Divergent requirements for the MAPK(ERK) signal transduction pathway during initial virus infection of quiescent primary B cells and disruption of Epstein-Barr virus latency by phorbol esters.
Quiescent primary B lymphocytes and Epstein-Barr virus (EBV)-immortalized lymphoblastoid cell lines express components of the extracellular response kinase arm of the mitogen-activated protein kinase (MAPK(ERK)) signal transduction pathway and transmit signals through the pathway when exposed to appropriate stimuli. Although the MAPK(ERK) pathway is activated following infection with EBV, MAPK/ERK kinase (MEK1) activity is not required to drive the proliferation of infected cells. However, MEK1 contributes to EBV latency control.
Fenton
M
M
School of Biological Sciences, University of Sussex, Brighton, East Sussex BN1 9QG, United Kingdom.
Sinclair
A J
AJ
D001402:B-Lymphocytes / Q000473:pathology / Q000502:physiology* / Q000821:virology*; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D002273:Carcinogens / Q000494:pharmacology; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D004854:Herpesvirus 4, Human / Q000502:physiology*; D006801:Humans; D015398:Signal Transduction; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D017735:Virus Latency / Q000187:drug effects / Q000502:physiology*
D002273:Carcinogens; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D013755:Tetradecanoylphorbol Acetate