ArticleProceedings of the National Academy of Sciences of the United States of America2009
Mutation of p107 exacerbates the consequences of Rb loss in embryonic tissues and causes cardiac and blood vessel defects.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The Tumor Suppressor p53 Downregulates p107 (International journal of molecular sciences · 2025Article
- Endothelial deletion of Ino80 disrupts coronary angiogenesis and causes congenital heart disease.Nature communications · 2018Article
- The p53 family members have distinct roles during mammalian embryonic development.Cell death and differentiation · 2017Article
- Transcriptional control of stem cell fate by E2Fs and pocket proteins.Frontiers in genetics · 2015Review
- Repression by RB1 characterizes genes involved in the penultimate stage of erythroid development.Cell cycle (Georgetown, Tex.) · 2015Article
- Loss of pRB and p107 disrupts cartilage development and promotes enchondroma formation.Oncogene · 2013Article
- Pocket proteins critically regulate cell cycle exit of the trabecular myocardium and the ventricular conduction system.Biology open · 2013Article
- miR than meets the eye.Genes & development · 2011Article
- Article
- G1 arrest and differentiation can occur independently of Rb family function.The Journal of cell biology · 2010Article
- Tandem E2F binding sites in the promoter of the p107 cell cycle regulator control p107 expression and its cellular functions.PLoS genetics · 2010Article
- p107 in the public eye: an Rb understudy and more.Cell division · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The retinoblastoma tumor-suppressor protein, pRb, is a member of the pocket protein family that includes p107 and p130. These proteins have well-defined roles in regulating entry into and exit from the cell cycle and also have cell cycle-independent roles in facilitating differentiation. Here we investigate the overlap between pocket protein's function during embryonic development by using conditional mutant alleles to generate Rb;p107 double-mutant embryos (DKOs) that develop in the absence of placental defects. These DKOs die between e13.5 and e14.5, much earlier than either the conditional Rb or the germline p107 single mutants, which survive to birth or are largely viable, respectively. Analyses of the e13.5 DKOs shows that p107 mutation exacerbates the phenotypes resulting from pRb loss in the central nervous system and lens, but not in the peripheral nervous system. In addition, these embryos exhibit novel phenotypes, including increased proliferation of blood vessel endothelial cells, and heart defects, including double-outlet right ventricle (DORV). The DORV is caused, at least in part, by a defect in blood vessel endothelial cells and/or heart mesenchymal cells. These findings demonstrate novel, overlapping functions for pRb and p107 in numerous murine tissues.
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Registered trials
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