Coughlin J P, Donahoe P K, Budzik G P, MacLaughlin D T
Mol Cell Endocrinol. 1987 Jan;49(1):75-86. doi: 10.1016/0303-7207(87)90065-7.
The fetal regressor Müllerian inhibiting substance (MIS), in concentrations as low as picomolar, inhibited the growth of A-431 cells and the autophosphorylation of its epidermal growth factor (EGF) receptor. The inhibition of membrane phosphorylation was due neither to the reduction of the total number of EGF receptor binding sites, nor to stimulation of intrinsic phosphates, but rather to inhibition of tyrosine kinase activity. MIS control of EGF receptor autophosphorylation by tyrosine kinase may be one mechanism by which Müllerian duct regression in the embryo and the inhibition of A-431 proliferation is initiated. In addition, MIS as an inhibitor of phosphorylation may furnish a tool to probe the role of membrane phosphorylation in growth control.
胎儿退化因子苗勒管抑制物质（MIS），即使浓度低至皮摩尔，也能抑制A - 431细胞的生长及其表皮生长因子（EGF）受体的自身磷酸化。膜磷酸化的抑制既不是由于EGF受体结合位点总数的减少，也不是由于内在磷酸酶的刺激，而是由于酪氨酸激酶活性的抑制。MIS通过酪氨酸激酶对EGF受体自身磷酸化的调控可能是胚胎中苗勒管退化和A - 431细胞增殖抑制启动的一种机制。此外，MIS作为一种磷酸化抑制剂，可能为探究膜磷酸化在生长调控中的作用提供一种工具。
