ArticleBone research2018
IGF-I induced phosphorylation of PTH receptor enhances osteoblast to osteocyte transition.
Article in Bone research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Using Mendelian randomization analyses in osteoarthritis: state of art and future perspectives.Annals of medicine · 2025Pooled it
- Genes and Pathways Associated with Skeletal Sagittal Malocclusions: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Regulation of cAMP levels in osteocytes by mechano-sensitive focal adhesion kinase and phosphodiesterase 8A.iScience · 2026Article
- PTH induced osteoblast Slit3 to decrease aberrant sensory innervation in degenerated vertebral endplates to relieve low back pain in mice.Bone research · 2026Article
- Integrating platelet-rich plasma therapy into nursing practice: a review of biological mechanisms and clinical applications.Frontiers in bioengineering and biotechnology · 2026Review
- Osteocyte Dendrites: How Do They Grow, Mature, and Degenerate in Mineralized Bone?Cytoskeleton (Hoboken, N.J.) · 2025Review
- Mechanosignaling in Osteoporosis: When Cells Feel the Force.International journal of molecular sciences · 2025Review
- Direct and indirect regulation of bone metabolism by lactoferrin.Frontiers in endocrinology · 2025Review
- Hypocalcemia in combination with hyperphosphatemia impairs muscle cell differentiation in vitro.Journal of endocrinological investigation · 2024Article
- Review
- Elastic porous microspheres/extracellular matrix hydrogel injectable composites releasing dual bio-factors enable tissue regeneration.Nature communications · 2024Article
- Enhanced molecular release from elderly bone samples using collagenase I: insights into fatty acid metabolism alterations.Journal of translational medicine · 2024Article
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Liquiritigenin promotes osteogenic differentiation and prevents bone loss via inducing auto-lysosomal degradation and inhibiting apoptosis.Genes & diseases · 2023Article
- Pathways Controlling Formation and Maintenance of the Osteocyte Dendrite Network.Current osteoporosis reports · 2022Review
- Mussel-Inspired Polydopamine-Based Multilayered Coatings for Enhanced Bone Formation.Frontiers in bioengineering and biotechnology · 2022Review
- FGF7-induced E11 facilitates cell-cell communication through connexin43.International journal of biological sciences · 2021Article
- Role of Metabolism in Bone Development and Homeostasis.International journal of molecular sciences · 2020Review
- Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption.International journal of molecular sciences · 2020Review
- IL-10 induces MC3T3-E1 cells differentiation towards osteoblastic fate in murine model.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Parathyroid hormone (PTH) regulates bone remodeling by activating PTH type 1 receptor (PTH1R) in osteoblasts/osteocytes. Insulin-like growth factor type 1 (IGF-1) stimulates mesenchymal stem cell differentiation to osteoblasts. However, little is known about the signaling mechanisms that regulates the osteoblast-to-osteocyte transition. Here we report that PTH and IGF-I synergistically enhance osteoblast-to-osteocyte differentiation. We identified that a specific tyrosine residue, Y494, on the cytoplasmic domain of PTH1R can be phosphorylated by insulin-like growth factor type I receptor (IGF1R) in vitro. Phosphorylated PTH1R localized to the barbed ends of actin filaments and increased actin polymerization during morphological change of osteoblasts into osteocytes. Disruption of the phosphorylation site reduced actin polymerization and dendrite length. Mouse models with conditional ablation of PTH1R in osteoblasts demonstrated a reduction in the number of osteoctyes and dendrites per osteocyte, with complete overlap of PTH1R with phosphorylated-PTH1R positioning in osteocyte dendrites in wild-type mice. Thus, our findings reveal a novel signaling mechanism that enhances osteoblast-to-osteocyte transition by direct phosphorylation of PTH1R by IGF1R.
Identifiers
What OpenQuestion holds
Registered trials
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.