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Stat1-Independent Regulation of Gene Expression in Response to IFN-γ

Chilakamarti V. Ramana, M. Pilar Gil, Yulong Han, Richard M. Ransohoff, Robert D. Schreiber and George R. Stark
Proceedings of the National Academy of Sciences of the United States of America
Vol. 98, No. 12 (Jun. 5, 2001), pp. 6674-6679
Stable URL: http://www.jstor.org/stable/3055870
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Stat1-Independent Regulation of Gene Expression in Response to IFN-γ
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Abstract

Although Stat1 is essential for cells to respond fully to IFN-γ, there is substantial evidence that, in the absence of Stat1, IFN-γ can still regulate the expression of some genes, induce an antiviral state and affect cell growth. We have now identified many genes that are regulated by IFN-γ in serum-starved Stat1-null mouse fibroblasts. The proteins induced by IFN-γ in Stat1-null cells can account for the substantial biological responses that remain. Some genes are induced in both wild-type and Stat1-null cells and thus are truly Stat1-independent. Others are subject to more complex regulation in response to IFN-γ, repressed by Stat1 in wild-type cells and activated in Stat1-null cells. Many genes induced by IFN-γ in Stat1-null fibroblasts also are induced by platelet-derived growth factor in wild-type cells and thus are likely to be involved in cell proliferation. In mouse cells expressing the docking site mutant Y440F of human IFN-γ receptor subunit 1, the mouse Stat1 is not phosphorylated in response to human IFN-γ, but c-myc and c-jun are still induced, showing that the Stat1 docking site is not required for Stat1-independent signaling.

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