The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
p53Ψ is a transcriptionally inactive p53 isoform able to reprogram cells toward a metastatic-like state
Abstract
Significance: p53 is one of the most intensively studied tumor-suppressor genes. We identified a naturally occurring p53 isoform, generated by an alternative-splicing event, that, although lacking transcriptional activity and canonical tumor suppressor functions, is able to reprogram cells toward the acquisition of metastatic features via a cyclophilin D interaction in the mitochondria matrix. Interestingly, this isoform is expressed on tissue injury and in tumors characterized by increased metastatic spread. In some of these tumors, p53-like isoforms are generated by intron 6 mutations. This suggests a possible physiological origin of certain p53 mutations and indicates that mutations resulting in the generation of truncated p53Ψ-like proteins do more than create a 53-null state.
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“p53Ψ cannot bind to DNA or transcriptionally activate p53 target genes.”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [565]
In the citing paper
“Fourteen isoforms of p53 have been identified: p53, p53β, p53γ, Δ40p53, Δ40p53β, Δ40p53γ, Δ133p53, Δ133p53β, Δ133p53γ, Δ160p53, Δ160p53β, Δ160p53γ, Δp53, and p53ψ.563–568”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [565]
In the citing paper
“However, it induces the expression of epithelial-mesenchymal transition markers and enhances the viability and invasiveness of cancer cells.565”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [565]
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Citations
Cites
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
p53 Regulates Mitochondrial Respiration
Matoba, S., Kang, J.-G., Patino, W. D., Wragg, A., Boehm, M., Gavrilova, O., Hurley, P. J., Bunz, F., & Hwang, P. M. (2006) · Science · doi:10.1126/science.1126863 · Cited by 1,650
p53 isoforms can regulate p53 transcriptional activity
Bourdon, J.-C., Fernandes, K., Murray-Zmijewski, F., Liu, G., Diot, A., Xirodimas, D. P., Saville, M. K., & Lane, D. P. (2005) · Genes & Development · doi:10.1101/gad.1339905 · Cited by 810
Selective fluorescent imaging of superoxide in vivo using ethidium-based probes
Robinson, K. M., Janes, M. S., Pehar, M., Monette, J. S., Ross, M. F., Hagen, T. M., Murphy, M. P., & Beckman, J. S. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0601945103 · Cited by 777
p53 Opens the Mitochondrial Permeability Transition Pore to Trigger Necrosis
Vaseva, A. V., Marchenko, N. D., Ji, K., Tsirka, S. E., Holzmann, S., & Moll, U. M. (2012) · Cell · doi:10.1016/j.cell.2012.05.014 · Cited by 740
Self-citationMonoubiquitylation promotes mitochondrial p53 translocation
Marchenko, N. D., Wolff, S., Erster, S., Becker, K., & Moll, U. M. (2007) · The EMBO Journal · doi:10.1038/sj.emboj.7601560 · Cited by 286
Self-citationRedox regulation of cell migration and adhesion
Hurd, T. R., DeGennaro, M., & Lehmann, R. (2012) · Trends in Cell Biology · doi:10.1016/j.tcb.2011.11.002 · Cited by 263
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Cited by
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Metadata
- Authors
- Senturk, S., Yao, Z., Camiolo, M., Stiles, B., Rathod, T., Walsh, A. M., Nemajerova, A., Lazzara, M. J., Altorki, N. K., Krainer, A., Moll, U. M., Lowe, S. W., Cartegni, L., & Sordella, R.
- Affiliations
- Cold Spring Harbor Laboratory Cancer Center, Cold Spring Harbor, NY 11724;
- Department of Cardiothoracic Surgery, Weill Cornell Medical Center, New York, NY 10065;
- Memorial Sloan-Kettering Cancer Center, New York, NY 10065;
- Bioengineering Department, University of Pennsylvania, Philadelphia, PA 19104; and
- Department of Pathology, Stony Brook University, Stony Brook, NY 11794
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2014-07-29
- Volume
- 111
- Issue
- 32
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 95
- References
- 7
- Language
- en
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- Senturk, S., Yao, Z., Camiolo, M., Stiles, B., Rathod, T., Walsh, A. M., Nemajerova, A., Lazzara, M. J., Altorki, N. K., Krainer, A., Moll, U. M., Lowe, S. W., Cartegni, L., & Sordella, R. (2014). p53Ψ is a transcriptionally inactive p53 isoform able to reprogram cells toward a metastatic-like state. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1321640111
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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