ArticlePLoS genetics2022
Aberrant expression and localization of the RAP1 shelterin protein contribute to age-related phenotypes.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
- Metformin exhibits gender specific impact on telomere dynamics by enhancing RAP1 expression in type-2 diabetes mellitus.Acta diabetologica · 2026Article
- Telomere attrition alters extracellular vesicles conferring adverse impacts on neuronal viability and inflammatory response.iScience · 2025Article
- The Role of Glia Telomere Dysfunction in the Pathogenesis of Central Nervous System Diseases.Molecular neurobiology · 2024Review
- Telomere Checkpoint in Development and Aging.International journal of molecular sciences · 2023Review
- The shelterin protein expansion of telomere dynamics: Linking early life adversity, life history, and the hallmarks of aging.Neuroscience and biobehavioral reviews · 2023Review
- The human RAP1 and GFAPɛ proteins increase γ-secretase activity in a yeast model system.G3 (Bethesda, Md.) · 2023Article
- Boosting NAD ameliorates hematopoietic impairment linked to short telomeres in vivo.GeroScience · 2023Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Short telomeres induce a DNA damage response (DDR) that evokes apoptosis and senescence in human cells. An extant question is the contribution of telomere dysfunction-induced DDR to the phenotypes observed in aging and telomere biology disorders. One candidate is RAP1, a telomere-associated protein that also controls transcription at extratelomeric regions. To distinguish these roles, we generated a knockin mouse carrying a mutated Rap1, which was incapable of binding telomeres and did not result in eroded telomeres or a DDR. Primary Rap1 knockin embryonic fibroblasts showed decreased RAP1 expression and re-localization away from telomeres, with an increased cytosolic distribution akin to that observed in human fibroblasts undergoing telomere erosion. Rap1 knockin mice were viable, but exhibited transcriptomic alterations, proinflammatory cytokine/chemokine signaling, reduced lifespan, and decreased healthspan with increased body weight/fasting blood glucose levels, spontaneous tumor incidence, and behavioral deficits. Taken together, our data present mechanisms distinct from telomere-induced DDR that underlie age-related phenotypes.
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Registered trials
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.