ArticleOncogene2009
p53 responsive elements in human retrotransposons.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Spatiotemporal dynamics of radioresistance: decoding macrophage-driven radioprotective niches through temporal-spatial reprogramming.Molecular cancer · 2026Review
- 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
- 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
- Causes and Consequences of Varying Transposable Element Activity: An Evolutionary Perspective.Annual review of genomics and human genetics · 2024Review
- Translating p53-based therapies for cancer into the clinic.Nature reviews. Cancer · 2024Review
- LINE-1 retrotransposition and its deregulation in cancers: implications for therapeutic opportunities.Genes & development · 2023Review
- Review
- A new human embryonic cell type associated with activity of young transposable elements allows definition of the inner cell mass.PLoS biology · 2023Article
- Transposon control as a checkpoint for tissue regeneration.Development (Cambridge, England) · 2022Article
- Role of Transposable Elements in Genome Stability: Implications for Health and Disease.International journal of molecular sciences · 2022Review
- Activating STING1-dependent immune signaling inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- NOS2 andProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Role of Transposable Elements of the Human Genome in Neuronal Function and Pathology.International journal of molecular sciences · 2022Review
- Transposable element regulation and expression in cancer.The FEBS journal · 2022Review
- Pharmacologic Activation of p53 Triggers Viral Mimicry Response Thereby Abolishing Tumor Immune Evasion and Promoting Antitumor Immunity.Cancer discovery · 2021Article
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Long interspersed nuclear elements-1 (L1s) are highly repetitive DNA elements that are capable of altering the human genome through retrotransposition. To protect against L1 retroposition, the cell downregulates the expression of L1 proteins by various mechanisms, including high-density cytosine methylation of L1 promoters and DICER-dependent destruction of L1 mRNAs. In this report, a large number of p53 responsive elements, or p53 DNA binding sites, were detected in L1 elements within the human genome. At least some of these p53 responsive elements are functional and can act to increase the levels of L1 mRNA expression. The p53 protein can directly bind to a short 15-nucleotide sequence within the L1 promoter. This p53 responsive element within L1 is a recent addition to evolution, appearing approximately 20 million years ago. This suggests an interplay between L1 elements, which have a rich history of causing changes in the genome, and the p53 protein, the function of which is to protect against genomic changes. To understand these observations, a model is proposed in which the increased expression of L1 mRNAs by p53 actually increases, rather than decreases, the genomic stability through amplification of p53-dependent processes for genomic protection.
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.