BIN1 regulates BACE1 intracellular trafficking and amyloid-β production
Miyagawa T, Ebinuma I, Morohashi Y, Hori Y, Young Chang M, Hattori H, Maehara T, Yokoshima S et al.. Human molecular genetics, 2016-05-14
Topic: Brain proteins, microglia and lab models
BIN1 is a genetic risk factor of late-onset Alzheimer disease (AD), which was identified in multiple genome-wide association studies. BIN1 is a member of the amphiphysin family of proteins, and contains N-terminal Bin-Amphiphysin-Rvs and C-terminal Src homology 3 domains. BIN1 is widely expressed in the mouse and human brains, and has been reported to function in the endocytosis and the endosomal sorting of membrane proteins. BACE1 is a type 1 transmembrane aspartyl protease expressed predominantly in neurons of the brain and responsible for the production of amyloid-β peptide (Aβ). Here we report that the depletion of BIN1 increases cellular BACE1 levels through impaired endosomal trafficking and reduces BACE1 lysosomal degradation, resulting in increased Aβ production. Our findings provide a mechanistic role of BIN1 in the pathogenesis of AD as a novel genetic regulator of BACE1 levels and Aβ production.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Miyagawa, T., Ebinuma, I., Morohashi, Y., Hori, Y., Young Chang, M., Hattori, H., et al. (2016). BIN1 regulates BACE1 intracellular trafficking and amyloid-β production. Human molecular genetics. https://doi.org/10.1093/hmg/ddw146
Vancouver
Miyagawa T, Ebinuma I, Morohashi Y, Hori Y, Young Chang M, Hattori H, et al. BIN1 regulates BACE1 intracellular trafficking and amyloid-β production. Human molecular genetics. 2016. doi:10.1093/hmg/ddw146. PMID: 27179792.
BibTeX
@article{miyagawa2016-27179792,
author = {Miyagawa, T. and Ebinuma, I. and Morohashi, Y. and Hori, Y. and Young Chang, M. and Hattori, H. and Maehara, T. and Yokoshima, S. and others},
title = {{BIN1 regulates BACE1 intracellular trafficking and amyloid-β production}},
journal = {Human molecular genetics},
year = {2016},
doi = {10.1093/hmg/ddw146},
pmid = {27179792},
url = {https://doi.org/10.1093/hmg/ddw146}
}
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Key findings
- Our findings provide a mechanistic role of BIN1 in the pathogenesis of AD as a novel genetic regulator of BACE1 levels and Aβ production.
Why it matters
In laboratory work, reducing BIN1 increased BACE1 levels and amyloid-beta production, suggesting BIN1 may regulate amyloid production. These are cell-based mechanistic findings and do not demonstrate a treatment for people.
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Study details
- Evidence strengthLow
How this study scored 43/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Human molecular genetics) |
| Journal's citation record | 3 / 4 | Human Molecular Genetics: journal h-index 356 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2016 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 96 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.0 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 3 / 6 | Cited 7.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Taisuke Tomita: h-index 65 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | The University of Tokyo: institution h-index 1,463 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27179792) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 43 / 100 | — |
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