ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Quaking Regulates Neurofascin 155 Expression for Myelin and Axoglial Junction Maintenance.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Isoform-specific roles of QKI-6 and QKI-7 direct Schwann cell lineage progression and enhance peripheral nerve regeneration.Experimental & molecular medicine · 2026Article
- Competition for the conserved branch point sequence influences physiological outcomes in pre-mRNA splicing.eLife · 2026Article
- Decoding exon inclusion in the human brain reveals more divergent splicing mechanisms in neurons than glia.Genome biology · 2026Article
- Quaking Protein in Myelin Maintenance and Regeneration in the Central Nervous System.Molecular neurobiology · 2025Review
- NF-κB RelA regulates temporal oligodendrocyte differentiation in the postnatal brains.Frontiers in cellular neuroscience · 2025Article
- Human-derived monoclonal autoantibodies as interrogators of cellular proteotypes in the brain.Trends in neurosciences · 2024Review
- Qki5 safeguards spinal motor neuron function by defining the motor neuron-specific transcriptome via pre-mRNA processing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Quaking regulates circular RNA production in cardiomyocytes.Journal of cell science · 2023Article
- The RNA-binding protein QKI governs a muscle-specific alternative splicing program that shapes the contractile function of cardiomyocytes.Cardiovascular research · 2023Article
- Myelin lipid metabolism and its role in myelination and myelin maintenance.Innovation (Cambridge (Mass.)) · 2023Review
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- Definition of germ layer cell lineage alternative splicing programs reveals a critical role for Quaking in specifying cardiac cell fate.Nucleic acids research · 2022Article
- Quaking but not parkin is the major tumor suppressor in 6q deleted region in glioblastoma.Frontiers in cell and developmental biology · 2022Article
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- GeneWalk identifies relevant gene functions for a biological context using network representation learning.Genome biology · 2021Article
- QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function.Nature communications · 2021Article
- Deletion of the Thrombin Proteolytic Site in Neurofascin 155 Causes Disruption of Nodal and Paranodal Organization.Frontiers in cellular neuroscience · 2021Article
- The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function.Frontiers in cell and developmental biology · 2021Review
- Transcriptional profiling of multiple system atrophy cerebellar tissue highlights differences between the parkinsonian and cerebellar sub-types of the disease.Acta neuropathologica communications · 2020Article
- Mature myelin maintenance requires Qki to coactivate PPARβ-RXRα-mediated lipid metabolism.The Journal of clinical investigation · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA binding proteins required for the maintenance of myelin and axoglial junctions are unknown. Herein, we report that deletion of the Quaking (QKI) RNA binding proteins in oligodendrocytes (OLs) using Olig2-Cre results in mice displaying rapid tremors at postnatal day 10, followed by death at postnatal week 3. Extensive CNS hypomyelination was observed as a result of OL differentiation defects during development. The QKI proteins were also required for adult myelin maintenance, because their ablation using PLP-CreERT resulted in hindlimb paralysis with immobility at ∼30 d after 4-hydroxytamoxifen injection. Moreover, deterioration of axoglial junctions of the spinal cord was observed and is consistent with a loss of Neurofascin 155 (Nfasc155) isoform that we confirmed as an alternative splice target of the QKI proteins. Our findings define roles for the QKI RNA binding proteins in myelin development and maintenance, as well as in the generation of Nfasc155 to maintain healthy axoglial junctions. SIGNIFICANCE STATEMENT: Neurofascin 155 is responsible for axoglial junction formation and maintenance. Using a genetic mouse model to delete Quaking (QKI) RNA-binding proteins in oligodendrocytes, we identify QKI as the long-sought regulator of Neurofascin alternative splicing, further establishing the role of QKI in oligodendrocyte development and myelination. We establish a new role for QKI in myelin and axoglial junction maintenance using an inducible genetic mouse model that deletes QKI in mature oligodendrocytes. Loss of QKI in adult oligodendrocytes leads to phenotypes reminiscent of the experimental autoimmune encephalomyelitis mouse model with complete hindlimb paralysis and death by 30 d after induction of QKI deletion.
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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.