All of these studies suggested a mechanism for IL-6 activation whose essential feature is the requirement for the bZIP region of C/EPBb to synergize with NF-kB, although this remains to be further investigated
burden in JNK1 2/2 mice. MLK3 2/2 mice, a kinase upstream of JNK1, display increased Influenza A burden due to increased epithelial cell survival and viral replication. The reason for…