By J. Esparza-Gordillo
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8, (August 2001), pp. , Takahata, N. & Yonekawa, H. (2005). Origins of mouse inbred strains deduced from whole- Mouse Models for Atopic Dermatitis Developed in Japan 37 genome scanning by polymorphic microsatellite loci. 1, (January 2005), pp. , Matsumoto, M. & Matsuda H. (2001). Atopic dermatitis-like skin lesions induced by topical application of mite antigens in NC/Nga mice. 3, (November 2001), pp. 239-247, ISSN 1018-2438 Schultz Larsen, F. (1993). Atopic dermatitis: a genetic-epidemiologic study in a populationbased twin sample.
A major determinant quantitative-trait locus responsible for atopic dermatitis-like skin lesions in NC/Nga mice is located on Chromosome 9. Immunogenetics, Vol. 9, (February 2001), pp. , & Hayakawa, J. (March 1983). ). , Tokyo. , Nagami, T. & Teramoto, S. (1969). Differences in hematopoietic death among inbred strains of mice. ), pp. , Satode, R. & Shiomoto, Y. (2006). Increased susceptibility to Staphylococcus aureus colonization of the skin of the NOA mouse: a potentially useful animal model for evaluating antiseptic effects.
2003b). , 2006). , 2006). Therefore, the DS-Nh mouse is a model of the pruritus associated with human AD. Fig. 3. Using (NC x MSM) N2 mice, a linkage disequilibrium analysis was performed, and a single significant genetic locus responsible for AD was identified on chromosome 9. We designated the locus derm1. Mouse Models for Atopic Dermatitis Developed in Japan 29 The Nh mutation is controlled by a single dominant mutation that occurred in the transient receptor potential (TRP) cation channel, subfamily V member 3 (Trpv3).
Atopic Dermatitis - Disease Etiology, Clinical Mgmt. by J. Esparza-Gordillo