ArticleEMBO reports2024
PRAMEL7 and CUL2 decrease NuRD stability to establish ground-state pluripotency.
Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- CtBP1/2 restrict DUX-dependent and independent 2C-like programs in mouse embryonic stem cells.EMBO reports · 2026Article
- PRAMEL12 orchestrates spermiogenesis to ensure male fertility in mice.The Journal of biological chemistry · 2026Article
- CUL2 confers ferroptosis resistance in pancreatic cancer by disrupting KEAP1-mediated NRF2 degradation.Cancer cell international · 2025Article
- An RNA-dependent and phase-separated active subnuclear compartment safeguards repressive chromatin domains.Molecular cell · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Pluripotency is established in E4.5 preimplantation epiblast. Embryonic stem cells (ESCs) represent the immortalization of pluripotency, however, their gene expression signature only partially resembles that of developmental ground-state. Induced PRAMEL7 expression, a protein highly expressed in the ICM but lowly expressed in ESCs, reprograms developmentally advanced ESC+serum into ground-state pluripotency by inducing a gene expression signature close to developmental ground-state. However, how PRAMEL7 reprograms gene expression remains elusive. Here we show that PRAMEL7 associates with Cullin2 (CUL2) and this interaction is required to establish ground-state gene expression. PRAMEL7 recruits CUL2 to chromatin and targets regulators of repressive chromatin, including the NuRD complex, for proteasomal degradation. PRAMEL7 antagonizes NuRD-mediated repression of genes implicated in pluripotency by decreasing NuRD stability and promoter association in a CUL2-dependent manner. Our data link proteasome degradation pathways to ground-state gene expression, offering insights to generate in vitro models to reproduce the in vivo ground-state pluripotency.
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Registered trials
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