ArticleStem cells and development2013
Geminin promotes an epithelial-to-mesenchymal transition in an embryonic stem cell model of gastrulation.
Article in Stem cells and development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting AXL and RAGE to prevent geminin overexpression-induced triple-negative breast cancer metastasis.Scientific reports · 2019Article
- Epithelial-mesenchymal transition (EMT): A biological process in the development, stem cell differentiation, and tumorigenesis.Journal of cellular physiology · 2017Review
- 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
- Site-specific Disruption of the Oct4/Sox2 Protein Interaction Reveals Coordinated Mesendodermal Differentiation and the Epithelial-Mesenchymal Transition.The Journal of biological chemistry · 2016Article
- Geminin restrains mesendodermal fate acquisition of embryonic stem cells and is associated with antagonism of Wnt signaling and enhanced polycomb-mediated repression.Stem cells (Dayton, Ohio) · 2013Article
- DNA Replication Inhibitor Geminin and Retinoic Acid Signaling Participate in Complex Interactions Associated With Pluripotency.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Geminin is a nuclear protein that performs the related functions of modulating cell cycle progression by binding Cdt1, and controlling differentiation by binding transcription factors. Since embryonic stem cells (ESC) and the epiblast share a similar gene expression profile and an attenuated cell cycle, ESC form an accessible and tractable model system to study lineage choice at gastrulation. We derived several ESC lines in which Geminin can be inducibly expressed, and employed short hairpin RNAs targeting Geminin. As in the embryo, a lack of Geminin protein resulted in DNA damage and cell death. In monolayer culture, in defined medium, Geminin supported neural differentiation; however, in three-dimensional culture, overexpression of Geminin promoted mesendodermal differentiation and epithelial-to-mesenchymal transition. In vitro, ESC overexpressing Geminin rapidly recolonized a wound, downregulated E-cadherin expression, and activated Wnt signaling. We suggest that Geminin may promote differentiation via binding Groucho/TLE proteins and upregulating canonical Wnt signaling.
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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.