ReviewInternational journal of molecular sciences2019
How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Loss of p53-DREAM-mediated repression of cell cycle genes as a driver of lymph node metastasis in head and neck cancer.Genome medicine · 2023Pooled it
- Deficient arsenic methylation and global proteomic reprogramming in human keratinocytes during arsenic-induced skin carcinogenesis.Archives of toxicology · 2026Article
- Frequency-specific photobiomodulation at theta and gamma enhances cognitive networks and mitigates age-related decline.GeroScience · 2026Article
- Efficacy of melflufen in multiple myeloma with mutated or deleted TP53.Experimental hematology & oncology · 2025Article
- A novel pyridazinone and thiophene compound IMB5043 activated apoptosis and autophagy in cisplatin-resistant non-small cell lung cancer cells.Translational cancer research · 2025Article
- Specific TP53 mutations impair the recruitment of 53BP1 to DNA double-strand breaks underlying the mechanism of radioresistance.European biophysics journal : EBJ · 2025Article
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.Nucleic acids research · 2025Article
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Evaluation of two algorithms measuring homologous recombination deficiency status in prognostic assessment for treatment-naïve non-small cell lung cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Article
- CCT8 drives colorectal cancer progression via the RPL4-MDM2-p53 axis and immune modulation.BMC medical genomics · 2025Article
- p53-dependent chromatin relaxation is required for DNA double-strand break repair.Acta biochimica et biophysica Sinica · 2025Article
- R-loop formation contributes to mTORC1 activation-dependent DNA replication stress induced by p53 deficiency.Acta biochimica et biophysica Sinica · 2024Article
- Targeting mutant p53: a key player in breast cancer pathogenesis and beyond.Cell communication and signaling : CCS · 2024Review
- Review
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- Structures of p53/BCL-2 complex suggest a mechanism for p53 to antagonize BCL-2 activity.Nature communications · 2023Article
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been four decades since the discovery of p53, the designated 'Guardian of the Genome'. P53 is primarily known as a master transcription factor and critical tumor suppressor, with countless studies detailing the mechanisms by which it regulates a host of gene targets and their consequent signaling pathways. However, transcription-independent functions of p53 also strongly define its tumor-suppressive capabilities and recent findings shed light on the molecular mechanisms hinted at by earlier efforts. This review highlights the transcription-independent mechanisms by which p53 influences the cellular response to genomic instability (in the form of replication stress, centrosome homeostasis, and transposition) and cell death. We also pinpoint areas for further investigation in order to better understand the context dependency of p53 transcription-independent functions and how these are perturbed when
Indexed as
Identifiers
What OpenQuestion holds
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.