The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
BIN1 localization is distinct from Tau tangles in Alzheimer’s disease
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Oligodendrocytes, which are enriched in white matter, mainly express BIN1 isoform 9.
“These investigators reported that oligodendrocytes, which are enriched in white matter, mainly express BIN1 isoform 9 [42]”
From BIN1 protein isoforms are differentially expressed in astrocytes, neurons, and microglia: neuronal and astrocyte BIN1 are implicated in tau pathology (2020) · cites this paper as [42]
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Zhang, Y., Chen, K., Sloan, S. A., Bennett, M. L., Scholze, A. R., O'Keeffe, S., Phatnani, H. P., Guarnieri, P., Caneda, C., Ruderisch, N., et al. (2014) · The Journal of Neuroscience · doi:10.1523/jneurosci.1860-14.2014 · Cited by 4,875
Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database
Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., & Tanzi, R. E. (2007) · Nature Genetics · doi:10.1038/ng1934 · Cited by 1,857
De Rossi, P., Buggia-Prévot, V., Clayton, B. L. L., Vasquez, J. B., van Sanford, C., Andrew, R. J., Lesnick, R., Botté, A., Deyts, C., Salem, S., et al. (2016) · Molecular Neurodegeneration · doi:10.1186/s13024-016-0124-1 · Cited by 151 · cited 7×
“Thus, additional studies are needed to fully understand the significance of the positive correlation between Tau pathology and the levels of the ubiquitous BIN1 isoform 9 [9], which in the brain appears to be mainly expressed by oligodendrocytes [4] and elucidates how BIN1 mechanistically participates as a risk factor…”
InfluentialSelf-citationSottejeau, Y., Bretteville, A., Cantrelle, F.-X., Malmanche, N., Demiaute, F., Mendes, T., Delay, C., Alves Dos Alves, H., Flaig, A., Davies, P., et al. (2015) · Acta Neuropathologica Communications · doi:10.1186/s40478-015-0237-8 · Cited by 98 · cited 3×
“BIN1 can directly bind to Tau, and the altered expression of Drosophila Amph (the fly BIN1 homolog) significantly modifies the human Tau-induced rough eye phenotype, leading to the suggestion that BIN1 mediates LOAD risk by modulating Tau pathology [6] [7] [8].”
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., Fukuyama, T., Tsuji, S., et al. (2016) · Human Molecular Genetics · doi:10.1093/hmg/ddw146 · Cited by 95 · cited 2×
“Our findings that BIN1 protein is not detected in ramified microglia, reactive microglia, and macrophages are notable because BIN1 mRNA expression in microglia and macrophages acutely isolated from mouse and human brain are reported in RNA-seq transcriptome databases [11] [12].”
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Research works printed but not linked: 8
- Alzheimer’s Disease Risk Genes and Mechanisms of Disease Pathogenesis, 10.1016/j.biopsych.2014.05.006 · DOI · Paper page
- Amphiphysin 2 (BIN1) in physiology and diseases, 10.1007/s00109-014-1138-1 · DOI · Paper page
- Subcellular Changes in Bridging Integrator 1 Protein Expression in the Cerebral Cortex During the Progression of Alzheimer Disease Pathology, 10.1093/jnen/nlw056 · DOI · Paper page
- Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology, 10.1038/mp.2013.1 · DOI · Paper page
- Intracellular Clusterin Interacts with Brain Isoforms of the Bridging Integrator 1 and with the Microtubule-Associated Protein Tau in Alzheimer's Disease, 10.1371/journal.pone.0103187 · DOI · Paper page
- Loss of Bin1 Promotes the Propagation of Tau Pathology, 10.1016/j.celrep.2016.09.063 · DOI · Paper page
- Purification and Characterization of Progenitor and Mature Human Astrocytes Reveals Transcriptional and Functional Differences with Mouse, 10.1016/j.neuron.2015.11.013 · DOI · Paper page
- Presynaptic dystrophic neurites surrounding amyloid plaques are sites of microtubule disruption, BACE1 elevation, and increased Aβ generation in Alzheimer’s disease, 10.1007/s00401-016-1558-9 · DOI · Paper page
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The BIN1 rs744373 SNP is associated with increased tau-PET levels and impaired memory
Franzmeier, N., Rubinski, A., Neitzel, J., Ewers, M., (ADNI), T. A. D. N. I., Weiner, M. W., Aisen, P., Petersen, R., Jack, C. R., Jagust, W., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09564-5 · Cited by 109
Self-citationTaga, M., Petyuk, V. A., White, C., Marsh, G., Ma, Y., Klein, H.-U., Connor, S. M., Kroshilina, A., Yung, C. J., Khairallah, A., et al. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00387-3 · Cited by 81
Metadata
- Authors
- De Rossi, P., Buggia-Prevot, V., Andrew, R., Krause, S., Woo, E., Nelson, P., Pytel, P., & Thinakaran, G.
- Venue
- Matters
- Publisher
- Sciencematters
- Published
- 2017-01-12
- ISSN
- 2297-8240
- PMC
- PMC5823513
- Cited by
- 19
- References
- 5
- Language
- en
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