A schematic which illustrates the contribution of EBNA3C to oncogenic transformation of B-cells through stabilization of IRF4 and degradation of IRF8 resulting in activation of IRF4 targeted proteins.

<p>EBNA3C interacts with IRF4 and IRF8 proteins and enhances the stability of IRF4 through inhibition of the poly-ubiquitination process. However, in the presence of EBNA3C, IRF4 targets IRF8 and facilitate the subsequent degradation of IRF8. EBNA3C can also contribute to B-cell proliferation by activating IRF4 downstream signaling as well as inhibiting the growth suppressive and apoptosis inducing properties of IRF8. This molecular strategy potentiates oncogenic activity of IRF4 in EBV transformed B-cell proliferation.