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p53 and E2f: partners in life and death
Abstract
During tumour development cells sustain mutations that disrupt normal mechanisms controlling proliferation. Remarkably, the Rb-E2f and MDM2-p53 pathways are both defective in most, if not all, human tumours, which underscores the crucial role of these pathways in regulating cell cycle progression and viability. A simple interpretation of the observation that both pathways are deregulated is that they function independently in the control of cell fate. However, a large body of evidence indicates that, in addition to their independent effects on cell fate, there is extensive crosstalk between these two pathways, and specifically between the transcription factors E2F1 and p53, which influences vital cellular decisions. This Review discusses the molecular mechanisms that underlie the intricate interactions between E2f and p53.
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“E2F1 signals positive and negative feedback to p53.225”
From Census and evaluation of p53 target genes (2017) · cites this paper as [225]
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Apoptosis Associated with Deregulated E2F Activity Is Dependent on E2F1 and Atm/Nbs1/Chk2
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Self-citationE2F1-induced apoptosis: turning killers into therapeutics
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E2F1 Induces Phosphorylation of p53 That Is Coincident with p53 Accumulation and Apoptosis
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p130/E2F4 Binds to and Represses the cdc2 Promoter in Response to p53
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The candidate tumor suppressor BTG3 is a transcriptional target of p53 that inhibits E2F1
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Specificity of E2F1, E2F2, and E2F3 in mediating phenotypes induced by loss of Rb.
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Self-citationApoptosis-stimulating protein of p53-2 (ASPP2/53BP2L) is an E2F target gene
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E2F3 is the main target gene of the 6p22 amplicon with high specificity for human bladder cancer
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Mutant p53: one name, many proteinsPreprint
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Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas
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The role of nuclear lamin B1 in cell proliferation and senescence
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Metadata
- Authors
- Polager, S., & Ginsberg, D.
- Affiliations
- Bar-Ilan University (IL)
- Corresponding author
- Ginsberg, Doron
- ORCID
- Ginsberg, Doron
- Venue
- Nature Reviews Cancer
- Published
- 2009-10
- Volume
- 9
- Issue
- 10
- Pages
- 738-748
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2019562165
- Cited by
- 498
- References
- 136
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 20 · 2023: 23 · 2022: 13 · 2021: 23 · 2020: 18 · 2019: 23 · 2018: 27 · 2017: 35 · 2016: 38 · 2015: 41 · 2014: 43 · 2013: 54 · 2012: 46
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, E2F1, Rb/E2F pathway, MDM2-p53 pathway, pathway crosstalk, cell cycle regulation, cell fate, carcinogenesis, transcription factors, tumor suppressor
- MeSH terms
- Cell Cycle, Cell Survival, Humans, Mutation, Neoplasms, Signal Transduction, Tumor Suppressor Protein p53, Apoptosis, Cell Proliferation, E2F Transcription Factors
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