Overexpression of wild-type Ras enhanced CpG ODN-induced ERK, JNK and NF-xJB reporter gene activation, On the contrary, RasN17 transfection inhibited CpG ODN-induced ERK1/2 and JNK1/2 phosphorylation and NF-KB reporter gene activation.

• 我们用免疫沉淀实验发现CpG ODN还能诱导Ras与TLRg的结合。 同样条件下non一CpG既不能活化Ras，也不能诱导Ras/T LRg复合物的形成，提示Ras活化以及Ras与TLRg的结合具有CpG基序特异性。