ArticleBone2011
PHOSPHO1 is essential for mechanically competent mineralization and the avoidance of spontaneous fractures.
Article in Bone, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- DNA methylation analysis is used to identify novel genetic loci associated with circulating fibrinogen levels in blood.Journal of thrombosis and haemostasis : JTH · 2023Pooled it
- TNAP and PHOSPHO1 Function Synergistically to Afford Critical Control Over the Mineralization of the Postnatal Murine Skeleton.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TNAP and PHOSPHO1 function synergistically to afford critical control over the mineralisation of the postnatal murine skeleton.bioRxiv : the preprint server for biology · 2026Article
- Osteoblasts sense extracellular levels of phosphate to control the local expression of phosphatases for matrix mineralisation.Bone reports · 2025Article
- Advances in graphene-based 2D materials for tendon, nerve, bone/cartilage regeneration and biomedicine.iScience · 2024Review
- Sexually dimorphic effects of prenatal alcohol exposure on the murine skeleton.Biology of sex differences · 2024Article
- Anti-RANKL Therapy Prevents Glucocorticoid-Induced Bone Loss and Promotes Muscle Function in a Mouse Model of Duchenne Muscular Dystrophy.Calcified tissue international · 2023Article
- Spatial Lipidomic Profiling of Mouse Joint Tissue Demonstrates the Essential Role of PHOSPHO1 in Growth Plate Homeostasis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Increased PHOSPHO1 and alkaline phosphatase expression during the anabolic bone response to intermittent parathyroid hormone delivery.Cell biochemistry and function · 2023Article
- Gene Therapy Using Recombinant AAV Type 8 Vector Encoding TNAP-DJBMR plus · 2023Article
- Matrix Vesicle-Mediated Mineralization and Osteocytic Regulation of Bone Mineralization.International journal of molecular sciences · 2022Review
- Combined growth hormone and insulin-like growth factor-1 rescues growth retardation in glucocorticoid-treated mdxmice but does not prevent osteopenia.The Journal of endocrinology · 2022Article
- Ablation ofJBMR plus · 2021Article
- Phosphatase orphan 1 inhibits myoblast proliferation and promotes myogenic differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Review
- Black phosphorus-based 2D materials for bone therapy.Bioactive materials · 2020Article
- Role of Metabolism in Bone Development and Homeostasis.International journal of molecular sciences · 2020Review
- PHOSPHO1 is a skeletal regulator of insulin resistance and obesity.BMC biology · 2020Article
- A comparison of the bone and growth phenotype ofDisease models & mechanisms · 2020Article
- How To Build a Bone: PHOSPHO1, Biomineralization, and Beyond.JBMR plus · 2019Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Phosphatases are essential for the mineralization of the extracellular matrix within the skeleton. Their precise identities and functions however remain unclear. PHOSPHO1 is a phosphoethanolamine/phosphocholine phosphatase involved in the generation of inorganic phosphate for bone mineralization. It is highly expressed at sites of mineralization in bone and cartilage. The bones of Phospho1(-/-) mice are hypomineralized, bowed and present with spontaneous greenstick fractures at birth. In this study we show that PHOSPHO1 is essential for mechanically competent mineralization that is able to withstand habitual load. Long bones from Phospho1(-/-) mice did not fracture during 3-point bending but deformed plastically. With dynamic loading nanoindentation the elastic modulus and hardness of Phospho1(-/-) tibiae were significantly lower than wild-type tibia. Raman microscopy revealed significantly lower mineral:matrix ratios and lower carbonate substitutions in Phospho1(-/-) tibia. The altered dihydroxylysinonorleucine/hydroxylysinonorleucine and pyridinoline/deoxypyridinoline collagen crosslink ratios indicated possible changes in lysyl hydroxylase-1 activity and/or bone mineralization status. The bone formation and resorption markers, N-terminal propeptide and C-terminal telopeptide of Type I collagen, were both increased in Phospho1(-/-) mice and this we associated with increased bone remodeling during fracture repair or an attempt to remodel a mechanically competent bone capable of withstanding physiological load. In summary these data indicate that Phospho1(-/-) bones are hypomineralized and, consequently, are softer and more flexible. An inability to withstand physiological loading may explain the deformations noted. We hypothesize that this phenotype is due to the reduced availability of inorganic phosphate to form hydroxyapatite during mineralization, creating an undermineralized yet active bone.
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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.