ArticleMobile genetic elements
Transposable elements and miRNA: Regulation of genomic stability and plasticity.
Article in Mobile genetic elements. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- The oncogenic microRNA miR-222 promotes human LINE-1 retrotransposition.RNA biology · 2025Article
- Non-Coding RNAs in Response to Drought Stress.International journal of molecular sciences · 2021Review
- Bioinformatics and Machine Learning Approaches to Understand the Regulation of Mobile Genetic Elements.Biology · 2021Review
- TRIM28 variants and Wilms' tumour predisposition.The Journal of pathology · 2021Review
- New Understanding of the Relevant Role of LINE-1 Retrotransposition in Human Disease and Immune Modulation.Frontiers in cell and developmental biology · 2020Review
- "Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma.PloS one · 2017Article
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2 authors at 1 institution in 1 country.
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Abstract
Transposable elements, the class of mobile DNA sequences that change their copies or positions within the genome have an ever increasing role in shaping the genetic and evolutionary landscape. Approximately half of the mammalian genome is composed of repetitive elements, including LINE-1 (L1) elements. Because of their ability to "copy and paste" into other regions of the genome, their activation represent an opportunity as well as a threat, as L1-induced mutations results in genomic instability and plasticity. On one hand L1 retrotransposition and integration fosters genomic diversity and on the other, de-repressed L1 functions as a driver of diseases such as cancer. The regulation of L1 is an area of intense research and novel epigenetic mechanisms have recently been discovered to now include DNA methylation, histone modifications, and miR-induced L1 silencing. During development, reprogramming and in transformed cells, specific classes of repetitive elements are upregulated, presumably due to the loss of epigenetic regulation in this process, increasing the risk of L1-induced mutations. Here we discuss how miR regulation of L1 activation fits into the complex picture of L1 repression in somatic cells and touch on some of the possible implications.
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