ArticleMolecular and cellular biology1995
E2F-1:DP-1 induces p53 and overrides survival factors to trigger apoptosis.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 165 citations in OpenAlex.
- BRD9-p53-E2F1 circuit orchestrates cell growth and DNA damage repair in gastric cancer.Molecular cancer · 2025Article
- A novel selenium analog of HDACi-based twin drug induces apoptosis and cell cycle arrest via CDC25A to improve prostate cancer therapy.Theranostics · 2024Article
- Transcriptome Sequencing Reveals Autophagy Networks in Rat Livers during the Development of NAFLD and Identifies Autophagy Hub Genes.International journal of molecular sciences · 2023Article
- Ethanolic extract of Ya-nang (PeerJ · 2022Article
- Arsenic trioxide reduces the expression of E2F1, cyclin E, and phosphorylation of PI3K signaling molecules in acute leukemia cells.Environmental toxicology · 2021Article
- TFDP3 as E2F Unique Partner, Has Crucial Roles in Cancer Cells and Testis.Frontiers in oncology · 2021Review
- Transcriptional control of stem cell fate by E2Fs and pocket proteins.Frontiers in genetics · 2015Review
- Regulation of E2F1 by APC/C Cdh1 via K11 linkage-specific ubiquitin chain formation.Cell cycle (Georgetown, Tex.) · 2012Article
- Article
- Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas.The American journal of pathology · 2009Article
- Antisense MDM2 enhances E2F1-induced apoptosis and the combination sensitizes androgen-sensitive [corrected] and androgen-insensitive [corrected] prostate cancer cells to radiation.Molecular cancer research : MCR · 2008Article
- Article
- Selection of novel mediators of E2F1-induced apoptosis through retroviral expression of an antisense cDNA library.Nucleic acids research · 2005Article
- Triggering of p73-dependent apoptosis in osteosarcoma is under the control of E2Fs-pRb2/p130 complexes.Oncogene · 2003Article
- Cell cycle and apoptosis.Cell proliferation · 2003Review
- E2F-1 overexpression sensitizes colorectal cancer cells to camptothecin.Cancer gene therapy · 2003Article
- E2F1 induces phosphorylation of p53 that is coincident with p53 accumulation and apoptosis.Molecular and cellular biology · 2002Article
- Gene expression changes in response to E2F1 activation.Nucleic acids research · 2002Article
- Regulation of E2F1-dependent gene transcription and apoptosis by the ETS-related transcription factor GABPgamma1.Molecular and cellular biology · 2002Article
- Mutant mouse models reveal the relative roles of E2F1 and E2F3 in vivo.Molecular and cellular biology · 2002Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The E2F DNA binding activity consists of a heterodimer between E2F and DP family proteins, and these interactions are required for association of E2F proteins with pRb and the pRb-related proteins p107 and p130, which modulate E2F transcriptional activities. E2F-1 expression is sufficient to release fibroblasts from G0 and induce entry into S phase, yet it also initiates apoptosis. To investigate the mechanisms of E2F-induced apoptosis, we utilized interleukin-3 (IL-3)-dependent 32D.3 myeloid cells, a model of hematopoietic progenitor programmed cell death. In the absence of IL-3, E2F-1 alone was sufficient to induce apoptosis, and p53 levels were diminished. DP-1 alone was not sufficient to induce cell cycle progression or alter rates of death following IL-3 withdrawal. However, overexpression of both E2F-1 and DP-1 led to the rapid death of cells even in the presence of survival factors. In the presence of IL-3, levels of endogenous wild-type p53 increased in response to E2F-1, and coexpression of DP-1 further augmented p53 levels. These results provide evidence that E2F is a functional link between the tumor suppressors p53 and pRb. However, induction of p53 alone was not sufficient to trigger apoptosis, suggesting that the ability of E2F to override survival factors involves additional effectors.
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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.