ArticleCurrent biology : CB2011
Geminin escapes degradation in G1 of mouse pluripotent cells and mediates the expression of Oct4, Sox2, and Nanog.
Article in Current biology : CB, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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Who cites it
46 citing papers in PubMed, 68 citations in OpenAlex.
- CD8 T lymphocytes deploy embryonic cell cycle control mechanisms for rapid cell proliferation.EMBO reports · 2026Article
- Maintenance of genome integrity and active homologous recombination in embryonic stem cells.Experimental & molecular medicine · 2020Review
- Proteomic Changes of Porcine Oocytes After Vitrification and SubsequentFrontiers in cell and developmental biology · 2020Article
- Cycling to Meet Fate: Connecting Pluripotency to the Cell Cycle.Frontiers in cell and developmental biology · 2018Review
- Assisted reproductive technologies to prevent human mitochondrial disease transmission.Nature biotechnology · 2017Article
- Geminin deletion in pre-meiotic DNA replication stage causes spermatogenesis defect and infertility.The Journal of reproduction and development · 2017Article
- Mechanisms of pluripotency maintenance in mouse embryonic stem cells.Cellular and molecular life sciences : CMLS · 2017Review
- Dual roles of Akirin2 protein duringThe Journal of biological chemistry · 2017Article
- Geminin Is Essential for Pluripotent Cell Viability During Teratoma Formation, but Not for Differentiated Cell Viability During Teratoma Expansion.Stem cells and development · 2017Article
- Review
- Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability.Genes · 2016Review
- Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes.Nature communications · 2016Article
- Role of Geminin in cell fate determination of hematopoietic stem cells (HSCs).International journal of hematology · 2016Review
- Concise Review: Control of Cell Fate Through Cell Cycle and Pluripotency Networks.Stem cells (Dayton, Ohio) · 2016Review
- Insights into APC/C: from cellular function to diseases and therapeutics.Cell division · 2016Review
- Manipulation of Cell Cycle and Chromatin Configuration by Means of Cell-Penetrating Geminin.PloS one · 2016Article
- Overexpression of cyclin D1 induces the reprogramming of differentiated epidermal cells into stem cell-like cells.Cell cycle (Georgetown, Tex.) · 2016Article
- ZD7288, a blocker of the HCN channel family, increases doubling time of mouse embryonic stem cells and modulates differentiation outcomes in a context-dependent manner.SpringerPlus · 2016Article
- Growing an Embryo from a Single Cell: A Hurdle in Animal Life.Cold Spring Harbor perspectives in biology · 2015Review
- Human cytomegalovirus infection interferes with the maintenance and differentiation of trophoblast progenitor cells of the human placenta.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Geminin is an essential cell-cycle protein that is only present from S phase to early mitosis in metazoan somatic cells. Genetic ablation of geminin in the mouse results in preimplantation embryonic lethality because pluripotent cells fail to form and all cells differentiate to trophoblast. Here we show that geminin is present in G1 phase of mouse pluripotent cells in contrast to somatic cells, where anaphase-promoting complex/cyclosome (APC/C)-mediated proteasomal destruction removes geminin in G1. Silencing geminin directly or by depleting the APC/C inhibitor Emi1 causes loss of stem cell identity and trophoblast differentiation of mouse embryonal carcinoma and embryonic stem cells. Depletion of cyclins A2 or B1 does not induce this effect, even though both of these APC/C substrates are also present during G1 of pluripotent cells. Crucially, geminin antagonizes the chromatin-remodeling protein Brg1 to maintain expression of Oct4, Sox2, and Nanog. Our results define a pluripotency pathway by which suppressed APC/C activity protects geminin from degradation in G1, allowing sustained expression of core pluripotency factors. Collectively, these findings link the cell cycle to the pluripotent state but also raise an unexplained paradox: How is cell-cycle progression possible in pluripotent cells when oscillations of key regulatory proteins are lost?
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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.