Genetic control of radiation leukemia virus-induced tumorigenesis II. Influence of Srlv-1, a locus not linked to H-2.
A single locus, tentatively denoted Srlv-1 (susceptibility to radiation leukemia virus [RadLV]-1), confers dominant susceptibility to RadLV-induced leukemogenesis. Srlv-1 is not linked to H-2, and appears to be distinct from Fv-1 and Fv-2. Preliminary data suggest that Srlv-1 affected virus proliferation. A striking feature of this system is that Srlv-1 overrides the protection afforded by the H2D-associated dominant resistance to RadLV-induced neoplasia.
D000818:Animals; D005796:Genes; D005799:Genes, Dominant; D008040:Genetic Linkage; D006649:Histocompatibility Antigens; D009052:Leukemia Virus, Murine; D007942:Leukemia, Experimental / Q000209:etiology / Q000235:genetics*; D051379:Mice
D006649:Histocompatibility Antigens