ArticleHaematologica2025
Rnf111 has a pivotal role in regulating development of definitive hematopoietic stem and progenitor cells through the Smad2/3-Gcsfr/NO axis in zebrafish.
Article in Haematologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Neighboring Gulf Killifish (Ecology and evolution · 2026Article
- Arkadia: a new player in hematopoietic stem and progenitor cell development.Haematologica · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
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12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The ubiquitination or SUMOylation of hematopoietic-related factors plays pivotal roles in hematopoiesis. RNF111, known as a ubiquitin ligase, is a newly discovered SUMO-targeted ubiquitin ligase involved in multiple signaling pathways mediated by transforming growth factor (TGF)-β family members. However, its role in hematopoiesis remains unclear. Herein, a heritable Rnf111 mutant zebrafish line was generated by CRISPR/Cas9-mediated genome editing. Impairment of hematopoietic stem and progenitor cells (HSPC) of definitive hematopoiesis was found in Rnf111-deficient mutants. Ablation of Rnf111 resulted in decreased phosphorylation of Smad2/3 in HSPC. Definitive endoderm 2 inducer (IDE2), which specifically activates TGF-β signaling and downstream Smad2 phosphorylation, could restore definitive hematopoiesis in Rnf111-deficient embryos. Further molecular mechanism studies revealed that Gcsfr/NO signaling was an important target pathway of Smad2/3 involved in Rnf111-mediated HSPC development. In conclusion, our study demonstrated that Rnf111 contributes to the development of HSPC by maintaining Smad2/3 phosphorylation and activation of the Gcsfr/NO signaling pathway.
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Registered trials
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