Polet H, Fryxell D
Department of Pathology, University of Illinois, College of Medicine, Chicago, IL 60612.
Biochim Biophys Acta. 1989 Oct 9;1013(3):279-86. doi: 10.1016/0167-4889(89)90147-x.
Stimulation of resting Chang liver or monkey kidney cells, prelabeled with [3H]leucine, by epidermal growth factor (EGF), caused inhibition of cellular protein degradation and a parallel increase nuclear translocation of 3H-labeled non-histone proteins and DNA synthesis. Nuclear translocation of these proteins was independent of protein synthesis. Fractionation of the nuclear 3H-labeled non-histone proteins in a pH gradient of 2.5-6.5 showed that the protein fractions with a high degree of proteolysis in resting cells corresponded to the protein fractions with a high extent of translocation in stimulated cells, suggesting that degradation and translocation of these proteins may be related. EGF inhibited cellular uptake of [3H]chloroquine, suggesting that EGF inhibits non-histone protein degradation via the lysosomal pathway. These observations support the hypothesis that EGF induces non-histone protein translocation to the nucleus by inhibiting lysosomal degradation of these proteins.
用[3H]亮氨酸预标记的静止的张氏肝细胞或猴肾细胞，经表皮生长因子（EGF）刺激后，细胞蛋白质降解受到抑制，同时3H标记的非组蛋白的核转位及DNA合成平行增加。这些蛋白质的核转位与蛋白质合成无关。在2.5 - 6.5的pH梯度中对核3H标记的非组蛋白进行分级分离，结果显示，静止细胞中具有高度蛋白水解作用的蛋白组分与受刺激细胞中具有高度转位作用的蛋白组分相对应，这表明这些蛋白质的降解和转位可能有关。EGF抑制细胞对[3H]氯喹的摄取，提示EGF通过溶酶体途径抑制非组蛋白的降解。这些观察结果支持了这样的假说，即EGF通过抑制这些蛋白质的溶酶体降解来诱导非组蛋白转位至细胞核。
