ArticleMolecular and cellular biology2000
Stimulation of p53 DNA binding by c-Abl requires the p53 C terminus and tetramerization.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 73 citations in OpenAlex.
- Unveiling the role of Ndrg1 gene on the oxidative stress induction behind the anticancer potential of styrylquinazoline derivatives.Scientific reports · 2025Article
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- Computational Identification of BCR-ABL Oncogenic Signaling as a Candidate Target of Withaferin A and Withanone.Biomolecules · 2022Article
- Protein of a thousand faces: The tumor-suppressive and oncogenic responses of p53.Frontiers in molecular biosciences · 2022Review
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- Mutant p53 dictates the oncogenic activity of c-Abl in triple-negative breast cancers.Cell death & disease · 2017Article
- Stabilization of the p53-DNA Complex by the Nuclear Protein Dmp1α.Cancer investigation · 2017Article
- p53 Proteoforms and Intrinsic Disorder: An Illustration of the Protein Structure-Function Continuum Concept.International journal of molecular sciences · 2016Review
- Cellular response to alkylating agent MNNG is impaired in STAT1-deficients cells.Journal of cellular and molecular medicine · 2016Article
- The secret life of kinases: functions beyond catalysis.Cell communication and signaling : CCS · 2011Article
- Tip60-mediated acetylation activates transcription independent apoptotic activity of Abl.Molecular cancer · 2011Article
- Cancer-associated p53 tetramerization domain mutants: quantitative analysis reveals a low threshold for tumor suppressor inactivation.The Journal of biological chemistry · 2011Article
- Tumour suppressor p53 down-regulates the expression of the human hepatocyte nuclear factor 4alpha (HNF4alpha) gene.The Biochemical journal · 2006Article
- Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).Molecular and cellular biology · 2006Article
- Characterization of cells and gene-targeted mice deficient for the p53-binding kinase homeodomain-interacting protein kinase 1 (HIPK1).Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Efficient specific DNA binding by p53 requires both its central and C-terminal domains as revealed by studies with high-mobility group 1 protein.Molecular and cellular biology · 2002Article
- Article
- Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation.The EMBO journal · 2002Article
- c-Abl regulates p53 levels under normal and stress conditions by preventing its nuclear export and ubiquitination.Molecular and cellular biology · 2001Article
- The role of tetramerization in p53 function.Oncogene · 2001Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The carboxyl terminus of p53 is a target of a variety of signals for regulation of p53 DNA binding. Growth suppressor c-Abl interacts with p53 in response to DNA damage and overexpression of c-Abl leads to G(1) growth arrest in a p53-dependent manner. Here, we show that c-Abl binds directly to the carboxyl-terminal regulatory domain of p53 and that this interaction requires tetramerization of p53. Importantly, we demonstrate that c-Abl stimulates the DNA-binding activity of wild-type p53 but not of a carboxyl-terminally truncated p53 (p53Delta363C). A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding. These data suggest that the binding to the p53 carboxyl terminus is necessary for c-Abl stimulation. To investigate the mechanism for this activation, we have also shown that c-Abl stabilizes the p53-DNA complex. These results led us to hypothesize that the interaction of c-Abl with the C terminus of p53 may stabilize the p53 tetrameric conformation, resulting in a more stable p53-DNA complex. Interestingly, the stimulation of p53 DNA-binding by c-Abl does not require its tyrosine kinase activity, indicating a kinase-independent function for c-Abl. Together, these results suggest a detailed mechanism by which c-Abl activates p53 DNA-binding via the carboxyl-terminal regulatory domain and tetramerization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.