The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Mutant p53 partners in crime
Open accessAbstract
Mutant p53 proteins impart changes in cellular behavior and function through interactions with proteins that alter gene expression. The milieu of intracellular proteins available to interact with mutant p53 is context specific and changes with disease, cell type, and environmental conditions. Varying conformations of mutant p53 largely dictate protein-protein interactions as different point mutations within protein-coding regions greatly alter the extent and array of gain-of-function (GOF) activities. Given such variables, how can knowledge regarding p53 missense mutations be translated into predicting or altering biologic activity for therapy? How may knowledge regarding mutant p53 functions within certain disease contexts be harnessed to blunt or ablate mutant p53 GOF for therapy? In this article, we review known proteins that interact with mutant p53 and result in the activation of genes that contribute to p53 GOF with particular emphasis on context dependency and an evolving appreciation of GOF mechanisms.
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“mutant p53 GOF activities, including the facilitation of cell proliferation, invasion, survival, cancer-promoting metabolism, protumorigenic inflammation, and drug resistance, have been observed in a series of experimental models, and multiple GOF mechanisms have been proposed.140,493,494”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [140]
In the citing paper
“Mutant p53 may not only lose the tumor suppressor function of wild-type p53 but also acquire new tumor-promoting functions, such as promoting tumor invasion, metastasis, and drug resistance.”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [140]
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Cites
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308
Mutant p53 Drives Pancreatic Cancer Metastasis through Cell-Autonomous PDGF Receptor β Signaling
Weissmueller, S., Manchado, E., Saborowski, M., Morris, J. P., Wagenblast, E., Davis, C. A., Moon, S.-H., Pfister, N. T., Tschaharganeh, D. F., Kitzing, T., et al. (2014) · Cell · doi:10.1016/j.cell.2014.01.066 · Cited by 466 · cited 1×
“In pancreatic cancer KPC cells, mutant p53R175H and R273H may bind to p73 and prevent its binding to NF-Y on the PDGFRβ promoter, allowing PDGFRβ expression.(18) The TF NF-Y binds the p53 missense mutants R175H and 273C, transactivating pro-cell cycle genes.”
BackgroundDi Agostino, S., Strano, S., Emiliozzi, V., Zerbini, V., Mottolese, M., Sacchi, A., Blandino, G., & Piaggio, G. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.013 · Cited by 418
Modulation of the Vitamin D3 Response by Cancer-Associated Mutant p53
Stambolsky, P., Tabach, Y., Fontemaggi, G., Weisz, L., Maor-Aloni, R., Sigfried, Z., Shiff, I., Kogan, I., Shay, M., Kalo, E., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.11.025 · Cited by 245
Walerych, D., Lisek, K., Sommaggio, R., Piazza, S., Ciani, Y., Dalla, E., Rajkowska, K., Gaweda-Walerych, K., Ingallina, E., Tonelli, C., et al. (2016) · Nature Cell Biology · doi:10.1038/ncb3380 · Cited by 239
Mutant p53 promotes tumor progression and metastasis by the endoplasmic reticulum UDPase ENTPD5
Vogiatzi, F., Brandt, D. T., Schneikert, J., Fuchs, J., Grikscheit, K., Wanzel, M., Pavlakis, E., Charles, J. P., Timofeev, O., Nist, A., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1612711114 · Cited by 99
Huang, X., Zhang, Y., Tang, Y., Butler, N., Kim, J., Guessous, F., Schiff, D., Mandell, J., & Abounader, R. (2013) · Neoplasia · doi:10.1593/neo.13376 · Cited by 53
Cited by
A dominant-negative effect drives selection of TP53 missense mutations in myeloid malignancies
Boettcher, S., Miller, P. G., Sharma, R., McConkey, M., Leventhal, M., Krivtsov, A. V., Giacomelli, A. O., Wong, W., Kim, J., Chao, S., et al. (2019) · Science · doi:10.1126/science.aax3649 · Cited by 441
p53, cancer and the immune response
Blagih, J., Buck, M. D., & Vousden, K. H. (2020) · Journal of Cell Science · doi:10.1242/jcs.237453 · Cited by 333
IFN-gamma-induced PD-L1 expression in melanoma depends on p53 expression
Thiem, A., Hesbacher, S., Kneitz, H., di Primio, T., Heppt, M. V., Hermanns, H. M., Goebeler, M., Meierjohann, S., Houben, R., & Schrama, D. (2019) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-019-1403-9 · Cited by 153
Regulation of Adult Neurogenesis in Mammalian Brain
Niklison-Chirou, M. V., Agostini, M., Amelio, I., & Melino, G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21144869 · Cited by 143
Cell of origin influences pancreatic cancer subtype
Flowers, B. M., Xu, H., Mulligan, A. S., Hanson, K. J., Seoane, J. A., Vogel, H., Curtis, C., Wood, L. D., & Attardi, L. D. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0633 · Cited by 118
Metadata
- Authors
- Kim, M. P., & Lozano, G.
- Venue
- Cell Death & Differentiation
- Published
- 2017-11-03
- Volume
- 25
- Issue
- 1
- Pages
- 161-168
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2767010895
- Cited by
- 311
- References
- 7
- FWCI
- 12.39
- Type
- journal article
- Language
- en
- Open access
- hybrid
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