ArticleCell cycle (Georgetown, Tex.)2015
E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
- Exploring the Research Progress of Vascular Dementia and Key Regulatory Molecules: E2F1.International journal of molecular sciences · 2026Review
- Casein kinase 1δ/ε inhibition suppresses CLL proliferation through cell-intrinsic and microenvironmental mechanisms.HemaSphere · 2026Article
- NR2F6 regulates Temozolomide resistance in glioma via the E2F2-PARP1 pathway.Cancer cell international · 2025Article
- Effects of E2F1 Point Acetylation at Lysine 117 or 125 on Neuronal Apoptosis After Ischemic Injury.Neurochemical research · 2025Article
- RNA-Seq of Chicken Embryo Liver Reveals Transcriptional Pathways Influenced by Egg Formaldehyde Treatment.Genes · 2025Article
- GCN5L: a critical target in energy metabolism pathways.Frontiers in cell and developmental biology · 2025Review
- Uncoupling of mTORC1 from E2F activity maintains DNA damage and senescence.Nature communications · 2024Article
- E2F1-Associated Purine Synthesis Pathway Is a Major Component of the MET-DNA Damage Response Network.Cancer research communications · 2024Article
- Authentication and validation of key genes in the treatment of atopic dermatitis with Runfuzhiyang powder: combined RNA-seq, bioinformatics analysis, and experimental research.Frontiers in genetics · 2024Article
- The effect of metformin on senescence of T lymphocytes.Immunity & ageing : I & A · 2023Article
- Transcriptional targets of senataxin and E2 promoter binding factors are associated with neuro-degenerative pathways during increased autophagic flux.Scientific reports · 2022Article
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- Receptor-Interacting Protein 140 Enhanced Temozolomide-Induced Cellular Apoptosis Through Regulation of E2F1 in Human Glioma Cell Lines.Neuromolecular medicine · 2022Article
- E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury.International journal of molecular sciences · 2022Article
- Decreased E2F2 Expression Correlates with Poor Prognosis and Immune Infiltrates in Patients with Colorectal Cancer.Journal of Cancer · 2022Article
- Peripheral Blood Circular RNAs as a Biomarker for Major Depressive Disorder and Prediction of Possible Pathways.Frontiers in neuroscience · 2022Article
- Transcriptome profiles associated with selenium-deficiency-dependent oxidative stress identify potential diagnostic and therapeutic targets in liver cancer cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- Low E2F2 activity is associated with high genomic instability and PARPi resistance.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which E2F1 and E2F2, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of de novo protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
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