ArticleNucleic acids research2014
A cytoplasmic quaking I isoform regulates the hnRNP F/H-dependent alternative splicing pathway in myelinating glia.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- NADScience advances · 2025Article
- Systematic Analysis of Alternative Splicing in Transcriptomes of Multiple Sclerosis Patient Brain Samples.International journal of molecular sciences · 2025Article
- Influence of ATXN2 intermediate CAG repeats, 9bp duplication and alternative splicing on SCA3 pathogenesis.Acta neuropathologica communications · 2025Article
- SRSF10 regulates oligodendrocyte differentiation during mouse central nervous system development by modulating pre-mRNA splicing.Nucleic acids research · 2025Article
- The Roles of hnRNP Family in the Brain and Brain-Related Disorders.Molecular neurobiology · 2024Review
- Development and disease-specific regulation of RNA splicing in cardiovascular system.Frontiers in cell and developmental biology · 2024Review
- Irrespective of Plaque Activity, Multiple Sclerosis Brain Periplaques Exhibit Alterations of Myelin Genes and a TGF-Beta Signature.International journal of molecular sciences · 2022Article
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- The Long Non-Coding RNACells · 2022Review
- Defective Oligodendroglial Lineage and Demyelination in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021Review
- Tau Modulates mRNA Transcription, Alternative Polyadenylation Profiles of hnRNPs, Chromatin Remodeling and Spliceosome Complexes.Frontiers in molecular neuroscience · 2021Article
- The role of hnRNPs in frontotemporal dementia and amyotrophic lateral sclerosis.Acta neuropathologica · 2020Review
- Could an Impairment in Local Translation of mRNAs in Glia be Contributing to Pathogenesis in ALS?Frontiers in molecular neuroscience · 2019Review
- New alternative splicing variants of the ATXN2 transcript.Neurological research and practice · 2019Article
- TCF3 alternative splicing controlled by hnRNP H/F regulates E-cadherin expression and hESC pluripotency.Genes & development · 2018Article
- ECD promotes gastric cancer metastasis by blocking E3 ligase ZFP91-mediated hnRNP F ubiquitination and degradation.Cell death & disease · 2018Article
- Noise-Induced Dysregulation ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Autogenous cross-regulation ofGenes & development · 2017Article
- The long and the short of TRF2 in neurogenesis.Cell cycle (Georgetown, Tex.) · 2016Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The selective RNA-binding protein quaking I (QKI) plays important roles in controlling alternative splicing (AS). Three QKI isoforms are broadly expressed, which display distinct nuclear-cytoplasmic distribution. However, molecular mechanisms by which QKI isoforms control AS, especially in distinct cell types, still remain elusive. The quakingviable (qk(v)) mutant mice carry deficiencies of all QKI isoforms in oligodendrocytes (OLs) and Schwann cells (SWCs), the myelinating glia of central and peripheral nervous system (CNS and PNS), respectively, resulting in severe dysregulation of AS. We found that the cytoplasmic isoform QKI-6 regulates AS of polyguanine (G-run)-containing transcripts in OLs and rescues aberrant AS in the qk(v) mutant by repressing expression of two canonical splicing factors, heterologous nuclear ribonucleoproteins (hnRNPs) F and H. Moreover, we identified a broad spectrum of in vivo functional hnRNP F/H targets in OLs that contain conserved exons flanked by G-runs, many of which are dysregulated in the qk(v) mutant. Interestingly, AS targets of the QKI-6-hnRNP F/H pathway in OLs are differentially affected in SWCs, suggesting that additional cell-type-specific factors modulate AS during CNS and PNS myelination. Together, our studies provide the first evidence that cytoplasmic QKI-6 acts upstream of hnRNP F/H, which forms a novel pathway to control AS in myelinating glia.
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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.