ArticlePLoS genetics2008
Context-dependent requirement for dE2F during oncogenic proliferation.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed.
- Hippo signaling is intrinsically regulated during cell cycle progression by APC/CProceedings of the National Academy of Sciences of the United States of America · 2019Article
- A Balance of Yki/Sd Activator and E2F1/Sd Repressor Complexes Controls Cell Survival and Affects Organ Size.Developmental cell · 2017Article
- Differential control of Yorkie activity by LKB1/AMPK and the Hippo/Warts cascade in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Protein phosphatase 2A promotes the transition to G0 during terminal differentiation in Drosophila.Development (Cambridge, England) · 2015Article
- PBK/TOPK mediates geranylgeranylation signaling for breast cancer cell proliferation.Cancer cell international · 2015Article
- mir-11 limits the proapoptotic function of its host gene, dE2f1.Genes & development · 2011Article
- Cooperation between dE2F1 and Yki/Sd defines a distinct transcriptional program necessary to bypass cell cycle exit.Genes & development · 2011Article
- Notch-dependent expression of the archipelago ubiquitin ligase subunit in the Drosophila eye.Development (Cambridge, England) · 2011Article
- dMyc functions downstream of Yorkie to promote the supercompetitive behavior of hippo pathway mutant cells.PLoS genetics · 2010Article
- Tuberous sclerosis complex 1 regulates dE2F1 expression during development and cooperates with RBF1 to control proliferation and survival.PLoS genetics · 2010Article
- Influence of fat-hippo and notch signaling on the proliferation and differentiation of Drosophila optic neuroepithelia.Development (Cambridge, England) · 2010Article
- Yorkie: the final destination of Hippo signaling.Trends in cell biology · 2010Review
- A robust cell cycle control mechanism limits E2F-induced proliferation of terminally differentiated cells in vivo.The Journal of cell biology · 2010Article
- Combined inactivation of pRB and hippo pathways induces dedifferentiation in the Drosophila retina.PLoS genetics · 2010Article
- Emerging roles of E2Fs in cancer: an exit from cell cycle control.Nature reviews. Cancer · 2009Review
- Comparative Generalized Logic Modeling Reveals Differential Gene Interactions during Cell Cycle Exit inGI-Edition. Proceedings · 2009Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The Hippo pathway negatively regulates the cell number in epithelial tissue. Upon its inactivation, an excess of cells is produced. These additional cells are generated from an increased rate of cell division, followed by inappropriate proliferation of cells that have failed to exit the cell cycle. We analyzed the consequence of inactivation of the entire E2F family of transcription factors in these two settings. In Drosophila, there is a single activator, dE2F1, and a single repressor, dE2F2, which act antagonistically to each other during development. While the loss of the activator dE2F1 results in a severe impairment in cell proliferation, this defect is rescued by the simultaneous loss of the repressor dE2F2, as cell proliferation occurs relatively normally in the absence of both dE2F proteins. We found that the combined inactivation of dE2F1 and dE2F2 had no significant effect on the increased rate of cell division of Hippo pathway mutant cells. In striking contrast, inappropriate proliferation of cells that failed to exit the cell cycle was efficiently blocked. Furthermore, our data suggest that such inappropriate proliferation was primarily dependent on the activator, de2f1, as loss of de2f2 was inconsequential. Consistently, Hippo pathway mutant cells had elevated E2F activity and induced dE2F1 expression at a point when wild-type cells normally exit the cell cycle. Thus, we uncovered a critical requirement for the dE2F family during inappropriate proliferation of Hippo pathway mutant cells.
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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.