ArticleDevelopmental biology2013
The EJC component Magoh regulates proliferation and expansion of neural crest-derived melanocytes.
Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 39 citations in OpenAlex.
- The Role of Splicing Machinery as a Promising Potential Therapeutic Target for Pituitary Neuroendocrine Tumors (PitNETs).Cancers · 2026Review
- Identification of a genetic locus responsible for the dominant white-spotting coat phenotype in mice spontaneously isolated from a Japanese wild-derived inbred strain.The Journal of veterinary medical science · 2026Article
- Pan-cancer analysis of oncogenic role of MAGOH and experiment validation in hepatocellular carcinoma.Scientific reports · 2025Article
- Transcriptomic Analyses of Brains of RBM8A Conditional Knockout Mice at Different Developmental Stages Reveal Conserved Signaling Pathways Contributing to Neurodevelopmental Diseases.International journal of molecular sciences · 2023Article
- The paralogues MAGOH and MAGOHB are oncogenic factors in high-grade gliomas and safeguard the splicing of cell division and cell cycle genes.RNA biology · 2023Article
- Article
- Diverse Roles of the Exon Junction Complex Factors in the Cell Cycle, Cancer, and Neurodevelopmental Disorders-Potential for Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Global ubiquitinome profiling identifies NEDD4 as a regulator of Profilin 1 and actin remodelling in neural crest cells.Nature communications · 2022Article
- Review
- The increasing expression of GPX7 related to the malignant clinical features leading to poor prognosis of glioma patients.Chinese neurosurgical journal · 2021Article
- Full function of exon junction complex factor, Rbm8a, is critical for interneuron development.Translational psychiatry · 2020Article
- The EJC component Magoh in non-vertebrate chordates.Development genes and evolution · 2020Article
- Zebrafish rbm8a and magoh mutants reveal EJC developmental functions and new 3'UTR intron-containing NMD targets.PLoS genetics · 2020Article
- The exon junction complex is required for stem and progenitor cell maintenance in planarians.Developmental biology · 2020Article
- Exon junction complex (EJC) core genes play multiple developmental roles in Physalis floridana.Plant molecular biology · 2018Article
- Systems analysis identifies melanoma-enriched pro-oncogenic networks controlled by the RNA binding protein CELF1.Nature communications · 2017Article
- EIF4A3 deficient human iPSCs and mouse models demonstrate neural crest defects that underlie Richieri-Costa-Pereira syndrome.Human molecular genetics · 2017Article
- Mouse models of Casc3 reveal developmental functions distinct from other components of the exon junction complex.RNA (New York, N.Y.) · 2017Article
- The exon junction complex in neural development and neurodevelopmental disease.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2016Review
- The RNA-binding profile of Acinus, a peripheral component of the exon junction complex, reveals its role in splicing regulation.RNA (New York, N.Y.) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Melanoblasts are a population of neural crest-derived cells that generate the pigment-producing cells of our body. Defective melanoblast development and function underlies many disorders including Waardenburg syndrome and melanoma. Understanding the genetic regulation of melanoblast development will help elucidate the etiology of these and other neurocristopathies. Here we demonstrate that Magoh, a component of the exon junction complex, is required for normal melanoblast development. Magoh haploinsufficient mice are hypopigmented and exhibit robust genetic interactions with the transcription factor, Sox10. These phenotypes are caused by a marked reduction in melanoblast number beginning at mid-embryogenesis. Strikingly, while Magoh haploinsufficiency severely reduces epidermal melanoblasts, it does not significantly affect the number of dermal melanoblasts. These data indicate Magoh impacts melanoblast development by disproportionately affecting expansion of epidermal melanoblast populations. We probed the cellular basis for melanoblast reduction and discovered that Magoh mutant melanoblasts do not undergo increased apoptosis, but instead are arrested in mitosis. Mitotic arrest is evident in both Magoh haploinsufficient embryos and in Magoh siRNA treated melanoma cell lines. Together our findings indicate that Magoh-regulated proliferation of melanoblasts in the dermis may be critical for production of epidermally-bound melanoblasts. Our results point to a central role for Magoh in melanocyte development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.