The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Mechanism for elimination of a tumor suppressor: Aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma
Open accessAbstract
Loss of tumor suppressors that restrain important oncoproteins such as c-Myc may contribute to malignant progression. Bin1 is an adapter protein with features of a tumor suppressor that was identified through its interaction with and inhibition of the oncogenic properties of c-Myc. In this study, we analyzed the patterns of Bin1 expression in normal melanocytes and melanoma cells at different stages of tumor progression. Evidence is provided that Bin1 function is abrogated in melanoma cells by a mechanism based on aberrant splicing of a tissue-specific exon. Specifically, most melanoma cells inappropriately expressed exon 12A, which is spliced alternately into Bin1 isoforms found in brain but not into isoforms found in melanocytes and many other nonneuronal cells. Exon 12A sequences abolished the ability of Bin1 to inhibit malignant transformation by c-Myc or adenovirus E1A. Similarly, these sequences abolished the ability of Bin1 to induce programmed cell death in melanoma cells that endogenously expressed exon 12A. Our findings suggest that aberrant splicing of Bin1 may contribute to melanoma progression, and they define a mechanism by which the activity of a tumor suppressor can be eliminated in cells.
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Cites
BIN1 is a novel MYC–interacting protein with features of a tumour suppressor
Sakamuro, D., Elliott, K. J., Wechsler-Reya, R., & Prendergast, G. C. (1996) · Nature Genetics · doi:10.1038/ng0996-69 · Cited by 387
Self-citationButler, 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
Structural Analysis of the Human BIN1 Gene
Wechsler-Reya, R., Sakamuro, D., Zhang, J., Duhadaway, J., & Prendergast, G. C. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.50.31453 · Cited by 142
Self-citationTsutsui, K., Maeda, Y., Tsutsui, K., Seki, S., & Tokunaga, A. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6927 · Cited by 68
Cited by
Muller, A. J., DuHadaway, J. B., Donover, P. S., Sutanto-Ward, E., & Prendergast, G. C. (2005) · Nature Medicine · doi:10.1038/nm1196 · Cited by 1,064
The gene encoding the splicing factor SF2/ASF is a proto-oncogene
Karni, R., de Stanchina, E., Lowe, S. W., Sinha, R., Mu, D., & Krainer, A. R. (2007) · Nature Structural & Molecular Biology · doi:10.1038/nsmb1209 · Cited by 934
Anczuków, O., Rosenberg, A. Z., Akerman, M., Das, S., Zhan, L., Karni, R., Muthuswamy, S. K., & Krainer, A. R. (2012) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2207 · Cited by 447
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
Ward, A. J., & Cooper, T. A. (2010) · The Journal of Pathology · doi:10.1002/path.2649 · Cited by 414
Metadata
- Authors
- Ge, K., DuHadaway, J., Du, W., Herlyn, M., Rodeck, U., & Prendergast, G. C.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-08-17
- Volume
- 96
- Issue
- 17
- Pages
- 9689-9694
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1989147967
- Cited by
- 195
- References
- 4
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Mechanism for elimination of a tumor suppressor: Aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma. https://app.cochat.ai/papers/10.1073/pnas.96.17.9689
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- Ge, K., DuHadaway, J., Du, W., Herlyn, M., Rodeck, U., & Prendergast, G. C. (1999). Mechanism for elimination of a tumor suppressor: Aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.17.9689
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
