ArticleScientific reports2015
Cytoplasmic hnRNPK interacts with GSK3β and is essential for the osteoclast differentiation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- A novel knockout mouse model to assess the impact of one-copy loss of Hnrnpk in CD4 + T cells in chronically inflamed skin as a prelude to CTCL.Scientific reports · 2025Article
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Neoandrographolide inhibits mature osteoclast differentiation to alleviate bone loss and treat osteoporosis.Frontiers in pharmacology · 2025Article
- Hnrnpk protects against osteoarthritis through targeting WWC1 mRNA and inhibiting Hippo signaling pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
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- An LGR4 agonist activates the GSK‑3β pathway to inhibit RANK‑RANKL signaling during osteoclastogenesis in bone marrow‑derived macrophages.International journal of molecular medicine · 2024Article
- Review
- Hnrnpk is essential for embryonic limb bud development as a transcription activator and a collaborator of insulator protein Ctcf.Cell death and differentiation · 2023Article
- Dlk2 interacts with Syap1 to activate Akt signaling pathway during osteoclast formation.Cell death & disease · 2023Article
- Casticin suppresses RANKL‑induced osteoclastogenesis and prevents ovariectomy‑induced bone loss by regulating the AKT/ERK and NF‑κB signaling pathways.International journal of molecular medicine · 2023Article
- Role of Heterogeneous Nuclear Ribonucleoproteins in the Cancer-Immune Landscape.International journal of molecular sciences · 2023Review
- Article
- High Throughput FISH Screening Identifies Small Molecules That Modulate Oncogenic lncRNA MALAT1 via GSK3B and hnRNPs.Non-coding RNA · 2023Article
- Hnrnpk maintains chondrocytes survival and function during growth plate development via regulating Hif1α-glycolysis axis.Cell death & disease · 2022Article
- LINC00162 regulates cell proliferation and apoptosis by sponging PAQR4-targeting miR-485-5p.Journal of cellular physiology · 2022Article
- Arginine Methylation of hnRNPK Inhibits the DDX3-hnRNPK Interaction to Play an Anti-Apoptosis Role in Osteosarcoma Cells.International journal of molecular sciences · 2021Article
- The RNA binding protein hnRNPK protects against adriamycin-induced podocyte injury.Annals of translational medicine · 2021Article
- Caveolin-1-driven membrane remodelling regulates hnRNPK-mediated exosomal microRNA sorting in cancer.Clinical and translational medicine · 2021Article
- A Novel Long Noncoding RNA lincRNA00892 Activates CD4Frontiers in pharmacology · 2021Article
- Ferric Ion Induction of Triggering Receptor Expressed in Myeloid Cells-2 Expression and PI3K/Akt Signaling Pathway in Preosteoclast Cells to Promote Osteoclast Differentiation.Orthopaedic surgery · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclast differentiation is a complex and finely regulated physiological process that involves a variety of signaling pathways and factors. Recent studies suggested that the Ser9 phosphorylation of Glycogen synthase kinase-3β (GSK3β) is required for the osteoclast differentiation. However, the precise underlying mechanism remains unclear. We have previously identified the heterogeneous nuclear ribonucleoprotein K (hnRNPK) as a putative GSK3β interactor. In the present study, we demonstrate that, during the RANKL-induced osteoclast differentiation, the PI3K/Akt-mediated Ser9 phosphorylation of GSK3β provokes the nuclear-cytoplasmic translocation of hnRNPK in an ERK-dependent manner, enhancing the cytoplasmic co-localization and interaction of GSK3β and hnRNPK. We show that hnRNPK is essential for the osteoclast differentiation, and is involved in several reported functions of GSK3β, including the activation of NF-κB, the expression of NFATc1, and the acetylation of tubulin, all known to be critical for osteoclast differentiation and functions. We find that hnRNPK is localized in the actin belt, and is important for the mature osteoclast formation. Taken together, we demonstrate here the critical role of hnRNPK in osteoclast differentiation, and depict a model in which the cytoplasmic hnRNPK interacts with GSK3β and regulates its function.
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