John M. Sedivy

This study shows that STING deficiency in mice increases median lifespan and reduces age-related liver damage.

This study shows that cGAS deficiency in mice leads to premature aging through inflammation and de-repression of LINE1 elements.

This study identifies LINE-1 retrotransposons as drivers of neuronal senescence in Alzheimer's disease through cytoplasmic DNA sensing and the cGAS-STING pathway.

This study uses AHARIBO to profile the translatome of human fibroblasts, revealing post-transcriptional regulation of senescence programs and identifying L1HS elements involved in inflammatory cDNA production.

This study characterizes replicative senescence in primary human astrocytes, identifying molecular features and L1HS retrotransposon activation associated with senescence.

The paper uses Nanopore long-read DNA sequencing to analyze retrotransposon activation in aged and Alzheimer's disease brains, identifying somatic insertions and epigenetic changes.

TE-Seq is an RNA-Seq pipeline that annotates transposable elements and analyzes their expression, supporting long-read DNA data for TE-complete genome assembly.

This study shows that reducing endogenous Myc levels in p53-deficient mice extends tumor-free survival and that tumors compensate by increasing Myc dosage or expression.

This study presents high-resolution Hi-C maps of human fibroblasts during senescence, revealing chromatin remodeling that promotes inflammation and transposable element activation.

This study uses single-cell whole-genome sequencing to compare mutation burdens in early passage and deeply senescent human fibroblasts, finding increased single-nucleotide variations and aneuploidies in senescent cells.

The paper identifies common transcriptional subpopulations across different senescence types and shows their differential response to a senolytic agent.

The paper develops a method to measure LINE-1 retrotransposon expression in single cells and identifies its presence in epithelial and neuronal cells, with age-related increases.

The paper shows that DNA double-strand breaks induce epigenomic changes that accelerate the aging clock in mammals.

This study shows that inhibiting L1 retrotransposition with NRTIs improves health and extends the lifespan of SIRT6 knockout mice by reducing type I interferon response and DNA damage.