Interleukin 6 enhances a cellular activity that functionally substitutes for E1A protein in transactivation.

TitleInterleukin 6 enhances a cellular activity that functionally substitutes for E1A protein in transactivation.
Publication TypeJournal Article
Year of Publication1991
AuthorsSpergel JM, Chen-Kiang S
JournalProc Natl Acad Sci U S A
Volume88
Issue15
Pagination6472-6
Date Published1991 Aug 01
ISSN0027-8424
KeywordsAdenovirus Early Proteins, Adenoviruses, Human, Base Sequence, Cell Line, Cell Nucleus, DNA Replication, DNA, Neoplasm, DNA, Viral, Fetus, Genes, Viral, HeLa Cells, Humans, Interleukin-6, Liver, Molecular Sequence Data, Oligonucleotide Probes, Oncogene Proteins, Viral, Promoter Regions, Genetic, Restriction Mapping, Transcription Factors, Transcription, Genetic, Transcriptional Activation
Abstract

An interleukin 6 (IL-6)-regulated cellular activity in HepG2 cells is found to functionally substitute for the transcriptional transactivator product of the adenovirus transforming gene E1A in transactivating E1A-dependent and E1A-responsive viral early genes. Mutant viruses deficient in E1A expression replicate in HepG2 cells. Induction with IL-6 leads to significant enhancement of synthesis of viral early E1B and E2ae mRNAs by greater than 30-fold and increases viral replication to the wild-type levels. The E1A-substituting activity activates E1A-responsive promoters in transient transfection, and this transcriptional activity is regulated by IL-6 induction. Formation of distinct protein-promoter complexes by binding of proteins in nuclear extracts prepared from HepG2 cells to the E1A-dependent E2ae promoter further supports the possibility that this activity may be a nuclear component in the IL-6 signal transduction pathway.

DOI10.1073/pnas.88.15.6472
Alternate JournalProc Natl Acad Sci U S A
PubMed ID1830663
PubMed Central IDPMC52107
Grant ListAI 24404 / AI / NIAID NIH HHS / United States
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Selina Chen-Kiang, Ph.D.

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