ArticleOncotarget2016
Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- p53-responsive TLR8 SNP enhances human innate immune response to respiratory syncytial virus.The Journal of clinical investigation · 2019Trial
- Toll-like Receptor 3 as a Context-Dependent Molecular Switch in Epithelial Cancers: Balancing Cell Death and Tumor-Supportive Programs.International journal of molecular sciences · 2026Review
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Mutant p53Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- APOBEC3G Is a p53-Dependent Restriction Factor in Respiratory Syncytial Virus Infection of Human Cells Included in the p53/Immune Axis.International journal of molecular sciences · 2023Article
- Mutant p53 gain of function mediates cancer immune escape that is counteracted by APR-246.British journal of cancer · 2022Article
- Review
- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- Tumor suppressor p53 regulates intestinal type 2 immunity.Nature communications · 2021Article
- The p53 status in rheumatoid arthritis with focus on fibroblast-like synoviocytes.Immunologic research · 2021Review
- Promising New Tools for Targeting p53 Mutant Cancers: Humoral and Cell-Based Immunotherapies.Frontiers in immunology · 2021Review
- P53 in the impaired lungs.DNA repair · 2020Review
- Dietary Flavonoids in p53-Mediated Immune Dysfunctions Linking to Cancer Prevention.Biomedicines · 2020Review
- Mutant p53 as an Antigen in Cancer Immunotherapy.International journal of molecular sciences · 2020Review
- P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020Review
- Role of p53 in the Regulation of the Inflammatory Tumor Microenvironment and Tumor Suppression.Cancers · 2018Review
- Molecularly targeted therapies for p53-mutant cancers.Cellular and molecular life sciences : CMLS · 2017Review
- Exploiting poly(I:C) to induce cancer cell apoptosis.Cancer biology & therapy · 2017Review
- The Cytidine Deaminase APOBEC3 Family Is Subject to Transcriptional Regulation by p53.Molecular cancer research : MCR · 2017Article
- Local Activation of p53 in the Tumor Microenvironment Overcomes Immune Suppression and Enhances Antitumor Immunity.Cancer research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Diversity within the p53 transcriptional network can arise from a matrix of changes that include target response element sequences and p53 expression level variations. We previously found that wild type p53 (WT p53) can regulate expression of most innate immune-related Toll-like-receptor genes (TLRs) in human cells, thereby affecting immune responses. Since many tumor-associated p53 mutants exhibit change-of-spectrum transactivation from various p53 targets, we examined the ability of twenty-five p53 mutants to activate endogenous expression of the TLR gene family in p53 null human cancer cell lines following transfection with p53 mutant expression vectors. While many mutants retained the ability to drive TLR expression at WT levels, others exhibited null, limited, or change-of-spectrum transactivation of TLR genes. Using TLR3 signaling as a model, we show that some cancer-associated p53 mutants amplify cytokine, chemokine and apoptotic responses after stimulation by the cognate ligand poly(I:C). Furthermore, restoration of WT p53 activity for loss-of-function p53 mutants by the p53 reactivating drug RITA restored p53 regulation of TLR3 gene expression and enhanced DNA damage-induced apoptosis via TLR3 signaling. Overall, our findings have many implications for understanding the impact of WT and mutant p53 in immunological responses and cancer therapy.
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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.