ArticleCell cycle (Georgetown, Tex.)2010
Disruption of calvarial ossification in E2f4 mutant embryos correlates with increased proliferation and progenitor cell populations.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Transglutaminase 2 regulates terminal erythroid differentiation via cross-linking activity.Frontiers in cell and developmental biology · 2023Article
- E2F8 as a Novel Therapeutic Target for Lung Cancer.Journal of the National Cancer Institute · 2015Article
- BCL11B expression in intramembranous osteogenesis during murine craniofacial suture development.Gene expression patterns : GEP · 2015Article
- Latent transforming growth factor β-binding protein 4 is downregulated in esophageal cancer via promoter methylation.PloS one · 2013Article
- Tissue-specific gene targeting by the multiprotein mammalian DREAM complex.The Journal of biological chemistry · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The E2F family of transcription factors, in association with pocket protein family members, are important for regulating genes required for cellular proliferation. The most abundant E2F, E2F4, is implicated in maintaining the G(0)/G(1) cell cycle state via transcriptional repression of genes that encode proteins required for S-phase progression. Here, we investigate E2F4's role in bone development using E2f4 germline mutant mice. We find that mutation of E2f4 impairs the formation of several bones that arise through intramembranous or endochondral ossification. The most severe defect occurred in the calvarial bones of the skull where we observed a striking delay in their ossification. In vivo and in vitro analyses established that E2F4 loss did not block the intrinsic differentiation potential of calvarial osteoblast progenitors. However, our data showed that E2f4 mutation elevated proliferation in the developing calvaria in vivo and it increased the endogenous pool of undifferentiated progenitor cells. These data suggest that E2F4 plays an important role in enabling osteoblast progenitors to exit the cell cycle and subsequently differentiate thereby contributing to the commitment of these cells to the bone lineage.
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Registered trials
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