ERK-INDEPENDENT PARTIAL ACTIVATION OF AP-1 SITES BY THE HEPATITIS-B VIRUS HBX PROTEIN

The hepatitis B virus X protein (HBx) is suggested to regulate transcr iption by stimulation of intracellular signalling pathways. We have an alysed the effects of HBx on activation of the MAP kinase (Erk) and JN K/SAPK signalling pathways and confirm a stimulation of the Erk/MAP ki nase in quiescent cells. However, a substantial Erk-independent activa tion of AP-1, and phosphorylation of c-Jun (serine-63), but not Erk-2, was induced by HBx in dividing, serum-maintained cells. These data su ggest that HBx promiscuously activates Erk and JNK responsive pathways and that its overall effect on signalling may be influenced by extern al mitogenic stimuli.