ArticleScience signaling2018
Mutant and wild-type p53 form complexes with p73 upon phosphorylation by the kinase JNK.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
The trial behind it
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Unveiling the Mechanism of Protective Effects of Tanshinone as a New Fighter Against Cardiovascular Diseases: A Systematic Review.Cardiovascular toxicology · 2024Pooled it
- Evaluation of novel targeted small-molecule therapeutics in desmoplastic small round cell tumor (DSRCT) cells.Journal of cancer research and clinical oncology · 2026Article
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- Reactivation ofInternational journal of molecular sciences · 2026Article
- Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions.FEBS letters · 2026Article
- Emerging links between TLR4 signaling and ferroptosis in heart failure.Frontiers in pharmacology · 2026Review
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- p53 in colorectal cancer: from a master player to a privileged therapy target.Journal of translational medicine · 2025Review
- Targeting mutant p53: Evaluation of novel anti-p53Scientific reports · 2025Article
- Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.Blood advances · 2024Article
- Mutant p53 in head and neck squamous cell carcinoma: Molecular mechanism of gain‑of‑function and targeting therapy (Review).Oncology reports · 2023Review
- JNK Cascade-Induced Apoptosis-A Unique Role in GqPCR Signaling.International journal of molecular sciences · 2023Review
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- Role of signal transduction pathways in IL-1β-induced apoptosis: Pathological and therapeutic aspects.Immunity, inflammation and disease · 2023Review
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- LRRC8A influences the growth of gastric cancer cells via the p53 signaling pathway.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021Article
- Tumor suppressor p53: Biology, signaling pathways, and therapeutic targeting.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Rab11-FIP1/RCP Functions as a Major Signalling Hub in the Oncogenic Roles of Mutant p53 in Cancer.Frontiers in oncology · 2021Article
- Clinical significance of CCN5 and mutant p53 in primary and recurrent lesions of breast cancer.American journal of translational research · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factors p53 and p73 are critical to the induction of apoptotic cell death, particularly in response to cell stress that activates c-Jun N-terminal kinase (JNK). Mutations in the DNA-binding domain of p53, which are commonly seen in cancers, result in conformational changes that enable p53 to interact with and inhibit p73, thereby suppressing apoptosis. In contrast, wild-type p53 reportedly does not interact with p73. We found that JNK-mediated phosphorylation of Thr
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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.