ArticleThe Journal of biological chemistry2013
Smad2 is essential for maintenance of the human and mouse primed pluripotent stem cell state.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Molecular Mechanisms Underlying Pluripotency and Self-Renewal of Embryonic Stem Cells.International journal of molecular sciences · 2023Pooled it
- TGFβ-dependent upregulation of OCIAD2 is essential for epithelial-to-mesenchymal transition during mesendoderm differentiation.Stem cell reports · 2026Article
- SMAD2 linker phosphorylation impacts overall survival, proliferation, TGFβ1-dependent gene expression and pluripotency-related proteins in NSCLC.British journal of cancer · 2025Article
- The regulatory architecture of the primed pluripotent cell state.Nature communications · 2025Article
- ModelingJournal of the American Heart Association · 2025Article
- TGFβ family signaling in human stem cell self-renewal and differentiation.Cell regeneration (London, England) · 2024Review
- Discovering genes and microRNAs involved in human lung development unveils IGFBP3/miR-34a dynamics and their relevance for alveolar differentiation.Stem cell research & therapy · 2024Article
- A single cell-based computational platform to identify chemical compounds targeting desired sets of transcription factors for cellular conversion.Stem cell reports · 2023Article
- Stabilization of hESCs in two distinct substates along the continuum of pluripotency.iScience · 2022Article
- Expression and Polymorphisms ofGenes · 2022Article
- PI3Kβ-regulated β-catenin mediates EZH2 removal from promoters controlling primed human ESC stemness and primitive streak gene expression.Stem cell reports · 2022Article
- Tanshinone IIA enhances the ovarian reserve and attenuates ovarian oxidative stress in aged mice.Veterinary medicine and science · 2022Article
- Smurf2-induced degradation of SMAD2 causes inhibition of hair follicle stem cell differentiation.Cell death discovery · 2022Article
- Dynamic Transcriptome Profiling Reveals LncRNA-Centred Regulatory Networks in the Modulation of Pluripotency.Frontiers in cell and developmental biology · 2022Article
- [Identification of potential regulatory genes for embryonic stem cell self-renewal and pluripotency by random forest].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Construction and characterization of EGFP reporter plasmid harboring putative human RAX promoter for in vitro monitoring of retinal progenitor cells identity.BMC molecular and cell biology · 2021Article
- Role of bone morphogenetic protein signaling in bovine early embryonic development and stage specific embryotropic actions of follistatin†.Biology of reproduction · 2020Article
- The Role of SMAD2/3 in Human Embryonic Stem Cells.Frontiers in cell and developmental biology · 2020Review
- TGF-beta and TNF-alpha cooperatively induce mesenchymal transition of lymphatic endothelial cells via activation of Activin signals.PloS one · 2020Article
- Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Human embryonic stem cells and mouse epiblast stem cells represent a primed pluripotent stem cell state that requires TGF-β/activin signaling. TGF-β and/or activin are commonly thought to regulate transcription through both Smad2 and Smad3. However, the different contributions of these two Smads to primed pluripotency and the downstream events that they may regulate remain poorly understood. We addressed the individual roles of Smad2 and Smad3 in the maintenance of primed pluripotency. We found that Smad2, but not Smad3, is required to maintain the undifferentiated pluripotent state. We defined a Smad2 regulatory circuit in human embryonic stem cells and mouse epiblast stem cells, in which Smad2 acts through binding to regulatory promoter sequences to activate Nanog expression while in parallel repressing autocrine bone morphogenetic protein signaling. Increased autocrine bone morphogenetic protein signaling caused by Smad2 down-regulation leads to cell differentiation toward the trophectoderm, mesoderm, and germ cell lineages. Additionally, induction of Cdx2 expression, as a result of decreased Smad2 expression, leads to repression of Oct4 expression, which, together with the decreased Nanog expression, accelerates the loss of pluripotency. These findings reveal that Smad2 is a unique integrator of transcription and signaling events and is essential for the maintenance of the mouse and human primed pluripotent stem cell state.
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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.