Structural Analysis of the Human BIN1 Gene
Open accessAbstract
BIN1 is a putative tumor suppressor that was identified through its interaction with the MYC oncoprotein. To begin to identify elements of BIN1 whose alteration may contribute to malignancy, we cloned and characterized the human BIN1 gene and promoter. Nineteen exons were identified in a region of >54 kilobases, six of which were alternately spliced in a cell type-specific manner. One alternately spliced exon encodes part of the MYC-binding domain, suggesting that splicing controls the MYC-binding capacity of BIN1 polypeptides. Four other alternately spliced exons encode amphiphysin-related sequences that were included in brain-specific BIN1 species, also termed amphiphysin isoforms or amphiphysin II. The 5'-flanking region of BIN1 is GC-rich and lacks a TATA box but directs transcriptional initiation from a single site. A approximately 0. 9-kilobase fragment from this region was sufficient for basal transcription and transactivation by MyoD, which may account for the high levels of BIN1 observed in skeletal muscle. This study lays the foundation for genetic and epigenetic investigations into the role of BIN1 in normal and neoplastic cell regulation.
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BIN1 undergoes complex alternative splicing to generate multiple isoforms with diverse functions in multiple cellular processes including endocytosis and membrane remodeling.
“BIN1 undergoes complex alternative splicing to generate multiple isoforms with diverse functions in multiple cellular processes including endocytosis and membrane remodeling.”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [12]
The BIN1 gene-structure section reports multiple alternatively spliced BIN1 RNA species, and the Discussion suggests that some splice forms may differ in MYC interaction or amphiphysin-like functions (page unavailable). Our copy does not establish that the isoforms function in endocytosis or membrane remodeling, so those specific processes are not supported by this source. (LLM, conf=0.88)
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Butler, M. H., David, C., Ochoa, G.-C., Freyberg, Z., Daniell, L., Grabs, D., Cremona, O., & Camilli, P. D. (1997) · The Journal of Cell Biology · doi:10.1083/jcb.137.6.1355 · Cited by 256 · see citing works
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- Wechsler-Reya, R., Elliott, K., and Prendergast, G. C. (1998) Mol. Cell. Biol., in press
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Nicot, A.-S., Toussaint, A., Tosch, V., Kretz, C., Wallgren-Pettersson, C., Iwarsson, E., Kingston, H., Garnier, J.-M., Biancalana, V., Oldfors, A., et al. (2007) · Nature Genetics · doi:10.1038/ng2086 · Cited by 434 · see citing works
Loss of Bin1 Promotes the Propagation of Tau Pathology
Calafate, S., Flavin, W., Verstreken, P., & Moechars, D. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.09.063 · Cited by 265 · see citing works
Genetic Variation and Neuroimaging Measures in Alzheimer Disease
Biffi, A. (2010) · Archives of Neurology · doi:10.1001/archneurol.2010.108 · Cited by 222 · see citing works
Tau Protein Interaction Partners and Their Roles in Alzheimer’s Disease and Other Tauopathies
Sinsky, J., Pichlerova, K., & Hanes, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22179207 · Cited by 220 · see citing works
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 · see citing works
Functional coordination of alternative splicing in the mammalian central nervous system
Fagnani, M., Barash, Y., Ip, J. Y., Misquitta, C., Pan, Q., Saltzman, A. L., Shai, O., Lee, L., Rozenhek, A., Mohammad, N., et al. (2007) · Genome Biology · doi:10.1186/gb-2007-8-6-r108 · Cited by 120 · see citing works
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 · see citing works
Self-citation
- Authors
- Wechsler-Reya, R., Sakamuro, D., Zhang, J., Duhadaway, J., & Prendergast, G. C.
- Affiliations
- The Wistar Institute (US)
- Corresponding author
- Prendergast, George C.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1997-12
- Volume
- 272
- Issue
- 50
- Pages
- 31453-31458
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2029383449
- Cited by
- 142
- References
- 1
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 2 · 2023: 5 · 2022: 3 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 2 · 2016: 8 · 2015: 5 · 2014: 6 · 2013: 5 · 2012: 5
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- Medical Research Council Canada
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- tumor suppressor, Myc oncoprotein, alternative splicing, exon structure, promoter, GC-rich promoter, TATA box, transcription initiation, skeletal muscle, gene structure
- MeSH terms
- Animals, Base Sequence, Carrier Proteins, Cell Line, Chromosome Mapping, DNA, Exons, Gene Expression Regulation, Humans, Introns, Molecular Sequence Data, Nerve Tissue Proteins, Nuclear Proteins, Promoter Regions, Genetic, RNA, RNA Caps, Transcription, Genetic, Genes, Tumor Suppressor, Alternative Splicing, MyoD Protein, Tumor Suppressor Proteins, Adaptor Proteins, Signal Transducing, Mice
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