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Ex and exacerbating tooth decay. They have been associated with mutations in collagen in cases of osteogenesis imperfecta (OI) [136]. Defects in the human DSPP gene are the major cause of dentin disorders identified to date [137,138,139]. Mutations in DSPP are associated with five different types of inherited dentin defects ?dentinogenesis imperfecta (DGI) types I, II, III and dentinal dysplasias
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Tta calculations and symmetric docking calculations starting from the CS-Rosetta monomers do not show convergence, indicating an interleaved dimer interface. The fold-and-dock protocol, supplemented by 45 RDCs, converges to a 2.5 ?structure, which shows the correct interleaved backbone topology (Supporting Information Figure 1). Very similar results were obtained for the structural genomics target
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Sociated with the retention of the mutant DSPP in odontoblasts, i.e. a failure to "traffic" the mature DSPP protein out of the cell. Thus if the protein, independent of its mutation, remains trapped in the cell and cannot interact with collagen so as to regulate the mineralization process, the hypo-mineralized phenotype persists. This is likely to be true of other IDPs where mutations could lead t