Further studies on ATP-mediated CA deposition by isolated matrix vesicles

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Summary

ATP at serum levels can support matrix vesicle-mediated Ca deposition even though the Ca × P ion product is held at physiological levels

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  • Inhibition of PHOSPHO1 activity results in impaired skeletal mineralization during limb development of the chick

    2010, Bone
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    The location of TNAP to the outer surface of MV membrane and the role of this enzyme as a pyrophosphatase suggest that other molecules or mechanisms are responsible for increasing intravesicular Pi levels to achieve a Pi/PPi ratio conducive for crystallization. The sodium-dependent phosphate type III transporter Pit-1 [43,44] and other phosphatases known to be present in MVs, including pyrophosphatase, AMPase, and ATPase [45–47] may be involved. Recent work has presented the first functional evidence that PHOSPHO1 is a MV phosphatase involved in skeletal mineralization [23].

  • PHOSPHO1 - A novel phosphatase specifically expressed at sites of mineralisation in bone and cartilage

    2004, Bone
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    The source of Pi in the TNAP mutant mouse is unclear and although it may be supplied through other routes such as intestinal absorption [38], it is also possible that an alternative phosphatase is responsible for the generation of Pi for hydroxyapatite formation in the mouse. Several authors have identified pyrophosphatase, ATPase and nucleoside triphosphate pyrophosphohydrolase activities in MVs [39,40] but these enzymes, and the reactions that they catalyze, have not been further characterised. We now propose that a previously unrecognized novel phosphatase, PHOSPHO1 [9,12], may also be a phosphatase involved in skeletal mineralisation.

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This paper was presented at the Fifth International Conference on Cell-Mediated Calcification and Matrix Vesicles, held November 16–20, 1991, Hilton Head, South Carolina.

Partially supported by NIH grant DE05262.

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