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- W623724467 abstract "Research Article1 December 1991free access Changes in NF-kappa B and ISGF3 DNA binding activities are responsible for differences in MHC and beta-IFN gene expression in Ad5- versus Ad12-transformed cells. U. Nielsch U. Nielsch Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author S.G. Zimmer S.G. Zimmer Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author L.E. Babiss L.E. Babiss Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author U. Nielsch U. Nielsch Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author S.G. Zimmer S.G. Zimmer Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author L.E. Babiss L.E. Babiss Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author Author Information U. Nielsch1, S.G. Zimmer1 and L.E. Babiss1 1Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021. The EMBO Journal (1991)10:4169-4175https://doi.org/10.1002/j.1460-2075.1991.tb04995.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Changes in MHC class I expression are frequently observed in tumors, which represents at least one mechanism by which tumor cells escape immune surveillance. MHC class I expression is often suppressed in type 12 adenovirus (Ad12)-transformed rodent cells, but is highly induced in Ad5-transformed cells. This difference helps to explain why Ad12 but not Ad5 can induce tumors in immunocompetent syngeneic rats. In this report we demonstrate that only Ad5- but not Ad12-transformed rodent fibroblasts constitutively express beta-IFN which results in ISGF3 factor induction, and stimulation of MHC class I expression. Furthermore, we demonstrate that in contrast to Ad12-transformed cells, Ad5-transformed cells show constitutive levels of nuclear NF-kappa B-like DNA binding activity. This is of particular interest since both the beta-IFN and the MHC class I promoters contain an NF-kappa B DNA binding site. Thus, high levels of MHC class I expression in Ad5-transformed cells are due to a combinatorial stimulation of two cis-regulatory sequences of the MHC class I promoter: the NF-kappa B binding site and the interferon stimulated response element (ISRE), which binds the ISGF3 factor complex. The failure of Ad12-transformed cells to activate this pathway explains their low levels of MHC class I expression and their greater oncogenicity. Previous ArticleNext Article Volume 10Issue 131 December 1991In this issue RelatedDetailsLoading ..." @default.
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- W623724467 title "Changes in NF-kappa B and ISGF3 DNA binding activities are responsible for differences in MHC and beta-IFN gene expression in Ad5- versus Ad12-transformed cells." @default.
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