机理研究表明,Tat通过增强NF-κB信号传导促进K1诱导的血管生成。从机制上讲,我们显示Tat与K1协同作用,诱导miR-891a-5p的表达,该表达直接靶向I alpha B alpha 3'非翻译区,从而导致NF-κB活化。因此,对miR-891a-5p的抑制作用会增加I alpha Bα水平,阻止NF-κB p65的核易位,并最终抑制Tat和K1诱导的血管生成的...
机译:NMMHC IIA抑制通过内皮中的Akt /GSK3β-NF-κB信号传导途径阻碍组织因子表达和静脉血栓形成 7. Poster session 2Morphogenetic mechanisms290MiR-133 regulates retinoic acid pathway during early cardiac chamber specification291Bmp2 regulates atrial differentiation through miR-130 during early heart looping...