ArticleCell cycle (Georgetown, Tex.)2010
pRB and E2F4 play distinct cell-intrinsic roles in fetal erythropoiesis.
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 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- C2H2 Zinc Finger Transcription Factors Associated with Hemoglobinopathies.Journal of molecular biology · 2024Review
- Phenotypic and proteomic characterization of the human erythroid progenitor continuum reveal dynamic changes in cell cycle and in metabolic pathways.American journal of hematology · 2024Article
- Functional interrelationship between TFII-I and E2F transcription factors at specific cell cycle gene loci.Journal of cellular biochemistry · 2018Article
- Revealing the action mechanisms of dexamethasone on the birth weight of infant using RNA-sequencing data of trophoblast cells.Medicine · 2018Article
- Interaction of the Macrophage and Primitive Erythroid Lineages in the Mammalian Embryo.Frontiers in immunology · 2016Review
- E2F8 as a Novel Therapeutic Target for Lung Cancer.Journal of the National Cancer Institute · 2015Article
- Aberrant splicing of U12-type introns is the hallmark of ZRSR2 mutant myelodysplastic syndrome.Nature communications · 2015Article
- Cytotoxicity of quantum dots and graphene oxide to erythroid cells and macrophages.Nanoscale research letters · 2013Article
- Hepatitis C virus-related hepatocellular carcinoma: An insight into molecular mechanisms and therapeutic strategies.World journal of hepatology · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The retinoblastoma tumor suppressor protein pRB functions, at least in part, by directly binding to and modulating the activity of the E2F transcription factors. Previous studies have shown that both E2F4 and pRB play important roles in fetal erythropoiesis. Given that these two proteins interact directly we investigated the overlap of E2F4 and pRB function in this process by analyzing E2f4(-/-), conditional Rb knockout (Rb(1lox/1lox)), and compound E2f4(-/-);Rb(1lox/1lox) embryos. At E15.5 E2f4(-/-) and Rb(1lox/1lox) fetal erythroid cells display distinct abnormalities in their differentiation profiles. When cultured in vitro, both E2f4(-/-) and Rb(1lox/1lox) erythroid cells show defects in cell cycle progression. Surprisingly, analysis of cell cycle profiling suggests that E2F4 and pRB control cell cycle exit through different mechanisms. Moreover, only pRB, but not E2F4, promotes cell survival in erythroid cells. We observed an additive rather than a synergistic impact upon the erythroid defects in the compound E2f4(-/-);Rb(1lox/1lox) embryos. We further found that fetal liver macrophage development is largely normal regardless of genotype. Taken together, our results show that E2F4 and pRB play independent cell-intrinsic roles in fetal erythropoiesis.
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