【摘要】 目的 探討佛波酯激活的蛋白激酶C與扭轉蛋白A在亞細胞成分中的表達之間的關系?！》椒ā〔捎妹庖邿晒夥ㄓ^察扭轉蛋白A在原代培養(yǎng)的神經(jīng)元和小鼠胚胎成纖維細胞（NIH 3T3細胞）中的分布。運用蛋白質(zhì)印跡法分析蛋白激酶C和扭轉蛋白A在細亞細胞成分中的表達。 結果 扭轉蛋白A在NIH 3T3細胞中的表達類似于神經(jīng)元。扭轉蛋白A在細胞質(zhì)溶質(zhì)、膜成分中均有分布。佛波酯活化蛋白激酶C后并不引起扭轉蛋白A在細胞質(zhì)成分和膜成分中表達含量的變化?！〗Y論 扭轉蛋白A可能是膜相關蛋白，細胞氧化應激中扭轉蛋白A表達上調(diào)和重分布變化不是由佛波酯誘導的蛋白激酶C活化途徑來實現(xiàn)的。鑒于扭轉蛋白A表達上調(diào)具有潛在的治療原發(fā)性早發(fā)扭轉性肌張力障礙的前景，影響其分布和表達的分子機制需要進一步研究?！続bstract】 Objective To investigate the relationship between the phorbol 12-myristate 13-acetate (PMA) activated protein kinase C (PKC) and the subcellular expression of TorsinA protein. Methods The expression of TorsinA in the primary cultured neurons and the NIH 3T3 cells was detected by immunofluorescence. The expression of PKC and TorsinA in subcellular fraction was analyzed by the western blotting. Results The expression pattern of TorsinA in NIH 3T3 cells was similar to neuron. PMA, an activator of PKC, did not promote the up-expression of TorsinA or redistribution in the subcellular fraction of NIH 3T3 cells. Conclusions TorsinA may be a membrane-associated protein. The up-regulation and redistribution of TorsinA is not caused by the pathway of the PMA activating PKC after cells insulted by oxidative stress. We should pay more attention on the mechanisms of the expression of TorsinA protein for the potential therapies to early-onset primary torsion dystonia (DYT1).