ArticleEMBO reports2012
Mutant p53 interactome identifies nardilysin as a p53R273H-specific binding partner that promotes invasion.
Article in EMBO reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- A systematic review and meta-analysis of somatic and germline DNA sequence biomarkers of esophageal cancer survival, therapy response and stage.Annals of oncology : official journal of the European Society for Medical Oncology · 2015Pooled it
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- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- p53 and Its Isoforms in Renal Cell Carcinoma-Do They Matter?Biomedicines · 2022Review
- Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The TRiCky Business of Protein Folding in Health and Disease.Frontiers in cell and developmental biology · 2022Review
- Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer.Redox biology · 2021Article
- Mutant TP53 interacts with BCAR1 to contribute to cancer cell invasion.British journal of cancer · 2021Article
- APOBEC3B expression in breast cancer cell lines and tumors depends on the estrogen receptor status.Carcinogenesis · 2020Article
- RANBP9 as potential therapeutic target in non-small cell lung cancer.Journal of cancer metastasis and treatment · 2020Article
- Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis.International journal of molecular sciences · 2019Review
- Integrating molecular networks with genetic variant interpretation for precision medicine.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Wild-type p53 oligomerizes more efficiently than p53 hot-spot mutants and overcomes mutant p53 gain-of-function via a "dominant-positive" mechanism.Oncotarget · 2018Article
- Potential therapeutic targets ofOncotarget · 2018Review
- Early-Stage Metastasis Requires Mdm2 and Not p53 Gain of Function.Molecular cancer research : MCR · 2017Article
- Li-Fraumeni Syndrome Disease Model: A Platform to Develop Precision Cancer Therapy Targeting Oncogenic p53.Trends in pharmacological sciences · 2017Review
- Proteomic identification of ERP29 as a key chemoresistant factor activated by the aggregating p53 mutant Arg282Trp.Oncogene · 2017Article
- Mutant p53 upregulates alpha-1 antitrypsin expression and promotes invasion in lung cancer.Oncogene · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The invasiveness of tumour cells depends on changes in cell shape, polarity and migration. Mutant p53 induces enhanced tumour metastasis in mice, and human cells overexpressing p53R273H have aberrant polarity and increased invasiveness, demonstrating the 'gain of function' of mutant p53 in carcinogenesis. We hypothesize that p53R273H interacts with mutant p53-specific binding partners that control polarity, migration or invasion. Here we analyze the p53R273H interactome using stable isotope labelling by amino acids in cell culture and quantitative mass spectrometry, and identify at least 15 new potential mutant p53-specific binding partners. The interaction of p53R273H with one of them--nardilysin (NRD1)--promotes an invasive response to heparin binding-epidermal growth factor-like growth factor that is p53R273H-dependant but does not require Rab coupling protein or p63. Advanced proteomics has thus allowed the detection of a new mechanism of p53-driven invasion.
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Registered trials
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.