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Gene Review:

ocd - osteochondrodystrophy

Mus musculus

Sweet, H.O. et al., Karaplis, A.C. et al., Lopez-Nieto, C.E. et al., Poirier, C. et al.

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High impact information on ocd

NKT was mapped by linkage disequilibrium to mouse chromosome 19, the same site to which several mouse mutations localize, including that for osteochondrodystrophy (ocd) [1].
These actions of PTHrP are probably responsible for the delay in chondrocyte development seen in Jansen osteochondrodystrophy, a disease caused by ligand-independent activation of the PTH-PTHrP receptor (Schipani et al., 1995) [2].
A high-resolution genetic map of mouse chromosome 19 encompassing the muscle-deficient osteochondrodystrophy (mdf-ocd) region [3].
Osteochondrodystrophy (ocd) is a new autosomal recessive mouse mutation characterized by a short, slightly domed head, reduced body size, disproportionately shortened long bones of the legs, supination of the forefeet, and short thickened tail [4].
Osteochondrodystrophy has been mapped to a position near the centromere of mouse chromosome (Chr) 19 [4].

References

Molecular cloning and characterization of NKT, a gene product related to the organic cation transporter family that is almost exclusively expressed in the kidney. Lopez-Nieto, C.E., You, G., Bush, K.T., Barros, E.J., Beier, D.R., Nigam, S.K. J. Biol. Chem. (1997) [Pubmed]
Physiological roles for parathyroid hormone-related protein: lessons from gene knockout mice. Karaplis, A.C., Kronenberg, H.M. Vitam. Horm. (1996) [Pubmed]
A high-resolution genetic map of mouse chromosome 19 encompassing the muscle-deficient osteochondrodystrophy (mdf-ocd) region. Poirier, C., Blot, S., Fernandes, M., Carle, G.F., Stanescu, V., Stanescu, R., Guénet, J.L. Mamm. Genome (1998) [Pubmed]
Osteochondrodystrophy (ocd): a new autosomal recessive mutation in the mouse. Sweet, H.O., Bronson, R.T. J. Hered. (1991) [Pubmed]

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