ArticleLife science alliance2023
c-JUN is a barrier in hESC to cardiomyocyte transition.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Deletion of activating transcription factor 3 (Atf3) promotes cardiomyocyte differentiation from embryonic stem cells.Scientific reports · 2026Article
- Review
- In vitro mimicking of humanized cardiogenesis under porcine condition.Cell & bioscience · 2026Article
- Causality of atrial fibrillation and left atrial traits: Genetic and epigenetic perspectives.Heart rhythm O2 · 2026Article
- In Vivo Models of Cardiovascular Disease:Biomedicines · 2025Review
- The role of ASS1 in mouse embryonic stem cell differentiation into mesendoderm lineages.Stem cell research & therapy · 2025Article
- Plasticity of Gene Expression in Spaceflight and Postflight in Relation to Cardiovascular Disease: Mechanisms and Candidate Repurposed Drugs.Proteomics · 2025Article
- ModelingJournal of the American Heart Association · 2025Article
- c-JUN: a chromatin repressor that limits mesoderm differentiation in human pluripotent stem cells.Nucleic acids research · 2025Article
- Impact of c-JUN deficiency on thalamus development in mice and human neural models.Cell & bioscience · 2024Article
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- Integrated multi-omics analysis identifies features that predict human pluripotent stem cell-derived progenitor differentiation to cardiomyocytes.Journal of molecular and cellular cardiology · 2024Article
- A Study ofGenes · 2024Article
- Endogenous retroviral ERVH48-1 promotes human urine cell reprogramming.Cell regeneration (London, England) · 2024Article
- Noncoding RNA-associated competing endogenous RNA networks in trastuzumab-induced cardiotoxicity.Non-coding RNA research · 2024Article
- Distinct roles of COMPASS subunits to Drosophila heart development.Biology open · 2024Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of c-JUN leads to early mouse embryonic death, possibly because of a failure to develop a normal cardiac system. How c-JUN regulates human cardiomyocyte cell fate remains unknown. Here, we used the in vitro differentiation of human pluripotent stem cells into cardiomyocytes to study the role of c-JUN. Surprisingly, the knockout of c-JUN improved cardiomyocyte generation, as determined by the number of TNNT2+ cells. ATAC-seq data showed that the c-JUN defect led to increased chromatin accessibility on critical regulatory elements related to cardiomyocyte development. ChIP-seq data showed that the knockout c-JUN increased RBBP5 and SETD1B expression, leading to improved H3K4me3 deposition on key genes that regulate cardiogenesis. The c-JUN KO phenotype could be copied using the histone demethylase inhibitor CPI-455, which also up-regulated H3K4me3 levels and increased cardiomyocyte generation. Single-cell RNA-seq data defined three cell branches, and knockout c-JUN activated more regulons that are related to cardiogenesis. In summary, our data demonstrated that c-JUN could regulate cardiomyocyte cell fate by modulating H3K4me3 modification and chromatin accessibility and shed light on how c-JUN regulates heart development in humans.
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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.