Veit M, Schmidt M F
Institut für Immunologie und Molekularbiologie, Freie Universität Berlin, Germany.
FEBS Lett. 1993 Dec 27;336(2):243-7. doi: 10.1016/0014-5793(93)80812-9.
The timing of the attachment of fatty acids to the hemagglutinin (HA) of influenza A virus was studied. Treatment of virus infected cells with brefeldin A (BFA), a drug which blocks intracellular transport along the exocytic pathway at a pre-Golgi site, does not prevent palmitoylation of HA. The relationship of HA-palmitoylation to the oligomerisation and to the proteolytical cleavage of the protein revealed that the uncleaved trimer of HA is the substrate for the acylating enzyme in virus infected cells. The results are discussed with regard to the intracellular site of palmitoylation.
研究了脂肪酸与甲型流感病毒血凝素(HA)结合的时间。用布雷菲德菌素A(BFA)处理病毒感染细胞,该药物在高尔基体前位点阻断沿胞吐途径的细胞内运输,但并不阻止HA的棕榈酰化。HA棕榈酰化与该蛋白的寡聚化和蛋白水解切割之间的关系表明,未切割的HA三聚体是病毒感染细胞中酰化酶的底物。结合棕榈酰化的细胞内位点对结果进行了讨论。