ArticleMolecular and cellular biology2013
The QKI-5 and QKI-6 RNA binding proteins regulate the expression of microRNA 7 in glial cells.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism.Nature genetics · 2016Pooled it
- Isoform-specific roles of QKI-6 and QKI-7 direct Schwann cell lineage progression and enhance peripheral nerve regeneration.Experimental & molecular medicine · 2026Article
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Diverse roles of quaking in endothelial cell biology.Angiogenesis · 2025Review
- Article
- Targeting the Hippo pathway in Schwann cells ameliorates peripheral nerve degeneration via a polypharmacological mechanism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- 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
- Use of microRNAs as Diagnostic, Prognostic, and Therapeutic Tools for Glioblastoma.International journal of molecular sciences · 2024Review
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- Alternative Transcripts Diversify Genome Function for Phenome Relevance to Health and Diseases.Genes · 2023Review
- QKI shuttles internal mCell · 2023Article
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- SOCS6 Promotes Mitochondrial Fission and Cardiomyocyte Apoptosis and Is Negatively Regulated by Quaking-Mediated miR-19b.Oxidative medicine and cellular longevity · 2022Article
- Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy throughMolecular therapy. Nucleic acids · 2021Article
- QKI 6 ameliorates CIRI through promoting synthesis of triglyceride in neuron and inhibiting neuronal apoptosis associated with SIRT1-PPARγ-PGC-1α axis.Brain and behavior · 2021Article
- RNA pull-down confocal nanoscanning (RP-CONA) detects quercetin as pri-miR-7/HuR interaction inhibitor that decreases α-synuclein levels.Nucleic acids research · 2021Article
- Article
- NRP1 and MMP9 are dual targets of RNA-binding protein QKI5 to alter VEGF-R/ NRP1 signalling in trophoblasts in preeclampsia.Journal of cellular and molecular medicine · 2021Article
- Matrix stiffening induces a pathogenic QKI-miR-7-SRSF1 signaling axis in pulmonary arterial endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- MiR-7 in Cancer Development.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The quaking (qkI) gene encodes 3 major alternatively spliced isoforms that contain unique sequences at their C termini dictating their cellular localization. QKI-5 is predominantly nuclear, whereas QKI-6 is distributed throughout the cell and QKI-7 is cytoplasmic. The QKI isoforms are sequence-specific RNA binding proteins expressed mainly in glial cells modulating RNA splicing, export, and stability. Herein, we identify a new role for the QKI proteins in the regulation of microRNA (miRNA) processing. We observed that small interfering RNA (siRNA)-mediated QKI depletion of U343 glioblastoma cells leads to a robust increase in miR-7 expression. The processing from primary to mature miR-7 was inhibited in the presence QKI-5 and QKI-6 but not QKI-7, suggesting that the nuclear localization plays an important role in the regulation of miR-7 expression. The primary miR-7-1 was bound by the QKI isoforms in a QKI response element (QRE)-specific manner. We observed that the pri-miR-7-1 RNA was tightly bound to Drosha in the presence of the QKI isoforms, and this association was not observed in siRNA-mediated QKI or Drosha-depleted U343 glioblastoma cells. Moreover, the presence of the QKI isoforms led to an increase presence of pri-miR-7 in nuclear foci, suggesting that pri-miR-7-1 is retained in the nucleus by the QKI isoforms. miR-7 is known to target the epidermal growth factor (EGF) receptor (EGFR) 3' untranslated region (3'-UTR), and indeed, QKI-deficient U343 cells had reduced EGFR expression and decreased ERK activation in response to EGF. Elevated levels of miR-7 are associated with cell cycle arrest, and it was observed that QKI-deficient U343 that harbor elevated levels of miR-7 exhibited defects in cell proliferation that were partially rescued by the addition of a miR-7 inhibitor. These findings suggest that the QKI isoforms regulate glial cell function and proliferation by regulating the processing of certain miRNAs.
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