P5L mutation in Ank results in an increase in extracellular inorganic pyrophosphate during proliferation and nonmineralizing hypertrophy in stably transduced ATDC5 cells 英文参考文献.docVIP

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P5L mutation in Ank results in an increase in extracellular inorganic pyrophosphate during proliferation and nonmineralizing hypertrophy in stably transduced ATDC5 cells 英文参考文献.doc

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P5L mutation in Ank results in an increase in extracellular inorganic pyrophosphate during proliferation and nonmineralizing hypertrophy in stably transduced ATDC5 cells 英文参考文献

Available online /content/8/6/R164 Research article Open Access Vol 8 No 6 P5L mutation in Ank results in an increase in extracellular inorganic pyrophosphate during proliferation and nonmineralizing hypertrophy in stably transduced ATDC5 cells Raihana Zaka1, David Stokes1, Arnold S Dion2, Anna Kusnierz1, Fei Han1 and Charlene J Williams1 1Division of Rheumatology, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA 2College of Graduate Studies, Thomas Jefferson University, Philadelphia, PA 19107, USA Corresponding author: Charlene J Williams, charlene.williams@ Received: 10 Aug 2006 Revisions requested: 30 Aug 2006 Revisions received: 5 Oct 2006 Accepted: 26 Oct 2006 Published: 26 Oct 2006 Arthritis Research Therapy 2006, 8:R164 (doi:10.1186/ar2072) This article is online at: /content/8/6/R164 ? 2006 Zaka et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Ank is a multipass transmembrane protein that regulates the cellular transport of inorganic pyrophosphate. In the progressive ankylosis (ank) mouse, a premature termination mutation at glutamic acid 440 results in a phenotype characterized by inappropriate deposition of basic calcium phosphate crystals in skeletal tissues. Mutations in the amino terminus of ANKH, the human homolog of Ank, result in familial calcium pyrophosphate dihydrate deposition disease. It has been hypothesized that these mutations result in a gain-of-function with respect to the elaboration of extracellular inorganic pyrophosphate. To explore this issue in a mineralization-competent system, we stably transduced ATDC5 cells with wild-type Ank as well as with transduced cells. The cell line expressing the proline to leuc