Examination of the roles of transcription factor Sp1-binding sites and an octamer motif in trans induction of the herpes simplex virus thymidine kinase gene.
Herpes simplex virus mutants with both Sp1-binding sites in the thymidine kinase (tk) promoter inactivated or an octamer motif deleted were at most modestly impaired for tk expression. Thus, no cellular transcription factor that binds upstream of the tk TATA box is solely required for trans induction of this gene.
Böni
J
J
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115.
Coen
D M
DM
D001483:Base Sequence; D001665:Binding Sites; D004268:DNA-Binding Proteins / Q000502:physiology*; D005814:Genes, Viral; D009154:Mutation; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000032:analysis; D018139:Simplexvirus / Q000235:genetics*; D016329:Sp1 Transcription Factor; D013937:Thymidine Kinase / Q000096:biosynthesis / Q000235:genetics*; D014157:Transcription Factors / Q000502:physiology*; D014158:Transcription, Genetic; D014759:Viral Envelope Proteins / Q000235:genetics
D004268:DNA-Binding Proteins; D012333:RNA, Messenger; D016329:Sp1 Transcription Factor; D014157:Transcription Factors; D014759:Viral Envelope Proteins; C038535:glycoprotein gC, herpes simplex virus type 1; D013937:Thymidine Kinase