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EC Number
General Information
Commentary
Reference
malfunction
both male and female Phospho1-/- mice are smaller than age-matched heterozygous and wild-type controls and exhibit growth retardation, where bones from 1-month-old male mice are shorter, phenotypes, overview
malfunction
long bones from Phospho1-/- mice do not fracture during 3-point bending but deform plastically. With dynamic loading nanoindentation the elastic modulus and hardness of Phospho1-/- tibiae are significantly lower than wild-type tibia. Mutant mice show significantly lower mineral:matrix ratios and lower carbonate substitutions in Phospho1-/- tibia, phenotype, overview
metabolism
the regulation of choline metabolism and consequently PchP synthesis may reflect an adaptive response of Pseudomonas aeruginosa to environmental conditions. Regulation of pchP gene expression, overview
more
catalytic mechanism of phosphocholine with Pcho as the substrate, Mg2+ or Zn2+ as activators, and alkylammonium compounds as inhibitors, overview. Zn2+ induces a conformational change in the active center that is communicated to the inhibitory site, producing a compact or closed structure. In contrast, Mg2+ produces a relaxed or open conformation
more
combination of molecular modeling, directed mutagenesis and enzyme kinetics to study the mode of interaction of PchP phosphatase with the choline moiety of the substrate
physiological function
calli of Phospho1-/- mice display a mild reduction of bone volume and an increase in trabecular number and a decrease in trabecular thickness and separation. There is a marked increase of osteoid volume over bone volume in the Phospho1-/- callus. Phospho1-/- fractured bone is more elastic than the wild-type bone
physiological function
cell line MC3T3-E1 clone 14 cells express high levels of Phospho1 and low levels of tissue-nonspecific alkalinephosphatase TNAP and they mineralize their matrix strongly. Clone 24 cells express high levels of TNAP and low levels of Phospho1 and mineralize their matrix poorly. Lentiviral Phospho1 overexpression in clone 24 cells results in higher Phospho1 and TNAP protein expression and increased levels of matrix mineralization. specific inhibition of Phospho1 individually reduces mineralization levels of Phospho1 overexpressing C24 cells, whereas the simultaneous addition of inhibitors of both Phospho1 and TNAP essentially abolishes matrix mineralization
physiological function
in Phospho1-/- mice, acellular cementum formation and mineralization are unaffected, whereas cellular cementum deposition increases despite delayed mineralization and cementoid. Phospho1-/- mice feature disturbances in alveolar bone mineralization. Parallel to other skeletal sites, deposition of mineral-regulating protein osteopontin is increased in alveolar bone in Phospho1-/- mice. Genetic ablation of Spp1, the gene encoding osteopontin, does not ameliorate dentoalveolar defects in Phospho1-/- mice
physiological function
loss of PECP1 activity exacerbates biochemical and morphological effects of phosphate starvation. Constitutive ectopic expression of PECP1 reduces phosphoethanolamine and phosphocholine levels
physiological function
PHOSPHO1 is a phosphoethanolamine/phosphocholine phosphatase involved in the generation of inorganic phosphate for bone mineralization
Results 1 - 10 of 15 > >>