Changes in alpha-1-antichymotrypsin expression in vaccinia virus infected HepG2 cells.
Human hepatoma cells (HepG2) synthesize and secrete several plasma proteins that are inhibited in a time- and dose-dependent manner after vaccinia virus infection. However, infection of the HepG2 cells with a low dose of the virus (up to 1 plaque forming unit/cell) stimulated the expression of alpha-1-antichymotrypsin, which was demonstrated by means of electroimmunoassay and Northern blot analysis. This stimulation appeared to be on the level of transcription as shown in transient transfection experiments using various alpha-1-antichymotrypsin gene promoter constructs. In contrast to interleukin-6, virus-induced activation of the alpha-1-antichymotrypsin gene transcription does not require the STAT (signal transducers and activators of transcription) binding elements present in the alpha-1-antichymotrypsin gene promoter. Furthermore, alpha-amanitin, which inhibits eukaryotic RNA polymerase II and III, did not affect alpha-1-antichymotrypsin stimulation by the virus, indicating involvement of the viral transcriptional apparatus in transient activation of alpha-1-antichymotrypsin gene expression.
Slezak
K
K
Institute of Molecular Biology, Jagiellonian University, Kraków, Poland.
Dobierzewska
A
A
Rokita
H
H
D000546:Amanitins / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger; D014407:Tumor Cells, Cultured; D014616:Vaccinia virus / Q000502:physiology*; D000514:alpha 1-Antichymotrypsin / Q000235:genetics / Q000378:metabolism*
D000546:Amanitins; D012333:RNA, Messenger; D000514:alpha 1-Antichymotrypsin