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The role of retrotransposons at the interface of DNA damage and the innate immune response.

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Current opinion in cell biology 2026 Vol.99() p. 102625 Chromosomal and Genetic Variations
TL;DR This mini-review discusses recent and still debated insights into L1's role in cancer, including non-cell-autonomous effects mediated by extracellular vesicles, its role in promoting cellular plasticity, and therapeutic opportunities through reverse transcriptase inhibition.
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PubMed DOI OpenAlex Semantic 마지막 보강 2026-05-01
OpenAlex 토픽 · Chromosomal and Genetic Variations Bacterial Genetics and Biotechnology DNA Repair Mechanisms

Vikraman P, Davoli T, Mita P

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This mini-review discusses recent and still debated insights into L1's role in cancer, including non-cell-autonomous effects mediated by extracellular vesicles, its role in promoting cellular plastici

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APA Pooja Vikraman, Teresa Davoli, Paolo Mita (2026). The role of retrotransposons at the interface of DNA damage and the innate immune response.. Current opinion in cell biology, 99, 102625. https://doi.org/10.1016/j.ceb.2026.102625
MLA Pooja Vikraman, et al.. "The role of retrotransposons at the interface of DNA damage and the innate immune response.." Current opinion in cell biology, vol. 99, 2026, pp. 102625.
PMID 41747652 ↗

Abstract

LINE-1 (L1) retrotransposons are increasingly recognized as key players in cancer biology. While traditionally viewed as mutators through their endonuclease (EN) activity, recent findings show that L1 elements can also activate innate immune pathways independently of EN activity, particularly type I interferon signaling via "viral mimicry." These dual functions position L1 at the intersection of genome regulation and innate immune response. From this perspective, this mini-review discusses recent and still debated insights into L1's role in cancer, including non-cell-autonomous effects mediated by extracellular vesicles, its role in promoting cellular plasticity, and therapeutic opportunities through reverse transcriptase inhibition. Together, these findings highlight L1 retrotransposons as drivers of tumor development and potential clinical targets.

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