ArticleMolecular and cellular biology2001
c-Abl regulates p53 levels under normal and stress conditions by preventing its nuclear export and ubiquitination.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 95 citations in OpenAlex.
- 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
- Anti-Apoptotic Effect of Chrysophanol Isolated fromInternational journal of molecular sciences · 2023Article
- Are off-target effects of imatinib the key to improving beta-cell function in diabetes?Upsala journal of medical sciences · 2022Review
- Targeting Mouse Double Minute 2: Current Concepts in DNA Damage Repair and Therapeutic Approaches in Cancer.Frontiers in pharmacology · 2020Review
- LAMP3 plays an oncogenic role in osteosarcoma cells partially by inhibiting TP53.Cellular & molecular biology letters · 2018Article
- Mathematical model identifies effective P53 accumulation with target gene binding affinity in DNA damage response for cell fate decision.Cell cycle (Georgetown, Tex.) · 2018Article
- BTK blocks the inhibitory effects of MDM2 on p53 activity.Oncotarget · 2017Article
- Combination therapy in a xenograft model of glioblastoma: enhancement of the antitumor activity of temozolomide by an MDM2 antagonist.Journal of neurosurgery · 2017Article
- Phosphorylation of the Mdm2 oncoprotein by the c-Abl tyrosine kinase regulates p53 tumor suppression and the radiosensitivity of mice.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Intra molecular interactions in the regulation of p53 pathway.Translational cancer research · 2016Article
- Regulation of the Mdm2-p53 signaling axis in the DNA damage response and tumorigenesis.Translational cancer research · 2016Article
- c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression.Oncotarget · 2016Article
- Cellular response to alkylating agent MNNG is impaired in STAT1-deficients cells.Journal of cellular and molecular medicine · 2016Article
- The kinase ABL phosphorylates the microprocessor subunit DGCR8 to stimulate primary microRNA processing in response to DNA damage.Science signaling · 2015Article
- Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Frontiers in oncology · 2015Review
- The MDM2 gene family.Biomolecular concepts · 2014Review
- Actin polymerization negatively regulates p53 function by impairing its nuclear import in response to DNA damage.PloS one · 2013Article
- Casein kinase 1α regulates an MDMX intramolecular interaction to stimulate p53 binding.Molecular and cellular biology · 2012Article
- MDM2 and MDMX: Alone and together in regulation of p53.Translational cancer research · 2012Article
- The Roles of MDM2 and MDMX Phosphorylation in Stress Signaling to p53.Genes & cancer · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 protein is subject to Mdm2-mediated degradation by the ubiquitin-proteasome pathway. This degradation requires interaction between p53 and Mdm2 and the subsequent ubiquitination and nuclear export of p53. Exposure of cells to DNA damage results in the stabilization of the p53 protein in the nucleus. However, the underlying mechanism of this effect is poorly defined. Here we demonstrate a key role for c-Abl in the nuclear accumulation of endogenous p53 in cells exposed to DNA damage. This effect of c-Abl is achieved by preventing the ubiquitination and nuclear export of p53 by Mdm2, or by human papillomavirus E6. c-Abl null cells fail to accumulate p53 efficiently following DNA damage. Reconstitution of these cells with physiological levels of c-Abl is sufficient to promote the normal response of p53 to DNA damage via nuclear retention. Our results help to explain how p53 is accumulated in the nucleus in response to DNA damage.
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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.