ArticleCell proliferation2023
BCL2 is a major regulator of haploidy maintenance in murine embryonic stem cells.
Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Metabolic Imbalance Triggers Adaptive Remodeling to Accelerate Diploidization in Murine Haploid Embryonic Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial metabolic imbalance drives diploidization in mouse haploid embryonic stem cells via NADPH overload.Nature communications · 2026Article
- Genetic Screening of Haploid Neural Stem Cells Reveals that Nfkbia and Atp2b4 are Key Regulators of Oxidative Stress in Neural Precursors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Development and application of haploid embryonic stem cells.Stem cell research & therapy · 2024Review
- BCL2 is a major regulator of haploidy maintenance in murine embryonic stem cells.Cell proliferation · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Mammalian haploid cells are important resources for forward genetic screening and are important in genetic medicine and drug development. However, the self-diploidization of murine haploid embryonic stem cells (haESCs) during daily culture or differentiation jeopardizes their use in genetic approaches. Here, we show that overexpression (OE) of an antiapoptosis gene, BCL2, in haESCs robustly ensures their haploidy maintenance in various situations, even under strict differentiation in vivo (embryonic 10.5 chimeric fetus or 21-day teratoma). Haploid cell lines of many lineages, including epiblasts, trophectodermal lineages, and neuroectodermal lineages, can be easily derived by the differentiation of BCL2-OE haESCs in vitro. Transcriptome analysis revealed that BCL2-OE activates another regulatory gene, Has2, which is also sufficient for haploidy maintenance. Together, our findings provide an effective and secure strategy to reduce diploidization during differentiation, which will contribute to the generation of haploid cell lines of the desired lineage and related genetic screening.
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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.