ArticleJournal of molecular cell biology2020
PIP5k1β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation.
Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Pip5k1α defines a mandible-specific phosphoinositide signaling axis in mice.Science China. Life sciences · 2026Article
- Sea cucumber-inspired dual-responsive black phosphorus/amorphous calcium-based bone-targeting nanoplatform for synergistic therapy of osteoporosis.Journal of nanobiotechnology · 2026Article
- VGF and the VGF-derived peptide AQEE30 stimulate osteoblastic bone formation through the C3a receptor.Experimental & molecular medicine · 2025Article
- Identification of Grb2 protein as a potential mediator of macrophage activation in acute pancreatitis based on bioinformatics and experimental verification.Frontiers in immunology · 2025Article
- TNF receptor-associated factors: promising targets of natural products for the treatment of osteoporosis.Frontiers in physiology · 2025Review
- Article
- Regulatory mechanisms of autophagy-related ncRNAs in bone metabolic diseases.Frontiers in pharmacology · 2023Review
- Fucoidan (Marine drugs · 2022Article
- lncRNA SNHG1 induced by SP1 regulates bone remodeling and angiogenesis via sponging miR-181c-5p and modulating SFRP1/Wnt signaling pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Macrophages Switch to an Osteo-Modulatory Profile Upon RANKL Induction in a Medaka (JBMR plus · 2020Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PIP5k1β is crucial to the generation of phosphotidylinosotol (4, 5)P2. PIP5k1β participates in numerous cellular activities, such as B cell and platelet activation, cell phagocytosis and endocytosis, cell apoptosis, and cytoskeletal organization. In the present work, we aimed to examine the function of PIP5k1β in osteoclastogenesis and osteogenesis to provide promising strategies for osteoporosis prevention and treatment. We discovered that PIP5k1β deletion in mice resulted in obvious bone loss and that PIP5k1β was highly expressed during both osteoclast and osteoblast differentiation. Deletion of the gene was found to enhance the proliferation and migration of bone marrow-derived macrophage-like cells to promote osteoclast differentiation. PIP5k1β-/- osteoclasts exhibited normal cytoskeleton architecture but stronger resorption activity. PIP5k1β deficiency also promoted activation of mitogen-activated kinase and Akt signaling, enhanced TRAF6 and c-Fos expression, facilitated the expression and nuclear translocation of NFATC1, and upregulated Grb2 expression, thereby accelerating osteoclast differentiation and function. Finally, PIP5k1β enhanced osteoblast differentiation by upregulating master gene expression through triggering smad1/5/8 signaling. Therefore, PIP5k1β modulates bone homeostasis and remodeling.
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