ArticleFundamental research2025
PIAS4 regulates pluripotency exit and cell fate commitment in porcine embryonic stem cells.
Article in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- RGTBind: RBF-gate graph transformer with spatially biased attention for protein-DNA binding-site prediction.Journal of molecular modeling · 2026Article
- CRISPR Screening Reveals a Novel Role for FOXH1 in Regulating Pluripotency of Porcine Embryonic Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-translational modifications (PTMs) are dynamic processes that regulate cell states by enhancing proteome diversity. However, the overall impact of PTMs on pluripotency exit in porcine embryonic stem cells (pESCs) remains largely unknown. Here, we present a systematic assay to identify E3 ubiquitin ligases for pluripotency exit by using CRISPR/Cas9 pooled screening and identified PIAS4 as a major regulator of pluripotency exit, as the cell differentiation was significantly impaired upon PIAS4 depletion in pESCs. PIAS4 shows a high degree of genomic occupation in promoter regions, particularly in key pluripotency maintenance genes. Moreover, we found that PIAS4 was recruited to the gene promoter marked by H3K4me3 and interacted with lysine demethylase KDM5B via SUMOylation, thereby affecting the stability of KDM5B and further facilitating the regulation of H3K4me3-mediated lineage-specific genes. Together, our findings reveal a regulatory mechanism by which PIAS4 modulates H3K4me3 modification on development-related genes, subsequently influencing pluripotency exit and cell fate commitment by interacting with KDM5B in pESCs.
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