Affinage

PHOSPHO1

Phosphoethanolamine/phosphocholine phosphatase · UniProt Q8TCT1

Length
267 aa
Mass
29.7 kDa
Annotated
2026-04-28
35 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PHOSPHO1 is a Mg2+-dependent HAD-superfamily phosphatase that generates inorganic phosphate within matrix vesicles by hydrolyzing phosphoethanolamine and phosphocholine, thereby initiating hydroxyapatite crystal nucleation during skeletal, dental, and vascular mineralization. Catalytic activity depends on conserved aspartate residues (Asp32, Asp203) for phosphoryl transfer and Asp43/Asp123 for substrate binding (PMID:15175005, PMID:16054448), and PHOSPHO1 operates nonredundantly with tissue-nonspecific alkaline phosphatase (TNAP): double ablation of Phospho1 and Alpl abolishes skeletal mineralization and causes perinatal lethality, whereas TNAP overexpression cannot rescue the Phospho1-null bone phenotype (PMID:20684022). The mineralization defect in Phospho1-/- mice is driven primarily by accumulation of phosphorylated osteopontin rather than elevated PPi, as genetic removal of Spp1 ameliorates the skeletal phenotype (PMID:24825455). Beyond mineralization, PHOSPHO1's hydrolysis of phosphocholine to choline regulates systemic choline levels, and its loss confers resistance to diet-induced obesity, improved glucose homeostasis, and enhanced brown adipose tissue thermogenesis—phenotypes reversed by dietary choline supplementation (PMID:33092598, PMID:32554489).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2003 Medium

    Structural modeling placed PHOSPHO1 within the HAD superfamily and identified candidate catalytic and substrate-specificity residues, providing the first framework for understanding its enzymatic mechanism.

    Evidence Comparative homology modeling based on Methanococcus jannaschii phosphoserine phosphatase crystal structure

    PMID:14983068

    Open questions at the time
    • Model-based predictions lacked experimental mutagenesis validation at time of publication
    • No crystal structure of PHOSPHO1 itself
  2. 2004 High

    Kinetic characterization established phosphoethanolamine and phosphocholine as high-affinity natural substrates and defined the strict Mg2+ dependence, answering the fundamental question of what PHOSPHO1 hydrolyzes and how it generates inorganic phosphate.

    Evidence In vitro enzymatic assay with recombinant PHOSPHO1; substrate kinetics, pH and metal ion dependence

    PMID:15175005

    Open questions at the time
    • In vivo substrate utilization within matrix vesicles not yet demonstrated
    • Product (Pi) contribution to mineral nucleation not directly shown
  3. 2004 Medium

    Immunolocalization of PHOSPHO1 protein exclusively to sites of active mineralization in bone and cartilage established the physiological context for its enzymatic activity.

    Evidence Immunohistochemistry with affinity-purified antibody on developing bone and growth plate sections

    PMID:15050893

    Open questions at the time
    • Single-lab IHC study
    • Sub-cellular localization to matrix vesicles not shown in this study
  4. 2005 High

    Site-directed mutagenesis confirmed the HAD-superfamily catalytic mechanism by showing Asp32 and Asp203 are essential for activity and Asp43/Asp123 mediate substrate binding, validating the earlier structural model.

    Evidence Site-directed mutagenesis of active-site residues with in vitro enzymatic assay

    PMID:16054448

    Open questions at the time
    • No crystal structure to visualize substrate-binding geometry
    • Distinction between PEA and PCho binding determinants not resolved
  5. 2006 High

    Direct immunoblot detection of PHOSPHO1 within isolated matrix vesicles and its upregulation during chondrocyte differentiation answered where within the extracellular space PHOSPHO1 acts and linked its expression to the onset of mineralization.

    Evidence MV fractionation with immunoblotting; whole-mount in situ hybridization in developing chick

    PMID:16837257

    Open questions at the time
    • Enzymatic activity within intact MVs not yet demonstrated
  6. 2007 High

    Demonstrating PHOSPHO1 enzymatic activity within matrix vesicles and showing that pharmacological PHOSPHO1 inhibition reduces MV-mediated mineralization established PHOSPHO1 as a functional mineralizing enzyme inside MVs, not merely a co-localized protein.

    Evidence PEA hydrolase activity in sonicated MVs from TNAP-null osteoblasts; HTS-derived inhibitors (lansoprazole, SCH202676); MV calcification assay

    PMID:17227223

    Open questions at the time
    • Inhibitor specificity for PHOSPHO1 over other phosphatases not fully characterized
    • Activity measured in sonicated, not intact, MVs
  7. 2010 High

    Genetic epistasis experiments using Phospho1-/-, TNAP transgenic rescue, and double Phospho1/Alpl knockout mice established that PHOSPHO1 has a nonredundant, TNAP-independent role in initiating mineralization, resolving the long-standing question of whether MV-intrinsic and extravesicular Pi-generating pathways are functionally separable.

    Evidence Phospho1-/- knockout; TNAP transgenic overexpression in Phospho1-/- background; double knockout causing perinatal lethality; MV calcification assay; plasma PPi measurement

    PMID:20684022

    Open questions at the time
    • Precise molecular product (Pi vs membrane lipid remodeling) driving mineral nucleation not distinguished
    • Human genetic validation lacking
  8. 2010 High

    In vivo pharmacological inhibition of PHOSPHO1 with lansoprazole completely prevented long bone mineralization in chick embryos, confirming the in vivo requirement and linking hedgehog-regulated chondrocyte differentiation upstream of PHOSPHO1 expression.

    Evidence Lansoprazole treatment of chick embryos; talpid3 hedgehog mutant expression analysis

    PMID:20053388

    Open questions at the time
    • Lansoprazole has off-target effects (proton pump); specificity for PHOSPHO1 in vivo uncertain
    • Hedgehog–PHOSPHO1 transcriptional pathway intermediates not identified
  9. 2014 High

    Identification of phosphorylated osteopontin accumulation—rather than elevated PPi—as the primary driver of the Phospho1-/- skeletal phenotype reframed the mechanism: PHOSPHO1 loss permits p-OPN to inhibit mineralization, and genetic removal of Spp1 rescues the defect.

    Evidence LC-MS/MS phosphoproteomics; double Phospho1-/-/Spp1-/- knockout with phenotypic rescue

    PMID:24825455

    Open questions at the time
    • Whether PHOSPHO1 directly dephosphorylates OPN or acts indirectly not resolved
    • Contribution of PPi versus p-OPN in vivo not fully quantified
  10. 2016 High

    Genetic interaction between Phospho1 and Pit1 (Slc20a1) revealed that PHOSPHO1-generated Pi and transporter-imported Pi act in parallel to load MVs with mineral; PHOSPHO1 deficiency also reduced MV number, suggesting an additional role in MV biogenesis.

    Evidence Conditional Phospho1-/-;Pit1col2/col2 double knockout; atomic force microscopy of MVs; bone histomorphometry

    PMID:26773408

    Open questions at the time
    • Mechanism by which PHOSPHO1 influences MV biogenesis unknown
    • Whether MV membrane lipid remodeling links phospholipid hydrolysis to budding not tested
  11. 2016 Medium

    Extension of PHOSPHO1's role to dental tissues showed it is required for alveolar bone and cellular cementum mineralization but dispensable for acellular cementum, distinguishing MV-dependent from MV-independent mineralization pathways in teeth.

    Evidence Phospho1-/- mouse dental histology, IHC, ISH, microCT

    PMID:27016531

    Open questions at the time
    • Molecular basis for why acellular cementum is PHOSPHO1-independent not explained
    • Single-lab observation
  12. 2020 High

    Discovery that Phospho1-/- mice are resistant to diet-induced obesity with improved insulin sensitivity, and that dietary choline supplementation normalizes these phenotypes, established a systemic metabolic function for PHOSPHO1 through its phosphocholine-to-choline conversion activity.

    Evidence Phospho1-/- mouse on high-fat diet; serum metabolomics (choline); dietary choline rescue

    PMID:33092598

    Open questions at the time
    • Tissue source of metabolically relevant PHOSPHO1 activity (bone vs adipose vs other) not delineated
    • Direct measurement of phosphocholine/choline flux in specific tissues lacking
  13. 2020 High

    Demonstration that phosphocholine supplementation alone induces cold tolerance and thermogenic gene expression established that PHOSPHO1's substrate phosphocholine, not its product choline, drives brown adipose tissue activation—resolving the directionality of the metabolic effect.

    Evidence Phospho1-/- mouse cold tolerance assay; exogenous phosphocholine treatment in vivo; BAT thermogenic gene expression

    PMID:32554489

    Open questions at the time
    • Direct sensor/receptor for phosphocholine in BAT not identified
    • Whether this is a cell-autonomous or systemic (endocrine) effect not resolved
  14. 2025 Medium

    Identification of phospholipase C activity on phosphatidylcholine and phosphatidylethanolamine, with diacylglycerol production and co-localization with DGKδ, expanded PHOSPHO1's substrate repertoire beyond soluble phosphomonoesters to intact phospholipids.

    Evidence In vitro PLC activity assay; HEK293 overexpression with DG lipid measurement; co-sedimentation and co-localization with DGKδ

    PMID:39992810

    Open questions at the time
    • Physiological relevance of PLC activity relative to PEA/PCho hydrolysis not established
    • Single-lab finding awaiting independent confirmation
    • Functional consequence of PHOSPHO1-DGKδ coupling not tested in mineralizing cells

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the crystal structure of PHOSPHO1, the identity of the tissue(s) and cell type(s) responsible for its systemic metabolic effects, whether its phospholipase C activity contributes to MV membrane remodeling and biogenesis, and whether human PHOSPHO1 loss-of-function mutations cause a recognizable skeletal or metabolic disease.
  • No crystal structure available
  • No human genetic disease association from direct evidence
  • Relative contribution of PEA/PCho hydrolysis versus PLC activity in vivo unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 4 GO:0140096 catalytic activity, acting on a protein 2 GO:0008289 lipid binding 1
Localization
GO:0031410 cytoplasmic vesicle 3 GO:0005576 extracellular region 2 GO:0005829 cytosol 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-1266738 Developmental Biology 3
Partners
ALPLDGKDSLC20A1SMPD3SPP1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 Human PHOSPHO1 exhibits high specific phosphatase activity toward phosphoethanolamine (PEA) and phosphocholine (PCho), with apparent Km values of 3.0 µM for PEA and 11.4 µM for PCho, optimal activity at pH 6.7, and strict Mg2+-dependence, establishing these as its natural substrates and providing a mechanism for inorganic phosphate generation in mineralizing cells. In vitro enzymatic assay with recombinant PHOSPHO1, substrate kinetics, pH and metal ion dependence studies The Biochemical journal High 15175005
2003 Comparative modeling of human PHOSPHO1 based on phosphoserine phosphatase (PSP) crystal structure identified a catalytic Mg2+-binding site coordinated by three conserved Asp residues (Asp32, Asp34, Asp203) and revealed that PHOSPHO1 belongs to a novel subgroup within the HAD superfamily distinct from PSPs, with Asp43 and Asp123 proposed to confer substrate specificity. Comparative homology modeling based on Methanococcus jannaschii PSP crystal structure; sequence conservation analysis Protein engineering Medium 14983068
2005 Mutagenesis of Asp32 and Asp203 abolished PHOSPHO1 phosphatase activity, confirming HAD superfamily membership and catalytic mechanism; Asp43 and Asp123 mutations impaired substrate hydrolysis, demonstrating their role in substrate binding. PHOSPHO2, despite 42% sequence identity, preferentially hydrolyzes pyridoxal-5-phosphate rather than PEA or PCho. Site-directed mutagenesis of active-site residues; in vitro enzymatic assay with recombinant proteins Biochimica et biophysica acta High 16054448
2004 PHOSPHO1 protein is localized by immunohistochemistry specifically to sites of active mineralization in bone and cartilage: osteoid layer of periosteum, forming surfaces of growing osteons, newly formed osteocytes, early hypertrophic chondrocytes of growth plate, and mineralizing surfaces of trabecular bone; absent from non-mineralizing soft tissues. Immunohistochemistry with affinity-purified antibody; RT-PCR in osteoblast cell lines Bone Medium 15050893
2006 PHOSPHO1 is present within matrix vesicles (MVs) isolated from growth plate chondrocytes as confirmed by immunoblotting, and its expression is upregulated in MVs from chondrocytes induced to differentiate, mirroring TNAP activity upregulation; its developmental expression in chick precedes mineralization onset, consistent with an initiating role. Immunoblotting of isolated MVs; whole-mount in situ hybridization; qPCR during chondrocyte differentiation Bone High 16837257
2007 PHOSPHO1 is functionally active within matrix vesicles: sonicated (but not intact) MVs from TNAP-deficient osteoblasts exhibit PEA hydrolase activity attributable to PHOSPHO1, and pharmacological inhibitors of PHOSPHO1 (lansoprazole, SCH202676) reduce MV-mediated mineralization by 56.8% and 70.7%, respectively. Enzyme activity assay in sonicated MVs; high-throughput screening for inhibitors; MV calcification assay in TNAP-null background Journal of bone and mineral research High 17227223
2010 Phospho1-/- mice display growth plate abnormalities, spontaneous fractures, bowed long bones, osteomalacia, and scoliosis; Phospho1-/- chondrocyte-derived MVs show reduced mineralizing ability; plasma PPi is elevated. Transgenic TNAP overexpression normalizes PPi but does not rescue the bone phenotype, indicating PHOSPHO1 has a nonredundant, TNAP-independent role in initiating skeletal mineralization. Double ablation of PHOSPHO1 and TNAP completely abolishes skeletal mineralization and causes perinatal lethality. Phospho1-/- knockout mouse; TNAP transgenic overexpression in Phospho1-/- background; double Phospho1/Alpl knockout; primary chondrocyte MV calcification assay; plasma PPi measurement Journal of bone and mineral research High 20684022
2010 PHOSPHO1 deficiency in MVs reduces ATP hydrolysis kinetics secondarily via reduction in TNAP levels within PHOSPHO1-deficient MVs; kinetic analysis establishes TNAP as the primary enzyme hydrolyzing ATP and PPi within the MV compartment, while PHOSPHO1 affects MV phosphosubstrate hydrolysis indirectly through regulation of TNAP levels. Kinetic substrate hydrolysis assays (ATP, ADP, PPi) on isolated MVs from WT, TNAP-/-, NPP1-/-, and PHOSPHO1-deficient osteoblasts Journal of bone and mineral research High 19874193
2010 In vivo inhibition of PHOSPHO1 with lansoprazole completely prevented mineralization of chick limb long bones, and the talpid3 chick mutant (defective hedgehog signaling, absent endochondral mineralization) lacked Phospho1 and Tnap expression, linking hedgehog-regulated chondrocyte differentiation to PHOSPHO1-mediated endochondral mineralization. Lansoprazole pharmacological inhibition in chick embryo in vivo; micromass cultures with PHOSPHO1 inhibitor; talpid3 mutant expression analysis; whole-mount in situ hybridization Bone High 20053388
2013 PHOSPHO1 is expressed and upregulated in mineralizing vascular smooth muscle cells (VSMCs); Phospho1-/- VSMCs fail to mineralize in vitro; pharmacological inhibition of PHOSPHO1 (MLS-0263839) reduces VSMC calcification to ~42% of control, and combined PHOSPHO1 + TNAP inhibition reduces it to ~21%, demonstrating PHOSPHO1 plays a critical initiating role in vascular smooth muscle cell calcification. Phospho1-/- VSMC cultures; PHOSPHO1-specific inhibitors identified by HTS; calcification assay; dual inhibitor experiment Journal of bone and mineral research High 22887744
2014 Phospho1-/- mice have elevated plasma osteopontin (OPN) with increased proportion of phosphorylated OPN (p-OPN) in skeleton as shown by LC-MS/MS; genetic ablation of Spp1 (OPN) in Phospho1-/- mice ameliorates scoliosis and long bone defects and corrects mineralization in vitro, identifying p-OPN accumulation (not elevated PPi) as the primary driver of the skeletal phenotype in PHOSPHO1 deficiency. LC-MS/MS phosphoproteomic analysis; double Phospho1-/-/Spp1-/- knockout mice; histology; in vitro mineralization assay Journal of bone and mineral research High 24825455
2016 Double knockout of Phospho1 and Pit1 (phosphate transporter Slc20a1 in chondrocytes) causes more severe skeletal mineralization defects than Phospho1-/- alone; ~80% of double-KO MVs lack mineral vs ~50% for Phospho1-/- and ~25% for WT, measured by atomic force microscopy. Phospho1-/- and double-KO chondrocytes also produce fewer MVs, implicating PHOSPHO1 in MV biogenesis. Conditional double knockout (Phospho1-/- ; Pit1col2/col2); atomic force microscopy of MVs; bone histomorphometry; biomechanical testing Journal of bone and mineral research High 26773408
2016 PTH-induced downregulation of PHOSPHO1 expression in osteoblasts is mediated through the cAMP/PKA signaling pathway, as demonstrated by mimicry with the cAMP agonist forskolin and blockade by PKA inhibitor PKI(5-24); PTH also coordinately suppresses nSMase2 (Smpd3) expression. Pharmacological pathway dissection (forskolin, PKA inhibitor PKI 5-24) in MC3T3-C14 osteoblast cultures; qPCR; hemi-calvaria organ culture Calcified tissue international Medium 27444010
2016 In Phospho1-/- mice, PHOSPHO1 loss leads to defects in alveolar bone and cellular cementum mineralization (cementoid accumulation, interglobular mineral deposition) with increased OPN deposition; acellular cementum is unaffected, indicating acellular cementum mineralization does not depend on matrix vesicle-mediated (PHOSPHO1-driven) initiation. Phospho1-/- mouse histology, immunohistochemistry, ISH, microCT; comparison of cellular vs acellular cementum phenotypes Journal of dental research Medium 27016531
2017 PHOSPHO1 is localized to ameloblast secretory vesicles and the enamel layer; Phospho1-/- mice show reduced enamel mineralization (2-fold reduction in von Kossa silver grain density), decreased phosphate incorporation by EDS, loss of enamel prism architecture, and 1.56-fold increase in prism width, establishing PHOSPHO1 as essential for enamel mineralization. Immunohistochemistry; Western blot; Phospho1-/- mouse; scanning electron microscopy; EDS elemental analysis; von Kossa staining Frontiers in physiology Medium 29089903
2020 PHOSPHO1 negatively regulates brown adipose tissue (BAT) thermogenesis: Phospho1-/- mice are cold-tolerant with higher thermogenic gene expression in BAT; treatment of mice with the PHOSPHO1 substrate phosphocholine is sufficient to induce cold tolerance and thermogenic gene expression, demonstrating the phosphocholine-to-choline conversion catalyzed by PHOSPHO1 suppresses BAT thermogenesis. Phospho1-/- mouse; cold tolerance assay; thermogenic gene expression (qPCR); exogenous phosphocholine treatment in vivo Proceedings of the National Academy of Sciences of the United States of America High 32554489
2020 Phospho1-/- mice exhibit improved glucose homeostasis and resistance to high-fat diet-induced obesity and insulin resistance independent of osteocalcin; decreased serum choline in Phospho1-/- mice is normalized by 2% dietary choline supplementation, which also normalizes insulin sensitivity and fat mass, linking PHOSPHO1's phosphocholine hydrolysis activity to systemic choline levels and metabolic regulation. Phospho1-/- mouse; high-fat diet challenge; metabolomics (serum choline); dietary choline rescue experiment; osteoblast transcriptomics BMC biology High 33092598
2021 Proton pump inhibitors (PPIs) directly inhibit PHOSPHO1 enzymatic activity in vitro (IC50 0.73–19.27 µM for different PPIs) and inhibit bone matrix mineralization in primary osteoblast cultures in a concentration-dependent manner; H2 receptor antagonists have no inhibitory effect on PHOSPHO1, suggesting PPI-specific inhibition. In vitro PHOSPHO1 enzymatic activity assay with PPIs; primary osteoblast mineralization assay Calcified tissue international Medium 34213594
2025 PHOSPHO1 (cytosolic protein) exhibits D609-sensitive phosphatidylcholine-phospholipase C (PC-PLC) and phosphatidylethanolamine-phospholipase C (PE-PLC) activities in vitro; overexpression in HEK293 cells increases cellular diacylglycerol (DG) levels; PHOSPHO1 co-sediments and co-localizes with diacylglycerol kinase δ (DGKδ), suggesting PHOSPHO1 supplies DG upstream of DGKδ. In vitro PLC activity assay; HEK293 overexpression with DG lipid measurement; co-sedimentation and co-localization assays FEBS letters Medium 39992810
2008 A novel alternatively spliced PHOSPHO1 transcript (PHOSPHO1-3a) was identified, encoding a 292 amino acid protein with a 40 amino acid N-terminal secretory signal while retaining all three HAD superfamily catalytic domains; expression confirmed in human and mouse osteoblast-like cells and chondrogenic ATDC5 cells. RT-PCR; sequence analysis; in silico signal peptide prediction; cell-line expression profiling Biochemical and biophysical research communications Low 18471996
2024 Lansoprazole acts as an efficient inhibitor of adipose PHOSPHO1 and produces metabolic benefits (reduced obesity, improved insulin resistance) in a PHOSPHO1-dependent manner; mechanistically, LPZ inhibition of PHOSPHO1 is proposed to suppress conversion of 2-AG-LPA to 2-AG, reducing thermogenic-suppressive cannabinoid receptor signaling. PHOSPHO1 enzymatic inhibition assay; Phospho1-/- mouse rescue/dependency experiment; adipocyte thermogenesis and mitochondrial respiration assays Acta pharmaceutica Sinica. B Medium 38572109

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Loss of skeletal mineralization by the simultaneous ablation of PHOSPHO1 and alkaline phosphatase function: a unified model of the mechanisms of initiation of skeletal calcification. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 177 20684022
2016 DNA methylation of loci within ABCG1 and PHOSPHO1 in blood DNA is associated with future type 2 diabetes risk. Epigenetics 150 27148772
2007 Functional involvement of PHOSPHO1 in matrix vesicle-mediated skeletal mineralization. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 142 17227223
2004 Human PHOSPHO1 exhibits high specific phosphoethanolamine and phosphocholine phosphatase activities. The Biochemical journal 111 15175005
2010 Kinetic analysis of substrate utilization by native and TNAP-, NPP1-, or PHOSPHO1-deficient matrix vesicles. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 109 19874193
2004 PHOSPHO1-A novel phosphatase specifically expressed at sites of mineralisation in bone and cartilage. Bone 80 15050893
2006 The presence of PHOSPHO1 in matrix vesicles and its developmental expression prior to skeletal mineralization. Bone 68 16837257
2010 Inhibition of PHOSPHO1 activity results in impaired skeletal mineralization during limb development of the chick. Bone 54 20053388
2013 Pharmacological inhibition of PHOSPHO1 suppresses vascular smooth muscle cell calcification. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 51 22887744
2019 How To Build a Bone: PHOSPHO1, Biomineralization, and Beyond. JBMR plus 49 31372594
2016 Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 47 26773408
2014 Ablation of osteopontin improves the skeletal phenotype of phospho1(-/-) mice. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 45 24825455
2003 Comparative modelling of human PHOSPHO1 reveals a new group of phosphatases within the haloacid dehalogenase superfamily. Protein engineering 40 14983068
2005 Probing the substrate specificities of human PHOSPHO1 and PHOSPHO2. Biochimica et biophysica acta 31 16054448
2015 The Functional co-operativity of Tissue-Nonspecific Alkaline Phosphatase (TNAP) and PHOSPHO1 during initiation of Skeletal Mineralization. Biochemistry and biophysics reports 27 26457330
2020 Phosphocholine accumulation and PHOSPHO1 depletion promote adipose tissue thermogenesis. Proceedings of the National Academy of Sciences of the United States of America 20 32554489
2016 Role of PHOSPHO1 in Periodontal Development and Function. Journal of dental research 19 27016531
2017 A distinctive patchy osteomalacia characterises Phospho1-deficient mice. Journal of anatomy 17 28737011
2022 Increased PHOSPHO1 expression mediates cortical bone mineral density in renal osteodystrophy. The Journal of endocrinology 16 35900032
2020 PHOSPHO1 is a skeletal regulator of insulin resistance and obesity. BMC biology 15 33092598
2002 Chromosomal localization of the chicken and mammalian orthologues of the orphan phosphatase PHOSPHO1 gene. Animal genetics 14 12464021
2021 Proton Pump Inhibitors Inhibit PHOSPHO1 Activity and Matrix Mineralisation In Vitro. Calcified tissue international 12 34213594
2017 Intravesicular Phosphatase PHOSPHO1 Function in Enamel Mineralization and Prism Formation. Frontiers in physiology 12 29089903
2016 The Expression of PHOSPHO1, nSMase2 and TNAP is Coordinately Regulated by Continuous PTH Exposure in Mineralising Osteoblast Cultures. Calcified tissue international 12 27444010
2022 Perspective on Dentoalveolar Manifestations Resulting From PHOSPHO1 Loss-of-Function: A Form of Pseudohypophosphatasia? Frontiers in dental medicine 8 36185572
2024 Repurposing lansoprazole to alleviate metabolic syndrome via PHOSPHO1 inhibition. Acta pharmaceutica Sinica. B 6 38572109
2008 Identification of a novel splice variant of the haloacid dehalogenase: PHOSPHO1. Biochemical and biophysical research communications 6 18471996
2025 Human PHOSPHO1 exhibits phosphatidylcholine- and phosphatidylethanolamine-phospholipase C activities and interacts with diacylglycerol kinase δ. FEBS letters 5 39992810
2025 Distinct bone metabolic networks identified in Phospho1-/- mice vs. wild type mice using [18F]FDG total-body PET. Frontiers in medicine 4 40470038
2022 PHOSPHO1 Serves as a Key Metabolism-Related Biomarker in the Tumorigenesis of Diffuse Large B-cell Lymphoma. Current medical science 3 35943680
2022 Increased PHOSPHO1 and alkaline phosphatase expression during the anabolic bone response to intermittent parathyroid hormone delivery. Cell biochemistry and function 3 36540015
2013 The use of tissue-nonspecific alkaline phosphatase (TNAP) and PHOSPHO1 inhibitors to affect mineralization by cultured cells. Methods in molecular biology (Clifton, N.J.) 2 23860651
2025 Co-overexpression of the caloric restriction-induced mitochondrial factors PGC-1α and MIPEP upregulates Phospho1 expression in adipocytes. FEBS open bio 1 40574346
2020 PHOSPHO1 Gene DNA Methylations are Associated with a Change in HDL-C Response to Simvastatin Treatment. Current pharmaceutical design 1 32693758
2026 Methylation analysis of PHOSPHO1 and ACACA gene promoters in whole blood samples: insights into metabolic syndrome and associated factors. Journal of diabetes and metabolic disorders 0 41664674