ArticleGenes & development2016
p53 genes function to restrain mobile elements.
Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 213 citations in OpenAlex.
- LINE-1 Deregulation in Ovarian Cancer: Implications for Diagnosis, Prognosis, and Therapeutic Targeting.Molecular diagnosis & therapy · 2026Review
- Transposable Element Activation: A Hallmark of Cancer.Cancer discovery · 2026Review
- Advancements and Clinical Applications Prospects of Epigenetic Biomarkers in Liquid Biopsy for Oral Squamous Cell Carcinoma.Current issues in molecular biology · 2026Review
- Functional analyses identify the L1 ORF2p Cryptic domain as a hub for intramolecular interfaces required for retrotransposition.Nucleic acids research · 2026Article
- Meiotic double-strand DNA breaks and spontaneous mutation in Drosophila melanogaster.G3 (Bethesda, Md.) · 2026Article
- The Chromaverse Is Colored by Triplexes Formed Through the Interactions of Noncoding RNAs with HNPRNPU, TP53, AGO, REL Proteins, Intrinsically-Disordered Regions, and Flipons.International journal of molecular sciences · 2026Article
- Article
- The guardian of the genome meets immunotherapy: p53-based strategies.Frontiers in immunology · 2026Review
- Hypomethylating agents increase L1 retroelement expression without inducing novel insertions in myeloid malignancies.Molecular oncology · 2025Article
- LINE1 insertion into the NACC2 locus disrupts the HDM2 axis and activates lung oncogenic signaling.NPJ precision oncology · 2025Article
- Co-option of an endogenous retrovirus (LTR7-HERVH) in early human embryogenesis: becoming useful and going unnoticed.Mobile DNA · 2025Review
- Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes.Communications biology · 2025Article
- An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility.Nucleic acids research · 2025Article
- Charting the regulatory landscape of TP53 on transposable elements in cancer.Genome research · 2025Article
- Pan-cancer multi-omic model of LINE-1 activity reveals locus heterogeneity of retrotransposition efficiency.Nature communications · 2025Article
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Transcriptional coupling of telomeric retrotransposons with the cell cycle.Science advances · 2025Article
- Cancer cells restrict immunogenicity of retrotransposon expression via distinct mechanisms.Immunity · 2024Article
- Elevated expression of the retrotransposon LINE-1 drives Alzheimer's disease-associated microglial dysfunction.Acta neuropathologica · 2024Article
- The transcription factor PAX5 activates human LINE1 retrotransposons to induce cellular senescence.EMBO reports · 2024Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Throughout the animal kingdom, p53 genes govern stress response networks by specifying adaptive transcriptional responses. The human member of this gene family is mutated in most cancers, but precisely how p53 functions to mediate tumor suppression is not well understood. Using Drosophila and zebrafish models, we show that p53 restricts retrotransposon activity and genetically interacts with components of the piRNA (piwi-interacting RNA) pathway. Furthermore, transposon eruptions occurring in the p53(-) germline were incited by meiotic recombination, and transcripts produced from these mobile elements accumulated in the germ plasm. In gene complementation studies, normal human p53 alleles suppressed transposons, but mutant p53 alleles from cancer patients could not. Consistent with these observations, we also found patterns of unrestrained retrotransposons in p53-driven mouse and human cancers. Furthermore, p53 status correlated with repressive chromatin marks in the 5' sequence of a synthetic LINE-1 element. Together, these observations indicate that ancestral functions of p53 operate through conserved mechanisms to contain retrotransposons. Since human p53 mutants are disabled for this activity, our findings raise the possibility that p53 mitigates oncogenic disease in part by restricting transposon mobility.
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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.