ArticleScientific reports2017
Determination of the physiological and pathological roles of E2F3 in adult tissues.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- A lactylation-associated gene signature predicts prognosis in neuroblastoma and identifies RPS6KA6 as a candidate biomarker.BMC cancer · 2026Article
- Synthetic lethality between RB-loss and E2F3 inhibition in small cell cancers targeted by pyrimidine synthesis blockade.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The cell-permeable iron chelator M606 inhibits MYCN-driven neuroblastoma via an E2F3-mediated response.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reversible Myc hypomorphism identifies a key Myc-dependency in early cancer evolution.Nature communications · 2022Article
- The Over-Expression of E2F3 Might Serve as Prognostic Marker for Neuroblastoma Patients with Stage 4S Disease.Diagnostics (Basel, Switzerland) · 2020Article
- Reactivation of Myc transcription in the mouse heart unlocks its proliferative capacity.Nature communications · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
While genetically engineered mice have made an enormous contribution towards the elucidation of human disease, it has hitherto not been possible to tune up or down the level of expression of any endogenous gene. Here we describe compound genetically modified mice in which expression of the endogenous E2f3 gene may be either reversibly elevated or repressed in adult animals by oral administration of tetracycline. This technology is, in principle, applicable to any endogenous gene, allowing direct determination of both elevated and reduced gene expression in physiological and pathological processes. Applying this switchable technology to the key cell cycle transcription factor E2F3, we demonstrate that elevated levels of E2F3 drive ectopic proliferation in multiple tissues. By contrast, E2F3 repression has minimal impact on tissue proliferation or homeostasis in the majority of contexts due to redundancy of adult function with E2F1 and E2F2. In the absence of E2F1 and E2F2, however, repression of E2F3 elicits profound reduction of proliferation in the hematopoietic compartments that is rapidly lethal in adult animals.
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Registered trials
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