ArticleCell cycle (Georgetown, Tex.)2016
Lysines in the tetramerization domain of p53 selectively modulate G1 arrest.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Functional Investigations of p53 Acetylation Enabled by Heterobifunctional Molecules.ACS chemical biology · 2024Article
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- GINS4 suppresses ferroptosis by antagonizing p53 acetylation with Snail.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- p53 Frameshift Mutations Couple Loss-of-Function with Unique Neomorphic Activities.Molecular cancer research : MCR · 2021Article
- Review
- Article
- UFMylation maintains tumour suppressor p53 stability by antagonizing its ubiquitination.Nature cell biology · 2020Article
- p53 tetramerization: at the center of the dominant-negative effect of mutant p53.Genes & development · 2020Review
- The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases.International journal of molecular sciences · 2019Review
- Aberrant expression of ETS1 and ETS2 proteins in cancer.Cancer reports and reviews · 2018Article
- p53 oligomerization status modulates cell fate decisions between growth, arrest and apoptosis.Cell cycle (Georgetown, Tex.) · 2016Article
- A new function for p53 tetramerization domain in cell fate control.Cell cycle (Georgetown, Tex.) · 2016Article
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10 authors.
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Abstract
Functional in a tetrameric state, the protein product of the p53 tumor suppressor gene confers its tumor-suppressive activity by transactivating genes which promote cell-cycle arrest, senescence, or programmed cell death. How p53 distinguishes between these divergent outcomes is still a matter of considerable interest. Here we discuss the impact of 2 mutations in the tetramerization domain that confer unique properties onto p53. By changing lysines 351 and 357 to arginine, thereby blocking all post-translational modifications of these residues, DNA binding and transcriptional regulation by p53 remain virtually unchanged. On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death. Surprisingly, when 2KQ-p53 is expressed at high levels in H1299 cells, it can bind to and transactivate numerous p53 target genes including p21, but not others such as miR-34a and cyclin G1 to the same extent as wild-type p53. Our findings show that strong induction of p21 is not sufficient to block H1299 cells in G1, and imply that modification of one or both of the lysines within the tetramerization domain may serve as a mechanism to shunt p53 from inducing cell cycle arrest.
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