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 transcription by stimulation of intracellular signalling pathways. We have analysed the effects of HBx on activation of the MAP kinase (Erk) and JNK/SAPK signalling pathways and confirm a stimulation of the Erk/MAP kinase in quiescent cells. However, a substantial Erk-independent activation 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 suggest that HBx promiscuously activates Erk and JNK responsive pathways and that its overall effect on signalling may be influenced by external mitogenic stimuli.
Henkler
F
F
Imperial College of Science, Technology and Medicine, Hammersmith Campus, Department of Infectious Diseases, London, UK. fhenkle@nimr.mrc.ac.uk
Lopes
A R
AR
Jones
M
M
Koshy
R
R
D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000502:physiology*; D002460:Cell Line; D006515:Hepatitis B virus / Q000502:physiology*; D006801:Humans; D010766:Phosphorylation; D015398:Signal Transduction; D015534:Trans-Activators / Q000502:physiology*; D018808:Transcription Factor AP-1 / Q000502:physiology*; D054334:Viral Regulatory and Accessory Proteins; D014779:Virus Replication
D015534:Trans-Activators; D018808:Transcription Factor AP-1; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein; D017871:Calcium-Calmodulin-Dependent Protein Kinases