【摘要】 以小鼠成纤维细胞为模型,探讨Nodal对趋化因子CCL5的调控作用。采用Western blotting、实时荧光定量PCR、小分子RNA干扰技术、质粒过表达技术等测试方法对Nodal调控的CCL5的机制进行探究。结果发现,Nodal可以引起NF-KappaB入核增加,从而促进CCL5的转录,并且Nodal还可以激活AKT/GSK-3β通路。由此可以得出,转录因子NF-KappaB在Nodal诱导的CCL5上调中发挥着重要作用,并且AKT/GSK-3β通路参与了Nodal诱导的CCL5的上调。更多还原

【Abstract】 Using mouse fibroblast as model,the regulation of Nodal on chemokine CCL5 was investigated.The mechanism of CCL5 regulation by Nodal was explored by Western blotting,quantitative real-time PCR,gene over-expression and RNA interference methods.The results indicate that Nodal can promote the location in nucleus of NF-KappaB,which make a contribution to the transcription of CCL5.Nodal also can activate AKT/GSK-3βpathway.Therefore,it can be concluded that transcription factor NF-KappaB plays an important role in Nodal induced upregulation of CCL5,and the AKT/GSK-3 beta pathway is involved in the upregulation of Nodal induced CCL5.更多还原