ArticleDevelopmental biology2009
E2F4 cooperates with pRB in the development of extra-embryonic tissues.
Article in Developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 0 citations in OpenAlex.
- E2F4DN Transgenic Mice: A Tool for the Evaluation of E2F4 as a Therapeutic Target in Neuropathology and Brain Aging.International journal of molecular sciences · 2022Review
- Revealing the action mechanisms of dexamethasone on the birth weight of infant using RNA-sequencing data of trophoblast cells.Medicine · 2018Article
- Silencing of E2F3 suppresses tumor growth of Her2+ breast cancer cells by restricting mitosis.Oncotarget · 2015Article
- Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.Molecular and cellular biology · 2014Article
- E2F activators signal and maintain centrosome amplification in breast cancer cells.Molecular and cellular biology · 2014Article
- Concomitant inactivation of Rb and E2f8 in hematopoietic stem cells synergizes to induce severe anemia.Blood · 2012Article
- pRB and E2F4 play distinct cell-intrinsic roles in fetal erythropoiesis.Cell cycle (Georgetown, Tex.) · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma gene, RB-1, was the first identified tumor suppressor. Rb(-/-) mice die in mid-gestation with defects in proliferation, differentiation and apoptosis. The activating E2F transcription factors, E2F1-3, contribute to these embryonic defects, indicating that they are key downstream targets of the retinoblastoma protein, pRB. E2F4 is the major pRB-associated E2F in vivo, yet its role in Rb(-/-) embryos is unknown. Here we establish that E2f4 deficiency reduced the lifespan of Rb(-/-) embryos by exacerbating the Rb mutant placental defect. We further show that this reflects the accumulation of trophectoderm-like cells in both Rb and Rb;E2f4 mutant placentas. Thus, Rb and E2f4 play cooperative roles in placental development. We used a conditional mouse model to allow Rb(-/-);E2f4(-/-) embryos to develop in the presence of Rb wild-type placentas. Under these conditions, Rb(-/-);E2f4(-/-) mutants survived to birth. These Rb(-/-);E2f4(-/-) embryos exhibited all of the defects characteristic of the Rb and E2f4 single mutants and had no novel defects. Taken together, our data show that pRB and E2F4 cooperate in placental development, but play largely non-overlapping roles in the development of many embryonic tissues.
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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.