ArticleOncogene2010
Accelerated DNA replication in E2F1- and E2F2-deficient macrophages leads to induction of the DNA damage response and p21(CIP1)-dependent senescence.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- E2F2 suppresses cell senescence and promotes odontogenic differentiation in dental pulp stem cells by stabilizing METTL3.Odontology · 2026Article
- Oxidative phosphorylation is a key feature of neonatal monocyte immunometabolism promoting myeloid differentiation after birth.Nature communications · 2025Article
- Epithelial-to-mesenchymal transition status correlated with ultrastructural features, and TP53 mutation in patient-derived oral cancer cell lines.Molecular biology reports · 2023Article
- Single-cell RNA sequencing reveals cellular and molecular reprograming landscape of gliomas and lung cancer brain metastases.Clinical and translational medicine · 2022Article
- Targeting E2F Sensitizes Prostate Cancer Cells to Drug-Induced Replication Stress by Promoting Unscheduled CDK1 Activity.Cancers · 2022Article
- Perspectives on the dynamic implications of cellular senescence and immunosenescence on macrophage aging biology.Biogerontology · 2021Review
- Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease.Cellular and molecular gastroenterology and hepatology · 2020Article
- An E2F7-dependent transcriptional program modulates DNA damage repair and genomic stability.Nucleic acids research · 2018Article
- High-concentration hydrogen protects mouse heart against ischemia/reperfusion injury through activation of thePI3K/Akt1 pathway.Scientific reports · 2017Article
- Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.Biological research · 2016Article
- The stress of coping with E2F loss.Molecular & cellular oncology · 2016Article
- E2F1 and E2F2 prevent replicative stress and subsequent p53-dependent organ involution.Cell death and differentiation · 2015Article
- E2F2 and CREB cooperatively regulate transcriptional activity of cell cycle genes.Nucleic acids research · 2013Article
- Bradykinin inhibits oxidative stress-induced cardiomyocytes senescence via regulating redox state.PloS one · 2013Article
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Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
E2F1-3 proteins appear to have distinct roles in progenitor cells and in differentiating cells undergoing cell cycle exit. However, the function of these proteins in paradigms of terminal differentiation that involve continued cell division has not been examined. Using compound E2F1/E2F2-deficient mice, we have examined the effects of E2F1 and E2F2 loss on the differentiation and simultaneous proliferation of bone-marrow-derived cells toward the macrophage lineage. We show that E2F1/E2F2 deficiency results in accelerated DNA replication and cellular division during the initial cell division cycles of bone-marrow-derived cells, arguing that E2F1/E2F2 are required to restrain proliferation of pro-monocyte progenitors during their differentiation into macrophages, without promoting their cell cycle exit. Accelerated proliferation is accompanied by early expression of DNA replication and cell cycle regulators. Remarkably, rapid proliferation of E2F1/E2F2 compound mutant cultures is temporally followed by induction of a DNA damage response and the implementation of a p21(CIP1)-dependent senescence. We further show that differentiating E2F1/E2F2-knockout macrophages do not trigger a DNA damage response pathway in the absence of DNA replication. These findings underscore the relevance of E2F1 and E2F2 as suppressors of hematopoietic progenitor expansion. Our data indicate that their absence in differentiating macrophages initiates a senescence program that results from enforcement of a DNA damage response triggered by DNA hyper-replication.
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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.