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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1991 Aug 1;88(15):6472–6476. doi: 10.1073/pnas.88.15.6472

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

J M Spergel 1, S Chen-Kiang 1
PMCID: PMC52107  PMID: 1830663

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.

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Selected References

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