ArticleThe Journal of biological chemistry2011
The cancer-associated K351N mutation affects the ubiquitination and the translocation to mitochondria of p53 protein.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Defects of mitochondria-lysosomes communication induce secretion of mitochondria-derived vesicles and drive chemoresistance in ovarian cancer cells.Cell communication and signaling : CCS · 2024Article
- Li-Fraumeni Syndrome-Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death.Cancer discovery · 2023Article
- E3 Ubiquitin Ligase in Anticancer Drugdsla Resistance: Recent Advances and Future Potential.Frontiers in pharmacology · 2021Review
- p53 tetramerization: at the center of the dominant-negative effect of mutant p53.Genes & development · 2020Review
- Inhibition of coiled coil domain containing protein 69 enhances platinum-induced apoptosis in ovarian cancer cells.Oncotarget · 2017Article
- Lysines in the tetramerization domain of p53 selectively modulate G1 arrest.Cell cycle (Georgetown, Tex.) · 2016Article
- External and internal triggers of cell death in yeast.Cellular and molecular life sciences : CMLS · 2016Review
- Drp1 stabilizes p53 on the mitochondria to trigger necrosis under oxidative stress conditions in vitro and in vivo.The Biochemical journal · 2014Article
- Tumor suppressor p53 and estrogen receptors in nuclear-mitochondrial communication.Mitochondrion · 2014Review
- p53 SUMOylation promotes its nuclear export by facilitating its release from the nuclear export receptor CRM1.Molecular biology of the cell · 2013Article
- Article
- Anticancer and antimicrobial activities of some antioxidant-rich cameroonian medicinal plants.PloS one · 2013Article
- It Takes 15 to Tango: Making Sense of the Many Ubiquitin Ligases of p53.Genes & cancer · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Stress-induced monoubiquitination of p53 is a crucial event for the nuclear-cytoplasm-mitochondria trafficking and transcription-independent pro-apoptotic functions of p53. Although an intact ubiquitination pathway and a functional nuclear export sequence are required for p53 nuclear export, the role of specific residues within this region in regulating both processes remains largely unknown. Here we characterize the mechanisms accounting for the nuclear accumulation of a new point mutation (Lys-351 to Asn) in the nuclear export sequence of p53 identified in a cisplatin-resistant ovarian carcinoma cell line (A2780 CIS). We found that K351N substitution abrogates the monoubiquitination of p53 induced by both Mdm2 and MSL2 E3-ligases. As a consequence, cells expressing p53 K351N mutant showed defects in cisplatin-induced translocation of p53 to mitochondria, Bax oligomerization, and mitochondrial membrane depolarization. These data identify K351N as a critical mutation of p53 that contributes to the development and maintenance of resistance to cisplatin.
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