ArticleScientific reports2018
Matrin-3 is essential for fibroblast growth factor 2-dependent maintenance of neural stem cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Nuclear structures and their emerging roles in cell differentiation and development.BMB reports · 2024Review
- The role of Matrin-3 in physiology and its dysregulation in disease.Biochemical Society transactions · 2024Review
- Review
- Matrin3 mediates differentiation through stabilizing chromatin loop-domain interactions and YY1 mediated enhancer-promoter interactions.Nature communications · 2024Article
- MATR3-antisense LINE1 RNA meshwork scaffolds higher-order chromatin organization.EMBO reports · 2023Article
- Prognostic significance of MATR3 in stage I and II non-small cell lung cancer patients.Journal of cancer research and clinical oncology · 2022Article
- Inner nuclear protein Matrin-3 coordinates cell differentiation by stabilizing chromatin architecture.Nature communications · 2021Article
- Multilayer and MATR3-dependent regulation of mRNAs maintains pluripotency in human induced pluripotent stem cells.iScience · 2021Article
- Matrin 3 in neuromuscular disease: physiology and pathophysiology.JCI insight · 2021Review
- Matrin3: Disorder and ALS Pathogenesis.Frontiers in molecular biosciences · 2021Review
- Review
- Review
- LncRNA TUG1 promoted osteogenic differentiation through promoting bFGF ubiquitination.In vitro cellular & developmental biology. Animal · 2020Article
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Authors and funding
4 authors.
Funding
Abstract
To investigate the mechanisms underlying the maintenance of neural stem cells, we performed two-dimensional fluorescence-difference gel electrophoresis (2D-DIGE) targeting the nuclear phosphorylated proteins. Nuclear phosphorylated protein Matrin-3 was identified in neural stem cells (NSCs) after stimulation using fibroblast growth factor 2 (FGF2). Matrin-3 was expressed in the mouse embryonic subventricular and ventricular zones. Small interfering RNA (siRNA)-mediated knockdown of Matrin-3 caused neuronal differentiation of NSCs in vitro, and altered the cerebral layer structure of foetal brain in vivo. Transfection of Matrin-3 plasmids in which the serine 208 residue was point-mutated to alanine (Ser208Ala mutant Matrin3) and inhibition of Ataxia telangiectasia mutated kinase (ATM kinase), which phosphorylates Matrin-3 Ser208 residue, caused neuronal differentiation and decreased the proliferation of neurosphere-forming stem cells. Thus, our proteomic approach revealed that Matrin-3 phosphorylation was essential for FGF2-dependent maintenance of NSCs in vitro and in vivo.
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Registered trials
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