ArticleMolecular and cellular biology2012
DNA damage signals through differentially modified E2F1 molecules to induce apoptosis.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Exploring the Research Progress of Vascular Dementia and Key Regulatory Molecules: E2F1.International journal of molecular sciences · 2026Review
- Orchestrating epigenetics: a comprehensive review of the methyltransferase SETD6.Experimental & molecular medicine · 2025Review
- CTSB Nuclear Translocation Facilitates DNA Damage and Lysosomal Stress to Promote Retinoblastoma Cell Death.Molecular biotechnology · 2024Article
- Comprehensive analysis of splicing factor SRs-related gene characteristics: predicting osteosarcoma prognosis and immune regulation status.Frontiers in oncology · 2024Article
- E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury.International journal of molecular sciences · 2022Article
- Understanding Retinoblastoma Post-Translational Regulation for the Design of Targeted Cancer Therapies.Cancers · 2022Review
- The nucleoplasmic interactions among Lamin A/C-pRB-LAP2α-E2F1 are modulated by dexamethasone.Scientific reports · 2021Article
- The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors.Cell cycle (Georgetown, Tex.) · 2020Review
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- A Novel Expression Profile of Cell Cycle and DNA Repair Proteins in Nonfunctioning Pituitary Adenomas.Endocrine pathology · 2020Article
- Transcriptional responses to DNA damage.DNA repair · 2019Review
- Loss of the tumor suppressor BIN1 enables ATM Ser/Thr kinase activation by the nuclear protein E2F1 and renders cancer cells resistant to cisplatin.The Journal of biological chemistry · 2019Article
- Non-canonical functions of the RB protein in cancer.Nature reviews. Cancer · 2018Review
- The Role of JMY in p53 Regulation.Cancers · 2018Review
- Aberrant rhythmic expression ofOncotarget · 2017Article
- The Retinoblastoma (RB) Tumor Suppressor: Pushing Back against Genome Instability on Multiple Fronts.International journal of molecular sciences · 2017Review
- Article
- Expression level is a key determinant of E2F1-mediated cell fate.Cell death and differentiation · 2017Article
- Synergistic functions of E2F7 and E2F8 are critical to suppress stress-induced skin cancer.Oncogene · 2017Article
- Combined analysis identifies six genes correlated with augmented malignancy from non-small cell to small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
E2F transcription can lead to cell proliferation or apoptosis, indicating that E2Fs control opposing functions. In a similar manner, DNA double-strand breaks can signal to induce cell cycle arrest or apoptosis. Specifically, pRB is activated following DNA damage, allowing it to bind to E2Fs and block transcription at cell cycle promoters; however, E2F1 is simultaneously activated, leading to transcription at proapoptotic promoters. We examined this paradoxical control of E2F transcription by studying how E2F1's interaction with pRB is regulated following DNA damage. Our work reveals that DNA damage signals create multiple forms of E2F1 that contain mutually exclusive posttranslational modifications. Specifically, E2F1 phospho-serine 364 is found only in complex with pRB, while E2F1 phosphorylation at serine 31 and acetylation function to create a pRB-free form of E2F1. Both pRB-bound and pRB-free modifications on E2F1 are essential for the activation of TA-p73 and the maximal induction of apoptosis. Chromatin immunoprecipitation demonstrated that E2F1 phosphorylated on serine 364 is also present at proapoptotic gene promoters during the induction of apoptosis. This indicates that distinct populations of E2F1 are organized in response to DNA damage signaling. Surprisingly, these complexes act in parallel to activate transcription of proapoptotic genes. Our data suggest that DNA damage signals alter pRB and E2F1 to engage them in functions leading to apoptotic induction that are distinct from pRB-E2F regulation in cell cycle control.
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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.