Miller A G, Israel D, Whitlock J P
J Biol Chem. 1983 Mar 25;258(6):3523-7.
We have analyzed wild type mouse hepatoma (Hepa 1c1c7) cells and variant cells which are defective in the induction of benzo(a)pyrene-metabolizing enzyme activity. One type of variant has no detectable basal or inducible aryl hydrocarbon hydroxylase activity. This class contains apparently normal cytosolic receptors for 2,3,7,8-tetrachlorodibenzo-p-dioxin, but is unable to translocate the inducer-receptor complex to the nucleus. The second type of variant has low levels of basal and inducible aryl hydrocarbon hydroxylase activity. This class contains cytosolic receptors which are decreased either in their number or in their ability to bind 2,3,7,8-tetrachlorodibenzo-p-dioxin; translocation of the inducer-receptor complex to the nucleus is apparently normal. Cell fusions indicate that both variant phenotypes are recessive with respect to wild type. Complementation analyses indicate that the defects are located on different genes.
我们分析了野生型小鼠肝癌（Hepa 1c1c7）细胞和在苯并(a)芘代谢酶活性诱导方面存在缺陷的变异细胞。一种变异细胞没有可检测到的基础或诱导性芳烃羟化酶活性。这类细胞含有明显正常的2,3,7,8 - 四氯二苯并 - p - 二恶英胞质受体，但无法将诱导剂 - 受体复合物转运至细胞核。第二种变异细胞具有低水平的基础和诱导性芳烃羟化酶活性。这类细胞含有数量减少或结合2,3,7,8 - 四氯二苯并 - p - 二恶英能力降低的胞质受体；诱导剂 - 受体复合物向细胞核的转运显然正常。细胞融合表明，相对于野生型，这两种变异表型都是隐性的。互补分析表明，缺陷位于不同的基因上。
