Vanacker J M, Laudet V, Adelmant G, Stéhelin D, Rommelaere J
Unité d'Oncologie Moléculaire, Institut Pasteur de Lille, Centre National de la Recherche Scientifique URA 1160, France.
J Virol. 1993 Dec;67(12):7668-72. doi: 10.1128/JVI.67.12.7668-7672.1993.
Nonstructural (NS) proteins of autonomous parvoviruses can repress expression driven by heterologous promoters, an activity which thus far has not been separated from their cytotoxic effects. It is shown here that, in transient transfection assays, the NS-1 protein of the parvovirus minute virus of mice (MVMp) activates the promoter of the human c-erbA1 gene, encoding the thyroid hormone (T3) receptor alpha. The endogenous c-erbA1 promoter is also a target for induction upon MVMp infection. Moreover, T3 was found to up-modulate the level of cell sensitivity to parvovirus attack. These data suggest an interconnection between T3 signalling and NS cytotoxic pathways.
自主细小病毒的非结构（NS）蛋白能够抑制由异源启动子驱动的表达，到目前为止，这种活性尚未与其细胞毒性作用区分开来。本文表明，在瞬时转染试验中，小鼠细小病毒（MVMp）的NS-1蛋白激活了人类c-erbA1基因的启动子，该基因编码甲状腺激素（T3）受体α。内源性c-erbA1启动子也是MVMp感染后诱导的靶点。此外，发现T3能上调细胞对细小病毒攻击的敏感性水平。这些数据表明T3信号传导与NS细胞毒性途径之间存在相互联系。
