Activation of the cellular transcription factor AP-1 in herpes simplex virus infected cells is dependent on the viral immediate-early protein ICPO
KL Jang, B Pulverer, JR Woodgett… - Nucleic acids …, 1991 - academic.oup.com
KL Jang, B Pulverer, JR Woodgett, DS Latchman
Nucleic acids research, 1991•academic.oup.comLytic infection with herpes simplex virus (HSV) results in the repression of most host cell
protein synthesis but produces an increased activity of the cellular AP-1 transcription factor.
This increase Is paralleled by an increase In the transcription rate of the proto-oncogene
encoding the AP-1 component, c-Jun resulting in an increase in c-Jun protein In infected
cells. The increased AP-1 activity in infected cells is dependent upon the HSV immediate-
early protein ICPO. Thus a mutant lacking the gene encoding this protein falls to increase AP …
protein synthesis but produces an increased activity of the cellular AP-1 transcription factor.
This increase Is paralleled by an increase In the transcription rate of the proto-oncogene
encoding the AP-1 component, c-Jun resulting in an increase in c-Jun protein In infected
cells. The increased AP-1 activity in infected cells is dependent upon the HSV immediate-
early protein ICPO. Thus a mutant lacking the gene encoding this protein falls to increase AP …
Abstract
Lytic infection with herpes simplex virus (HSV) results in the repression of most host cell protein synthesis but produces an increased activity of the cellular AP-1 transcription factor. This increase Is paralleled by an increase In the transcription rate of the proto-oncogene encoding the AP-1 component, c-Jun resulting in an increase in c-Jun protein In infected cells. The increased AP-1 activity in infected cells is dependent upon the HSV immediate-early protein ICPO. Thus a mutant lacking the gene encoding this protein falls to increase AP-1 activity whilst an ICPO expression plasmid can specifically increase the activity of an AP-1 dependent promoter in co-transfection experiments. The Implications of these effects in the interaction of HSV with cultured cells are discussed.
Oxford University Press