ArticleNucleic acids research2014
Potential for genomic instability associated with retrotranspositionally-incompetent L1 loci.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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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
38 citing papers in PubMed, 58 citations in OpenAlex.
- AcutebioRxiv : the preprint server for biology · 2026Article
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Locus-specific LINE-1 mRNA expression reflects cell-type- and stimulus-specific senescence states.Nucleic acids research · 2026Article
- Functional analyses identify the L1 ORF2p Cryptic domain as a hub for intramolecular interfaces required for retrotransposition.Nucleic acids research · 2026Article
- Reactivation of retrotransposable elements is associated with environmental stress and ageing.Nature reviews. Genetics · 2025Review
- Identification and characterization of small molecule inhibitors of the LINE-1 retrotransposon endonuclease.Nature communications · 2024Article
- Article
- Lamivudine modulates the expression of neurological impairment-related genes and LINE-1 retrotransposons in brain tissues of a Down syndrome mouse model.Frontiers in aging neuroscience · 2024Article
- Aging differentially alters the transcriptome and landscape of chromatin accessibility in the male and female mouse hippocampus.Frontiers in molecular neuroscience · 2024Article
- A novel role of TRIM28 B box domain in L1 retrotransposition and ORF2p-mediated cDNA synthesis.Nucleic acids research · 2023Article
- The Immunological Conundrum of Endogenous Retroelements.Annual review of immunology · 2023Review
- SCIFER: approach for analysis of LINE-1 mRNA expression in single cells at a single locus resolution.Mobile DNA · 2022Article
- Analysis of epigenetic features characteristic of L1 loci expressed in human cells.Nucleic acids research · 2022Article
- Structural dissection of sequence recognition and catalytic mechanism of human LINE-1 endonuclease.Nucleic acids research · 2021Article
- Review
- Organ-, sex- and age-dependent patterns of endogenous L1 mRNA expression at a single locus resolution.Nucleic acids research · 2021Article
- Measuring and interpreting transposable element expression.Nature reviews. Genetics · 2020Review
- New Understanding of the Relevant Role of LINE-1 Retrotransposition in Human Disease and Immune Modulation.Frontiers in cell and developmental biology · 2020Review
- RNA Next-Generation Sequencing and a Bioinformatics Pipeline to Identify Expressed LINE-1s at the Locus-Specific Level.Journal of visualized experiments : JoVE · 2019Article
- LINE1 Derepression in Aged Wild-Type and SIRT6-Deficient Mice Drives Inflammation.Cell metabolism · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Expression of the L1 retrotransposon can damage the genome through insertional mutagenesis and the generation of DNA double-strand breaks (DSBs). The majority of L1 loci in the human genome are 5'-truncated and therefore incapable of retrotransposition. While thousands of full-length L1 loci remain, most are retrotranspositionally-incompetent due to inactivating mutations. However, mutations leading to premature stop codons within the L1 ORF2 sequence may yield truncated proteins that retain a functional endonuclease domain. We demonstrate that some truncated ORF2 proteins cause varying levels of toxicity and DNA damage when chronically overexpressed in mammalian cells. Furthermore, transfection of some ORF2 constructs containing premature stop codons supported low levels of Alu retrotransposition, demonstrating the potential for select retrotranspositionally-incompetent L1 loci to generate genomic instability. This result suggests yet another plausible explanation for the relative success of Alu elements in populating the human genome. Our data suggest that a subset of retrotranspositionally-incompetent L1s, previously considered to be harmless to genomic integrity, may have the potential to cause chronic DNA damage by introducing DSBs and mobilizing Alu. These results imply that the number of known L1 loci in the human genome that potentially threaten its stability may not be limited to the retrotranspositionally active loci.
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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.