ArticleGenesis (New York, N.Y. : 2000)2014
Generation of a Magoh conditional allele in mice.
Article in Genesis (New York, N.Y. : 2000), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Impaired cortical development and translational control in a missense mouse model of DDX3X syndrome.Disease models & mechanisms · 2025Article
- Interneuron migration impairment and brain region-specific DNA damage response following irradiation during early neurogenesis in mice.Cellular and molecular life sciences : CMLS · 2025Article
- The RNA-binding protein EIF4A3 promotes axon development by direct control of the cytoskeleton.Cell reports · 2024Article
- Significance of an altered lncRNA landscape in schizophrenia and cognition: clues from a case-control association study.European archives of psychiatry and clinical neuroscience · 2023Article
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
- Genes for RNA-binding proteins involved in neural-specific functions and diseases are downregulated in Rubinstein-Taybi iNeurons.Neural regeneration research · 2022Article
- Exon junction complex dependent mRNA localization is linked to centrosome organization during ciliogenesis.Nature communications · 2021Article
- Dosage-dependent requirements ofDevelopment (Cambridge, England) · 2020Article
- RNA on the brain: emerging layers of post-transcriptional regulation in cerebral cortex development.Wiley interdisciplinary reviews. Developmental biology · 2018Review
- 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
- ATR maintains chromosomal integrity during postnatal cerebellar neurogenesis and is required for medulloblastoma formation.Development (Cambridge, England) · 2016Article
- Haploinsufficiency for Core Exon Junction Complex Components Disrupts Embryonic Neurogenesis and Causes p53-Mediated Microcephaly.PLoS genetics · 2016Article
- Article
- A critical role of RBM8a in proliferation and differentiation of embryonic neural progenitors.Neural development · 2015Article
- Rbm8a haploinsufficiency disrupts embryonic cortical development resulting in microcephaly.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Post-transcriptional regulation in corticogenesis: how RNA-binding proteins help build the brain.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Magoh encodes a core component of the exon junction complex (EJC), which binds mRNA and regulates mRNA metabolism. Magoh is highly expressed in proliferative tissues during development. EJC components have been implicated in several developmental disorders including TAR syndrome, Richieri-Costa-Pereira syndrome, and intellectual disability. Existing germline null Magoh mice are embryonic lethal as homozygotes and perinatal lethal as heterozygotes, precluding detailed analysis of embryonic and postnatal functions. Here, we report the generation of a new genetic tool to dissect temporal and tissue-specific roles for Magoh in development and adult homeostasis. This Magoh conditional allele has two loxP sites flanking the second exon. Ubiquitous Cre-mediated deletion of the floxed allele in a heterozygous mouse (Magoh(del/+) ) causes 50% reduction of both Magoh mRNA and protein. Magoh(del/+) mice exhibit both microcephaly and hypopigmentation, thus phenocopying germline haploinsufficient Magoh mice. Using Emx1-Cre, we further show that conditional Magoh deletion in neural progenitors during embryonic development also causes microcephaly. We anticipate this novel conditional allele will be a valuable tool for assessing tissue-specific roles for Magoh in mammalian development and postnatal processes.
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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.