<i>In vivo</i> inactivation of RAD51-mediated homologous recombination leads to premature aging, but not to tumorigenesis is a research paper. On theSindex it has a DataRank of 0.145. It has been cited 1 time, with 1 citing works in its 1-hop citation network.
Abstract Genetic instability is a hallmark of both cancer and aging. Homologous recombination (HR) is a prominent DNA repair pathway maintaining genomic integrity. Mutations in many HR genes lead to cancer predisposition. Paradoxically, the consequences of mutations in the pivotal HR player, RAD51 , on cancer development remain puzzling. Moreover, in contrast with other HR genes, RAD51 mouse models are not available to experimentally address the role of RAD51 on aging and carcinogenesis, in vivo . Here, we engineered a mouse model with an inducible dominant negative form of RAD51 ( SMRad51 ) that suppresses RAD51-mediated HR without stimulating alternative non-conservative repair pathways. We found that, in vivo expression of SMRad51 did not trigger tumorigenesis, but instead induced premature aging. We propose that these in vivo phenotypes result from the exhaustion of proliferating progenitors submitted to chronic endogenous replication stress resulting from RAD51-mediated HR suppression. Our data underline the importance of the RAD51 activity for progenitors homeostasis, preventing aging, and more generally for the balance between cancer and aging.
FAIR checklist signals are shown for context only and do not affect DataRank scoring.
Base Score Contribution
0.104
From this paper's citation signal
Citation Network Contribution
0.0415
From 1 citing papers with measurable signal
Ranked by citation count — the same ordering the engine uses when summing log1p(Cq) over citers.
DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 71% comes from its base citations and 29% from the citation network (1 citing paper contributed measurable signal).
Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.
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