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Gene Review:

Dxcp2 - dexamethasone induced cleft palate 2

Mus musculus

Synonyms: Cps-1, Dcp-2, Dcp2

Tyan, M.L. et al., Gasser, D.L. et al., Gasser, D.L. et al., Gasser, D.L. et al.

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Disease relevance of Dxcp2

The enhancement of susceptibility to glucocorticosteroid-induced cleft palate by vitamin A appears to be a recessive trait and the locus, called Acp, maps centromeric to another corticosteroid-induced cleft palate gene (Dcp-2) that also is in the C4:B144 interval [1].

High impact information on Dxcp2

Polymorphic DNA markers within the cloned region were used to map the cleft palate susceptibility-1 (Cps-1) locus to the interval between Hsp70.1 and BAT6 (valyl-tRNA synthetase) [2].
These data therefore suggest that a gene coding for susceptibility, which we designate Cps-1, maps in the 350-kb interval between H-2S and H-2D, and the congenic strains that we have found to be different have different crossover points within this interval [3].
The Cps-1 gene does not appear to affect the level of glucocorticoid receptors or the susceptibility of mice to phenytoin-induced cleft palate [4].

References

Vitamin A-enhanced cleft palate susceptibility gene maps between C4 and B144 within the H-2 complex. Tyan, M.L., Tyan, D.B. Proc. Soc. Exp. Biol. Med. (1993) [Pubmed]
P1 and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci. Gasser, D.L., Sternberg, N.L., Pierce, J.C., Goldner-Sauve, A., Feng, H., Haq, A.K., Spies, T., Hunt, C., Buetow, K.H., Chaplin, D.D. Immunogenetics (1994) [Pubmed]
Recombinants in the H-2S/H-2D interval of mouse chromosome 17 define the map position of a gene for cleft palate susceptibility. Gasser, D.L., Yadvish, K.N., Trammell, M.A., Goldman, A.S. Teratology (1988) [Pubmed]
Restriction fragment length polymorphisms, glucocorticoid receptors, and phenytoin-induced cleft palate in congenic strains of mice with steroid susceptibility differences. Gasser, D.L., Goldner-Sauvé, A., Katsumata, M., Goldman, A.S. J. Craniofac. Genet. Dev. Biol. (1991) [Pubmed]

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