ArticleMolecules and cells2014
Developmental roles of D-bifunctional protein-A zebrafish model of peroxisome dysfunction.
Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Modelling Peroxisomal Disorders in Zebrafish.Cells · 2025Review
- Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria, mTOR, and autophagy.Cellular and molecular life sciences : CMLS · 2023Article
- Insights Into the Peroxisomal Protein Inventory of Zebrafish.Frontiers in physiology · 2022Article
- Emerging cellular themes in leukodystrophies.Frontiers in cell and developmental biology · 2022Review
- Metabolic etiologies in West syndrome.Epilepsia open · 2018Review
- The fatty acid chain elongase, Elovl1, is required for kidney and swim bladder development during zebrafish embryogenesis.Organogenesis · 2016Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The peroxisome is an intracellular organelle that responds dynamically to environmental changes. Various model organisms have been used to study the roles of peroxisomal proteins in maintaining cellular homeostasis. By taking advantage of the zebrafish model whose early stage of embryogenesis is dependent on yolk components, we examined the developmental roles of the D-bifunctional protein (Dbp), an essential enzyme in the peroxisomal β-oxidation. The knockdown of dbp in zebrafish phenocopied clinical manifestations of its deficiency in human, including defective craniofacial morphogenesis, growth retardation, and abnormal neuronal development. Overexpression of murine Dbp rescued the morphological phenotypes induced by dbp knockdown, indicative of conserved roles of Dbp during zebrafish and mammalian development. Knockdown of dbp impaired normal development of blood, blood vessels, and most strikingly, endoderm-derived organs including the liver and pancreas - a phenotype not reported elsewhere in connection with peroxisome dysfunction. Taken together, our results demonstrate for the first time that zebrafish might be a useful model animal to study the role of peroxisomes during vertebrate development.
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Registered trials
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