The DOI matches its Crossref record; 132 of the 133 references it cites were found in a registry or an index.
Sibling rivalry in the E2F family
Abstract
The E2F transcription factor family determines whether or not a cell will divide by controlling the expression of key cell-cycle regulators. The individual E2Fs can be divided into distinct subgroups that act in direct opposition to one another to promote either cellular proliferation or cell-cycle exit and terminal differentiation. What is the underlying molecular basis of this 'push-me-pull-you' regulation, and what are its biological consequences?
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In the citing paper
“Many of these repressed genes are activation targets of E2F transcription factors (Narita et al., 2003), some of which are converted to transcriptional repressors when complexed with pRB (Trimarchi and Lees, 2002).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Trimarchi and Lees, 2002
In the citing paper
“Together, these results implied that the role of CDK4/6 was to phosphorylate RB, priming it for inactivation by other CDKs later in G1, and releasing E2F transcription factors from RB constraint to allow their coordinate induction of a suite of genes whose activities are jointly required for initiation of S phase [reviewed in detail in (16) (29-31)].”
From Targeting CDK4 and CDK6: From Discovery to Therapy (2016) · cites this paper as [30]
Citations
Cites
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Oncomirs—MicroRNAs with a role in cancer
Esquela-Kerscher, A., & Slack, F. J. (2006) · Nature Reviews Cancer · doi:10.1038/nrc1840 · Cited by 5,884
BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc
Delmore, J. E., Issa, G. C., Lemieux, M. E., Rahl, P. B., Shi, J., Jacobs, H. M., Kastritis, E., Gilpatrick, T., Paranal, R. M., Qi, J., et al. (2011) · Cell · doi:10.1016/j.cell.2011.08.017 · Cited by 2,888
The role of MicroRNAs in human cancer
Peng, Y., & Croce, C. M. (2016) · Signal Transduction and Targeted Therapy · doi:10.1038/sigtrans.2015.4 · Cited by 2,566
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
Campisi, J. (2005) · Cell · doi:10.1016/j.cell.2005.02.003 · Cited by 2,379
Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
Narita, M., Nuñez, S., Heard, E., Narita, M., Lin, A. W., Hearn, S. A., Spector, D. L., Hannon, G. J., & Lowe, S. W. (2003) · Cell · doi:10.1016/s0092-8674(03)00401-x · Cited by 2,278
Metadata
- Authors
- Trimarchi, J. M., & Lees, J. A.
- Affiliations
- Massachusetts Institute of Technology (US)
- Corresponding author
- Lees, Jacqueline A.
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2002-01
- Volume
- 3
- Issue
- 1
- Pages
- 11-20
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2791873134
- Cited by
- 1,158
- References
- 133
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 19 · 2023: 21 · 2022: 27 · 2021: 29 · 2020: 43 · 2019: 42 · 2018: 20 · 2017: 39 · 2016: 35 · 2015: 31 · 2014: 27 · 2013: 51 · 2012: 62
- FWCI
- 9.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- E2F transcription factors, cell cycle regulation, cell proliferation, cell cycle exit, terminal differentiation, cell division, transcriptional regulation
- MeSH terms
- Animals, Cell Cycle, Cell Differentiation, Cell Division, Chromatin, DNA-Binding Proteins, Gene Expression Regulation, Humans, Models, Genetic, Neoplasms, Transcription Factors, Retinoblastoma Protein, Apoptosis, Protein Structure, Tertiary, Cell Cycle Proteins, E2F Transcription Factors, E2F6 Transcription Factor, Mice
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