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Defective Gene Causes Bone Defects.
Mice lacking a protein called SHIP (Src homology 2-containing inositol-5-phosphatase) have twice as many cells that break down bone as normal mice, according to a study led by F. Patrick Ross at the Washington University School of Medicine (660 Euclid Ave., No. 8057, St. Louis, MO; Tel: 314/362-3567). The extra cells, called osteoclasts, cause the mice to lose a significant amount of bone density and thickness. The mouse strain used in the study also may be the first animal model of a rare genetic disease called juvenile Paget's disease (JPD). Results of the study appear appeared online in Nature Medicine on August 5 and will be published in the September print issue of the journal.
JPD, also known as hereditary hyperphosphatasia or hyperostosis corticalis deformans juvenilis, is a painful skeletal disease characterized by abnormally fast formation and breakdown of bone throughout the body that leads to debilitating fractures and deformities beginning soon after birth.
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