ArticleNature communications2014
SIRT6 represses LINE1 retrotransposons by ribosylating KAP1 but this repression fails with stress and age.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers.
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Who cites it
248 citing papers in PubMed.
- Microglia activation by derepression of endogenous retroviruses drives inflammation and cellular senescence.Nature neuroscience · 2026Article
- Preserving genome integrity to combat cardiac aging: beyond LINE-1 and cGAS-STING.Journal of thoracic disease · 2026Article
- Mechanisms of Brain Aging and Their Links to Alzheimer's and Parkinson's Disease Pathology.International journal of molecular sciences · 2026Review
- Coincidence of L1 retrotransposition and DNA repair deficiency elicits synthetic lethality in S-phase mature neurons.iScience · 2026Article
- SIRT1 Silences L1 Retrotransposons by Stabilizing Heterochromatin-Modifying Complexes.Aging cell · 2026Article
- cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation.Nature aging · 2026Article
- Transposable Element Activation: A Hallmark of Cancer.Cancer discovery · 2026Review
- Review
- Emerging roles of SIRT6 and its modulators in kidney diseases.Cell death discovery · 2026Review
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Conserved Transcriptomic Signatures of Sirt6 Activity: A Cross-Species RNA-seq Meta-analysis.bioRxiv : the preprint server for biology · 2026Article
- Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation.Epigenomics · 2026Review
- Centenarian SIRT6 variants elevate SIRT6 protein and enhance cellular senescence resistance.Research square · 2026Article
- Locus-specific LINE-1 mRNA expression reflects cell-type- and stimulus-specific senescence states.Nucleic acids research · 2026Article
- Beyond deacetylation: crosstalk mechanisms and context-dependent regulation of sirtuin non-classical enzymatic functions in disease.Molecular medicine (Cambridge, Mass.) · 2026Review
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 2026Review
- Long-lived mammals contain more phosphorylation sites in the SIRT6 C-terminus that enhance PARP1 interaction and resistance to oxidative stress.bioRxiv : the preprint server for biology · 2026Article
- Role of Sirtuin 6 in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Current issues in molecular biology · 2026Review
- Human cGAS Drives LINE-1 Transcriptional Activation to Trigger MAVS-Dependent Cellular Senescence.Aging cell · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
188 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
L1 retrotransposons are an abundant class of transposable elements that pose a threat to genome stability and may have a role in age-related pathologies such as cancer. Recent evidence indicates that L1s become more active in somatic tissues during the course of ageing; however the mechanisms underlying this phenomenon remain unknown. Here we report that the longevity regulating protein, SIRT6, is a powerful repressor of L1 activity. Specifically, SIRT6 binds to the 5'-UTR of L1 loci, where it mono-ADP ribosylates the nuclear corepressor protein, KAP1, and facilitates KAP1 interaction with the heterochromatin factor, HP1α, thereby contributing to the packaging of L1 elements into transcriptionally repressive heterochromatin. During the course of ageing, and also in response to DNA damage, however, we find that SIRT6 is depleted from L1 loci, allowing the activation of these previously silenced retroelements.
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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.