ArticleCell death & disease2021
The endoribonuclease N4BP1 prevents psoriasis by controlling both keratinocytes proliferation and neutrophil infiltration.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- N4BP1 uses tandem KH domains to associate with EDC4 and mRNA decapping factors in P-bodies.Communications biology · 2026Article
- Identification of UBE2T as a novel diagnostic biomarker of psoriasis and proliferating UBE2T+ Keratinocyte in psoriasis.Journal of translational medicine · 2026Article
- N4BP1 is essential for the development of oral cancer via controlling both cancer cells and immune microenvironment.Cell death & disease · 2026Article
- N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Dual role of N4BP1 in neutrophil-epithelial crosstalk in periodontitis.Frontiers in immunology · 2026Article
- Enteroviral 3C protease cleaves N4BP1 to impair the host inflammatory response.Journal of virology · 2025Article
- Trifolirhizin improves the hyperproliferation and excessive inflammatory response in human HaCaT keratinocytes and ameliorates skin lesions in psoriasis-like mouse models.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Article
- N4BP1 coordinates ubiquitin-dependent crosstalk within the IκB kinase family to limit Toll-like receptor signaling and inflammation.Immunity · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- Alendronate augments lipid A‑induced IL‑1β release by ASC‑deficient RAW264 cells via AP‑1 activation.Experimental and therapeutic medicine · 2023Article
- N4BP1 mediates RAM domain-dependent notch signaling turnover during neocortical development.The EMBO journal · 2023Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a common chronic skin disease, characterized by abnormal interplay between hyperproliferative epidermal keratinocytes and self-reactive immune cells with not fully addressed molecular mechanism. N4BP1 (NEDD4-binding protein 1) is considered as an immune regulator for a long time but its physiological role is not determined yet. Here, we found that the expression of N4BP1 in skin was highest among all 54 tested tissues, and its expression was further upregulated in psoriatic skin. N4BP1-deficient mice exhibited normal grossly, but developed severe and prolonged IMQ-induced psoriasis-like disease comparing to controls. N4BP1 mainly expressed in keratinocytes and located on nucleus. Up- but not downregulated genes in N4BP1-deficient skin were specifically enriched in keratinocyte proliferation and differentiation. The proliferation of N4BP1-deficient primary keratinocytes was faster compared to that of controls. The upregulated genes upon ablation of N4BP1 were highly enriched in targets of AP-1 transcription factor. Knocking out N4BP1 resulted in upregulation of JunB and FosB, and conversely, overexpression of N4BP1 greatly reduced their expression. Furthermore, N4BP1 binds with JunB and FosB encoding mRNAs and greatly reduces their stability. In addition, with a high expression in neutrophils, N4BP1 limits survival of neutrophils in blood and infiltration of neutrophils in psoriatic skin by targeting CXCL1, CCL20, and S100A8. These findings demonstrate that N4BP1 controls the proper function of keratinocytes and neutrophils by negatively regulating JunB, FosB, and CXCL1, respectively, and that is critical for psoriasis prevention.
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