ArticleThe Journal of biological chemistry2011
BRI2 protein regulates β-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 44 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
- Exploratory Mass Spectrometry of Cerebrospinal Fluid from Persons with Autopsy-Confirmed LATE-NC.Journal of molecular neuroscience : MN · 2024Article
- Autoantibodies involved in primary and secondary adrenal insufficiency following treatment with immune checkpoint inhibitors.Immuno-oncology technology · 2023Review
- Ginsenoside ompound K reduces neuronal damage and improves neuronal synaptic dysfunction by targeting Aβ.Frontiers in pharmacology · 2023Article
- Finding New Ways How to Control BACE1.The Journal of membrane biology · 2022Article
- Genetic Inactivation of Free Fatty Acid Receptor 3 Impedes Behavioral Deficits and Pathological Hallmarks in the APPInternational journal of molecular sciences · 2022Article
- The role of the integral type II transmembrane protein BRI2 in health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- Biological Bases of Immune-Related Adverse Events and Potential Crosslinks With Immunogenic Effects of Radiation.Frontiers in pharmacology · 2021Review
- The biomarkers related to immune related adverse events caused by immune checkpoint inhibitors.Journal of experimental & clinical cancer research : CR · 2020Review
- Autoimmune antibodies correlate with immune checkpoint therapy-induced toxicities.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Powering Amyloid Beta Degrading Enzymes: A Possible Therapy for Alzheimer's Disease.Neurochemical research · 2019Review
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Insulin-degrading enzyme is not secreted from cultured cells.Scientific reports · 2018Article
- Insulin-degrading enzyme secretion from astrocytes is mediated by an autophagy-based unconventional secretory pathway in Alzheimer disease.Autophagy · 2016Article
- BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells.Cellular and molecular life sciences : CMLS · 2015Article
- Generalised Anxiety Disorder--A Twin Study of Genetic Architecture, Genome-Wide Association and Differential Gene Expression.PloS one · 2015Article
- Organotypic vibrosections from whole brain adult Alzheimer mice (overexpressing amyloid-precursor-protein with the Swedish-Dutch-Iowa mutations) as a model to study clearance of beta-amyloid plaques.Frontiers in aging neuroscience · 2015Article
- BRI2 interacts with BACE1 and regulates its cellular levels by promoting its degradation and reducing its mRNA levels.Current Alzheimer research · 2013Article
- Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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9 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The amyloid precursor protein (APP) is one of the major proteins involved in Alzheimer disease (AD). Proteolytic cleavage of APP gives rise to amyloid-β (Aβ) peptides that aggregate and deposit extensively in the brain of AD patients. Although the increase in levels of aberrantly folded Aβ peptide is considered to be important to disease pathogenesis, the regulation of APP processing and Aβ metabolism is not fully understood. Recently, the British precursor protein (BRI2, ITM2B) has been implicated in influencing APP processing in cells and Aβ deposition in vivo. Here, we show that the wild type BRI2 protein reduces plaque load in an AD mouse model, similar to its disease-associated mutant form, ADan precursor protein (ADanPP), and analyze in more detail the mechanism of how BRI2 and ADanPP influence APP processing and Aβ metabolism. We find that overexpression of either BRI2 or ADanPP reduces extracellular Aβ by increasing levels of secreted insulin-degrading enzyme (IDE), a major Aβ-degrading protease. This effect is also observed with BRI2 lacking its C-terminal 23-amino acid peptide sequence. Our results suggest that BRI2 might act as a receptor protein that regulates IDE levels that in turn influences APP metabolism in a previously unrecognized way. Targeting the regulation of IDE may be a promising therapeutic approach to sporadic AD.
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