ArticleDisease models & mechanisms2014
Heme acts through the Bach1b/Nrf2a-MafK pathway to regulate exocrine peptidase precursor genes in porphyric zebrafish.
Article in Disease models & mechanisms, 2014. 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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12 citing papers in PubMed, 24 citations in OpenAlex.
- Time-series single-cell transcriptomics reveals pervasive daily rhythmicity and nocturnal spermatogenesis in the zebrafish testis.Science advances · 2026Article
- Multi-endpoint assessment of tunnel wash water and tyre-particle leachate in zebrafish larvae.Toxicology reports · 2025Article
- Acute anxiogenic effect of lisdexamphetamine dimesylate in zebrafish: implications of off-label cognitive enhancement use.Toxicology research · 2025Article
- A miR-219-5p-bmal1b negative feedback loop contributes to circadian regulation in zebrafish.Communications biology · 2024Article
- Gene Characterization of Nocturnin Paralogues in Goldfish: Full Coding Sequences, Structure, Phylogeny and Tissue Expression.International journal of molecular sciences · 2023Article
- BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression.Life science alliance · 2020Article
- Hepcidin protects against iron overload-induced inhibition of bone formation in zebrafish.Fish physiology and biochemistry · 2019Article
- Redox stress and signaling during vertebrate embryonic development: Regulation and responses.Seminars in cell & developmental biology · 2018Review
- The Transcription Factor Bach1 Suppresses the Developmental Angiogenesis of Zebrafish.Oxidative medicine and cellular longevity · 2017Article
- Article
- Nrf2 and Nrf2-related proteins in development and developmental toxicity: Insights from studies in zebrafish (Danio rerio).Free radical biology & medicine · 2015Review
- Spotlight on zebrafish: translational impact.Disease models & mechanisms · 2014Article
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8 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Using a zebrafish model of hepatoerythropoietic porphyria (HEP), we identify a previously unknown mechanism underlying heme-mediated regulation of exocrine zymogens. Zebrafish bach1b, nrf2a and mafK are all expressed in the zebrafish exocrine pancreas. Overexpression of bach1b or knockdown of nrf2a result in the downregulation of the expression of the exocrine zymogens, whereas overexpression of nrf2a or knockdown of bach1b cause their upregulation. In vitro luciferase assays demonstrate that heme activates the zymogens in a dosage-dependent manner and that the zymogen promoter activities require the integral Maf recognition element (MARE) motif. The Bach1b-MafK heterodimer represses the zymogen promoters, whereas the Nrf2a-MafK heterodimer activates them. Furthermore, chromatin immunoprecipitation (ChIP) assays show that MafK binds to the MARE sites in the 5' regulatory regions of the zymogens. Taken together, these data indicate that heme stimulates the exchange of Bach1b for Nrf2a at MafK-occupied MARE sites and that, particularly in heme-deficient porphyria, the repressive Bach1b-MafK heterodimer dominates, which can be exchanged for the activating Nrf2a-MafK heterodimer upon treatment with hemin. These results provide novel insights into the regulation of exocrine function, as well as the pathogenesis of porphyria, and should be useful for designing new therapies for both types of disease.
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