Lee K A, Edery I, Hanecak R, Wimmer E, Sonenberg N
J Virol. 1985 Aug;55(2):489-93. doi: 10.1128/JVI.55.2.489-493.1985.
Infection of HeLa cells by poliovirus results in proteolysis of the large subunit (P220) of the cap-binding protein complex. This is believed to cause the rapid shut-off of host protein synthesis during poliovirus infection. In this communication we examined the possible involvement of poliovirus proteins 3C (a proteinase) and 2C in cleavage of P220. Using antisera against these two viral polypeptides, we were unable to inhibit proteolysis of P220 in an in vitro assay. These results indicate that viral proteins 3C and 2C are not directly involved in cleaving P220 and hence do not cause shut-off of cellular protein synthesis.
脊髓灰质炎病毒感染HeLa细胞会导致帽结合蛋白复合体的大亚基(P220)发生蛋白水解。据信,这会导致脊髓灰质炎病毒感染期间宿主蛋白质合成的迅速停止。在本通讯中,我们研究了脊髓灰质炎病毒蛋白3C(一种蛋白酶)和2C在P220裂解过程中可能的作用。使用针对这两种病毒多肽的抗血清,我们无法在体外试验中抑制P220的蛋白水解。这些结果表明,病毒蛋白3C和2C不直接参与裂解P220,因此不会导致细胞蛋白质合成的停止。