Fournier A, Zhang Z Q, Tan Y H
Somat Cell Mol Genet. 1985 May;11(3):291-5. doi: 10.1007/BF01534686.
The binding of human interferons to their binding site(s) was measured by the amount of radioiodinated human beta interferon (HuIFNbeta) displaceable by unlabeled human beta, alpha, and gamma interferon (HuIFNbeta, alpha, and gamma). By this approach, HuIFNbeta and HuIFNalpha were found to interact with specific binding sites in cell membranes derived from human cells and mouse-human cell hybrids containing chromosome 21 as their only human chromosome. Specific binding was not observed with cell membranes derived from parental mouse cells or from mouse-human cell hybrids in subsequent generations that have lost human chromosome 21. Although the chromosome 21-positive mouse-human cell hybrids are sensitive to the antiviral effects of HuIFNbeta and HuIFNalpha, they are found to be insensitive to the antiviral effect of HuIFNgamma and to lack specific HuIFNgamma binding sites. These results suggest that the HuIFNbeta and HuIFNalpha but not HuIFNgamma binding sites are coded for by genes located on chromosome 21. The lack of a chromosome 21 gene dosage effect on the inducibility of the antiviral state by HuIFNgamma is consistent with this hypothesis.
通过未标记的人β、α和γ干扰素(HuIFNβ、α和γ)置换的放射性碘化人β干扰素(HuIFNβ)的量来测定人干扰素与其结合位点的结合情况。通过这种方法,发现HuIFNβ和HuIFNα与来源于人细胞以及仅含21号染色体作为其唯一人类染色体的小鼠 - 人细胞杂种的细胞膜中的特异性结合位点相互作用。在亲本小鼠细胞或在随后几代中丢失了人类21号染色体的小鼠 - 人细胞杂种的细胞膜中未观察到特异性结合。虽然21号染色体阳性的小鼠 - 人细胞杂种对HuIFNβ和HuIFNα的抗病毒作用敏感,但发现它们对HuIFNγ的抗病毒作用不敏感且缺乏特异性HuIFNγ结合位点。这些结果表明,HuIFNβ和HuIFNα而非HuIFNγ的结合位点由位于21号染色体上的基因编码。HuIFNγ对抗病毒状态诱导性缺乏21号染色体基因剂量效应与该假设一致。