Lack of gene complementation prevents expression of I-Ek in recombinant A.TFR5.
Lack of gene complementation prevents expression of I-Ek in recombinant A.TFR5.
复制标题
缺乏基因互补会阻碍重组 A.TFR5 中 I-Ek 的表达。
作者：
W. Lafuse;J. Mccormick;C. David
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.
