ArticleGenetics1999
A genetic screen for modifiers of E2F in Drosophila melanogaster.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 81 citations in OpenAlex.
- An RNAi Screen for Genes Required for Growth ofG3 (Bethesda, Md.) · 2019Article
- An alternatively spliced form affecting the Marked Box domain of Drosophila E2F1 is required for proper cell cycle regulation.PLoS genetics · 2018Article
- Modelling Cooperative Tumorigenesis inBioMed research international · 2018Review
- Phosphorylation of Drosophila Brahma on CDK-phosphorylation sites is important for cell cycle regulation and differentiation.Cell cycle (Georgetown, Tex.) · 2018Article
- Identification of novel direct targets of Drosophila Sine oculis and Eyes absent by integration of genome-wide data sets.Developmental biology · 2016Article
- Coordinating cell proliferation and differentiation: Antagonism between cell cycle regulators and cell type-specific gene expression.Cell cycle (Georgetown, Tex.) · 2016Review
- Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer--mechanisms and potential therapeutic insights.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- In vivo regulation of E2F1 by Polycomb group genes in Drosophila.G3 (Bethesda, Md.) · 2012Article
- The role of components of the chromatin modification machinery in carcinogenesis of clear cell carcinoma of the ovary (Review).Oncology letters · 2011Article
- A screen for conditional growth suppressor genes identifies the Drosophila homolog of HD-PTP as a regulator of the oncoprotein Yorkie.Developmental cell · 2011Article
- The chromatin-remodeling protein Osa interacts with CyclinE in Drosophila eye imaginal discs.Genetics · 2010Article
- Article
- Chapter 5. Nuclear actin-related proteins in epigenetic control.International review of cell and molecular biology · 2009Review
- Transcriptional regulation of the Drosophila moira and osa genes by the DREF pathway.Nucleic acids research · 2008Article
- Zebrafish brd2a and brd2b are paralogous members of the bromodomain-ET (BET) family of transcriptional coregulators that show structural and expression divergence.BMC developmental biology · 2008Article
- A suppressor screen in chlamydomonas identifies novel components of the retinoblastoma tumor suppressor pathway.Genetics · 2008Article
- dE2F2-independent rescue of proliferation in cells lacking an activator dE2F1.Molecular and cellular biology · 2007Article
- A genome-wide RNA interference screen identifies putative chromatin regulators essential for E2F repression.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The Trithorax group protein Lid is a trimethyl histone H3K4 demethylase required for dMyc-induced cell growth.Genes & development · 2007Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The activity of the E2F transcription factor is regulated in part by pRB, the protein product of the retinoblastoma tumor suppressor gene. Studies of tumor cells show that the p16(ink4a)/cdk4/cyclin D/pRB pathway is mutated in most forms of cancer, suggesting that the deregulation of E2F, and hence the cell cycle, is a common event in tumorigenesis. Extragenic mutations that enhance or suppress E2F activity are likely to alter cell-cycle control and may play a role in tumorigenesis. We used an E2F overexpression phenotype in the Drosophila eye to screen for modifiers of E2F activity. Coexpression of dE2F and its heterodimeric partner dDP in the fly eye induces S phases and cell death. We isolated 33 enhancer mutations of this phenotype by EMS and X-ray mutagenesis and by screening a deficiency library collection. The majority of these mutations sorted into six complementation groups, five of which have been identified as alleles of brahma (brm), moira (mor) osa, pointed (pnt), and polycephalon (poc). osa, brm, and mor encode proteins with homology to SWI1, SWI2, and SWI3, respectively, suggesting that the activity of a SWI/SNF chromatin-remodeling complex has an important impact on E2F-dependent phenotypes. Mutations in poc also suppress phenotypes caused by p21(CIP1) expression, indicating an important role for polycephalon 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.