Telomeres, Telomerase, and Senescence

This study shows RTEL1 ATPase activity is essential for both telomere strand synthesis and TERT regulation, with reduced TERT providing an adaptive survival mechanism in RTEL1-defective cells.

This study identifies senescent cancer-associated fibroblasts (senCAFs) driven by MK2 that promote immunosuppression in bone metastases and shows that combining MK2 inhibition with OX40 agonists enhances immunotherapy efficacy.

This paper identifies Cx43 as a target that enhances CDK4/6 inhibitor efficacy and promotes elimination of therapy-induced senescent tumor cells through senolytic agents.

The paper identifies age-dependent senescent endothelial cells in adipose tissue using snRNA-Seq and finds ion channel genes as predictive biomarkers.

The paper investigates the role of CST-PP complex in protecting telomeric ss-dsDNA junctions from damage and resection in yeast, showing that Rif1 supports this protection.

This study shows that excess cell size drives senescence by altering mRNA homeostasis and reorganizing the genome, leading to the secretory phenotype and cell cycle arrest.

The paper develops a mathematical model to infer telomere dynamics parameters from telomere length distributions in yeast using long-read sequencing data.

This paper introduces TeloXplorer, a framework for analyzing telomere features in long-read data, showing how telomere diversity is inherited across species and populations.

The paper shows that escaping replicative crisis and achieving immortality precedes complex genome evolution in cancer cells.

This study identifies an ammonia-senescence ratchet mechanism that drives tumor cells from metabolic adaptation to senescence and ultimately to ammonioptosis.

This study shows TRF2 mediates force-resistant tethering of telomeric DNA repeats, which may be a step in T-loop formation.

The paper identifies Nutlin3a as a senolytic compound that reduces radiation-induced salivary gland dysfunction by transiently activating p53 in a two-step organoid screening approach.

The paper uses super-resolution microscopy to show that single-stranded telomeric repeats are spatially segregated within ALT-associated PML bodies.

This study evaluates thiomorpholino antisense oligonucleotides (TMOs) as telomerase inhibitors, showing they reduce telomerase activity and limit cancer cell proliferation.

This study identifies GPR81 loss as a driver of vascular senescence and shows that its activation can reverse age-related metabolic dysfunction in arteries.

The paper develops a computational systems biology framework to model metabolic-epigenetic coupling in cellular senescence, showing how mitochondrial remodeling and alpha-ketoglutarate depletion inhibit KDM4/KDM6 and amplify SASP.

This study identifies mitochondrial dysfunction and impaired osteogenic capacity as key features of stress-induced osteoblast senescence using in vitro models and transcriptomic analysis.

This study shows that chronic genotoxic and metabolic stress induce distinct yet overlapping senescence programs in human microglia, characterized by morphological changes, mitochondrial remodelling, and inflammatory activation.

Merging CellAge, GenAge, SenMayo and Reactome senescence genes onto Ensembl IDs yields 1,250 provenance-tracked genes, most also annotated with mouse/zebrafish orthologs, tissue expression and STRING interactions.

This study shows that combining sacituzumab govitecan with the senolytic ABT-263 effectively overcomes chemoresistance in HNSCC by targeting senescent cells.

This study shows Cdc13 initially binds telomeres as a monomer, then forms a stable dimer, revealing a sequential mechanism for telomere protection and length regulation.

This paper shows that tumour telomere length is influenced by patient-specific telomere length, replicating this across two cancer cohorts.

This study investigates the role of human PIF1 in ALT telomere maintenance, showing its involvement in DNA damage, G4 formation, and replication stress response, with implications for cancer therapy.

This study identifies mitochondrial dysfunction as a key feature of brain senescence in telomerase-deficient mice, linking telomere attrition to impaired mitochondrial function and region-specific neuronal vulnerability.

This paper develops a standardized in vitro model for senolytic drug screening using human intervertebral disc cells and validates a metabolic activity assay as a scalable method to assess senolytic activity.

This study identifies two HES1-expressing senescent CTC subpopulations with distinct metabolic and clinical outcomes, showing HES1-SOD1 antagonism influences metastatic relapse.

This paper introduces a method using Oxford Nanopore long-read sequencing to measure chromosome-specific telomere lengths in human cells.

This study identifies the BLM DHBN domain and the roles of WRN, MUS81, and GEN1 in mitotic arrest-dependent telomere deprotection, showing TRF2's protective role.

The paper analyzes the transcriptomic effects of PCC1 treatment on senescent human stromal cells, identifying gene expression changes in ribosomal, lysosomal, and membrane-lipid pathways.