title: Lack of gene complementation prevents expression of I-Ek in recombinant A.TFR5.
abstract: The I-E molecule is produced by complementation of genes in I-A (Ae) and I-E (E alpha). Ia specificities 22 and 23 are generated by the hybrid molecule, whereas Ia.7 is an allotypic determinant presumably on the alpha-chain of the I-E molecule. Recombinant A.TFR5 (AfEk) lacks detectable I-E molecule since Af and Ek cannot complement. In a cross between A.TFR5 and B10.A(4R) (AkEb), Aek and E alpha k can successfully complement to express the I-Ek molecule on the cell surface of the heterozygote. Haplotypes H-2b and H-2s can also provide the permissive Abe and Ase molecules for complementation with Ek alpha of A.TFR5.
mesh_terms: D000042:Absorption; D000818:Animals; D003433:Crosses, Genetic; D006649:Histocompatibility Antigens / Q000235:genetics*; D007106:Immune Sera / Q000494:pharmacology; D051379:Mice; D008805:Mice, Inbred A; D014176:Protein Biosynthesis; D011487:Protein Conformation; D011995:Recombination, Genetic; D013154:Spleen / Q000276:immunology
chemical_list: D006649:Histocompatibility Antigens; D007106:Immune Sera