ArticleThe Journal of biological chemistry2013
Dhrs3 protein attenuates retinoic acid signaling and is required for early embryonic patterning.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- The retinol-metabolizing enzyme DHRS3 coordinates antigen presentation, endothelial stability, and cholesterol metabolism to suppress hepatocellular carcinoma progression.The Journal of biological chemistry · 2026Article
- Retinoic Acid Receptor γ Activity Plays a Critical Role in Regulating Early Mouse Gastruloid Development.International journal of molecular sciences · 2026Article
- Identification of immunometabolism-associated genes and immune infiltration in sepsis-induced cardiomyopathy using integrated bioinformatics and machine learning approaches.The Journal of international medical research · 2025Article
- Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis.FEBS letters · 2025Article
- Wnt signalling facilitates neuronal differentiation of cochlear Frizzled10-positive cells in mouse cochlea via glypican 6 modulation.Cell communication and signaling : CCS · 2025Article
- Identification and characterization of short-chain dehydrogenase/reductase 3 (DHRS3) deficiency, a retinoic acid embryopathy of humans.Genetics in medicine open · 2025Article
- Human intestinal stromal cells promote homeostasis in normal mucosa but inflammation in Crohn's disease in a retinoic acid-deficient manner.Mucosal immunology · 2024Article
- Oncometabolite D-2-hydroxyglutarate-dependent metabolic reprogramming induces skeletal muscle atrophy during cancer cachexia.Communications biology · 2023Article
- In Vitro Transfection of Up-Regulated Genes Identified in Favorable-Outcome Neuroblastoma into Cell Lines.Cells · 2022Article
- Mechanisms of Feedback Regulation of Vitamin A Metabolism.Nutrients · 2022Review
- Enhanced Loss of Retinoic Acid Network Genes inCells · 2022Article
- Favored single nucleotide variants identified using whole genome Re-sequencing of Austrian and Chinese cattle breeds.Frontiers in genetics · 2022Article
- A virus-free cellular model recapitulates several features of severe COVID-19.Scientific reports · 2021Article
- Inhibition of retinoic acid receptor α phosphorylation represses the progression of triple-negative breast cancer via transactivating miR-3074-5p to target DHRS3.Journal of experimental & clinical cancer research : CR · 2021Article
- Retinoid signaling in skeletal development: Scoping the system for predictive toxicology.Reproductive toxicology (Elmsford, N.Y.) · 2021Review
- Retinoic Acid Fluctuation Activates an Uneven, Direction-Dependent Network-Wide Robustness Response in Early Embryogenesis.Frontiers in cell and developmental biology · 2021Article
- Spermatozoa induce transcriptomic alterations in bovine oviductal epithelial cells prior to initial contact.Journal of cell communication and signaling · 2020Article
- Role of carotenoids and retinoids during heart development.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- Retinoic Acid Organizes the Zebrafish Vagus Motor Topographic Map via Spatiotemporal Coordination of Hgf/Met Signaling.Developmental cell · 2020Article
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9 authors at 4 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
All-trans-retinoic acid (atRA) is an important morphogen involved in many developmental processes, including neural differentiation, body axis formation, and organogenesis. During early embryonic development, atRA is synthesized from all-trans-retinal (atRAL) in an irreversible reaction mainly catalyzed by retinal dehydrogenase 2 (aldh1a2), whereas atRAL is converted from all-trans-retinol via reversible oxidation by retinol dehydrogenases, members of the short-chain dehydrogenase/reductase family. atRA is degraded by cytochrome P450, family 26 (cyp26). We have previously identified a short-chain dehydrogenase/reductase 3 (dhrs3), which showed differential expression patterns in Xenopus embryos. We show here that the expression of dhrs3 was induced by atRA treatment and overexpression of Xenopus nodal related 1 (xnr1) in animal cap assay. Overexpression of dhrs3 enhanced the phenotype of excessive cyp26a1. In embryos overexpressing aldh1a2 or retinol dehydrogenase 10 (rdh10) in the presence of their respective substrates, Dhrs3 counteracted the action of Aldh1a2 or Rdh10, indicating that retinoic acid signaling is attenuated. Knockdown of Dhrs3 by antisense morpholino oligonucleotides resulted in a phenotype of shortened anteroposterior axis, reduced head structure, and perturbed somitogenesis, which were also found in embryos treated with an excess of atRA. Examination of the expression of brachyury, not, goosecoid, and papc indicated that convergent extension movement was defective in Dhrs3 morphants. Taken together, these studies suggest that dhrs3 participates in atRA metabolism by reducing atRAL levels and is required for proper anteroposterior axis formation, neuroectoderm patterning, and somitogenesis.
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