Saito M, Ueno I, Egawa K
Biochim Biophys Acta. 1982 Aug 6;717(2):301-4. doi: 10.1016/0304-4165(82)90183-0.
Binding of 125I-labelled epidermal growth factor (EGF) to C3H/2K cells and the effect of a tumor promotor, 12-O-tetradecanoyl phorbol-13-acetate (TPA) and of a tumor promotor antagonist, retinoic acid, on the binding was studied. Scatchard plot analysis of the binding showed the presence of two types of binding sites with different affinity to EGF. Treatment of the cells with retinoic acid for 1 h resulted in elevation of the affinity of both sites without changing their number per cell. Prolonged exposure to retinoic acid abrogated this elevation of the affinity and caused cycloheximide-sensitive increase of the number of the binding sites of both types. TPA inhibited binding of EGF to the cells by abolishing the binding to the high affinity sites, whereas retinoic acid, in the presence of TPA, enhanced it by increasing the number of the low affinity sites.
研究了125I标记的表皮生长因子（EGF）与C3H/2K细胞的结合，以及肿瘤促进剂12-O-十四酰佛波醇-13-乙酸酯（TPA）和肿瘤促进剂拮抗剂视黄酸对该结合的影响。对结合进行的Scatchard图分析表明存在两种对EGF具有不同亲和力的结合位点。用视黄酸处理细胞1小时导致两个位点的亲和力升高，而每个细胞的位点数量不变。长时间暴露于视黄酸消除了这种亲和力的升高，并导致两种类型结合位点数量的环己酰亚胺敏感增加。TPA通过消除与高亲和力位点的结合来抑制EGF与细胞的结合，而在TPA存在的情况下，视黄酸通过增加低亲和力位点的数量来增强结合。
