Distinctive Chaperones.Biomolecules · 2023Review
- The brain on time: links between development and neurodegeneration.Development (Cambridge, England) · 2023Article
- Gene-educational attainment interactions in a multi-population genome-wide meta-analysis identify novel lipid loci.Frontiers in genetics · 2023Article
- Finding New Ways How to Control BACE1.The Journal of membrane biology · 2022Article
- Affinity Proteomics Identifies Interaction Partners and Defines Novel Insights into the Function of the Adhesion GPCR VLGR1/ADGRV1.Molecules (Basel, Switzerland) · 2022Article
- Immune infiltration landscape and immune-marker molecular typing of pulmonary fibrosis with pulmonary hypertension.BMC pulmonary medicine · 2021Article
- Recombinant Bri3 BRICHOS domain is a molecular chaperone with effect against amyloid formation and non-fibrillar protein aggregation.Scientific reports · 2020Article
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Association between miRNAs expression and cognitive performances of Pediatric Multiple Sclerosis patients: A pilot study.Brain and behavior · 2019Article
- Mining the Plasma Cell Transcriptome for Novel Cell Surface Proteins.International journal of molecular sciences · 2018Article
- The Bri2 and Bri3 BRICHOS Domains Interact Differently with AβJournal of Alzheimer's disease reports · 2018Article
- Clptm1 Limits Forward Trafficking of GABANeuron · 2018Article
- Not just amyloid: physiological functions of the amyloid precursor protein family.Nature reviews. Neuroscience · 2017Review
- A Greek Tragedy: The Growing Complexity of Alzheimer Amyloid Precursor Protein Proteolysis.The Journal of biological chemistry · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of beta amyloid (Abeta) peptides. Abeta is cleaved off from amyloid precursor protein (APP) with consecutive proteolytic processing: beta-secretase, followed by gamma-secretase. Here, we show that BRI3, a member of the BRI gene family that includes the familial British and Danish dementia gene BRI2, interacts with APP and serves as an endogenous negative regulator of Abeta production. BRI3 colocalizes with APP along neuritis in differentiated N2a cells; endogenous BRI3-APP complexes are readily detectable in mouse brain extract; reducing endogenous BRI3 levels by RNA interference results in increased Abeta secretion. BRI3 resembles BRI2, because BRI3 overexpression reduces both alpha- and beta-APP cleavage. We propose that BRI3 inhibits the various processing of APP by blocking the access of alpha- and beta-secretases to APP. However, unlike BRI2, the binding of BRI3 to the beta-secretase cleaved APP C-terminal fragment is negligible and BRI3 does not cause the massive accumulation of this APP fragment, suggesting that, unlike BRI2, BRI3 is a poor gamma-cleavage inhibitor. Competitive inhibition of APP processing by BRI3 may provide a new approach to AD therapy and prevention.
Indexed as
Identifiers
What OpenQuestion holds
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.