BIN1 is a novel MYC–interacting protein with features of a tumour suppressor
Abstract
BIN1 is a novel protein that interacts with the functionally critical Myc box regions at the N terminus of the MYC oncoprotein. BIN1 is structurally related to amphiphysin, a breast cancer-associated autoimmune antigen, and RVS167, a negative regulator of the yeast cell cycle, suggesting roles in malignancy and cell cycle control. Consistent with this likelihood, BIN1 inhibited malignant cell transformation by MYC. Although BIN1 is expressed in many normal cells, its levels were greatly reduced or undetectable in 14/27 carcinoma cell lines and 3/6 primary breast tumours. Deficits were functionally significant because ectopic expression of BIN1 inhibited the growth of tumour cells lacking endogenous message. We conclude that BIN1 is an MYC-interacting protein with features of a tumour suppressor.
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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 [2]
BIN1 is broadly expressed in several tissues, with the highest expression in skeletal muscle.
“Unlike its close paralog Amphiphysin 1, BIN1 is broadly expressed in several tissues, with the highest expression in skeletal muscle [2, 4, 6, 11].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [2]
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Self-citation
- Authors
- Sakamuro, D., Elliott, K. J., Wechsler-Reya, R., & Prendergast, G. C.
- Affiliations
- The Wistar Institute (US)
- Corresponding author
- Prendergast, George C.
- Venue
- Nature Genetics
- Published
- 1996-09
- Volume
- 14
- Issue
- 1
- Pages
- 69-77
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W1972402664
- Cited by
- 387
- References
- 2
- Citations by year
- 2026: 2 · 2025: 15 · 2024: 8 · 2023: 10 · 2022: 19 · 2021: 11 · 2020: 15 · 2019: 12 · 2018: 8 · 2017: 12 · 2016: 10 · 2015: 10 · 2014: 19 · 2013: 10 · 2012: 11
- FWCI
- 7.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA09171, CA66179, CA-10815, T32CA009171, P30CA010815)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- BIN1, c-Myc, protein-protein interaction, tumour suppressor, amphiphysin, cell cycle regulation, cell transformation, breast cancer, carcinoma cell lines, ectopic expression
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Carrier Proteins, Cell Division, Cell Line, Cell Transformation, Neoplastic, Fungal Proteins, HeLa Cells, Humans, Microfilament Proteins, Molecular Sequence Data, Nerve Tissue Proteins, Nuclear Proteins, Transformation, Genetic, Tumor Cells, Cultured, Genes, Tumor Suppressor, Genes, myc, DNA Primers, Tumor Suppressor Proteins, Saccharomyces cerevisiae Proteins, Adaptor Proteins, Signal Transducing
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