Open AccessInterferon‐Modulated Expression of Genes Encoding the Nuclear‐Dot‐Associated Proteins Sp100 and Promyelocytic Leukemia Protein (PML)
Author(s) -
Grötzinger Thilo,
Sternsdorf Thomas,
Jensen Kirsten,
Will Hans
Publication year - 1996
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1996.0554z.x
Subject(s) - promyelocytic leukemia protein , gene , nuclear protein , acute promyelocytic leukemia , encoding (memory) , leukemia , cancer research , interferon , biology , microbiology and biotechnology , genetics , transcription factor , retinoic acid , neuroscience
Promyelocytic leukemia protein (PML) and Sp100 are transcription‐regulatory proteins which colocalize in discrete nuclear dots and play a role in autoimmunity, oncogenesis and virus‐host interaction. Interferons (IFNs) were shown previously to increase strongly the levels of Sp100 mRNA and protein. Here, we examined which mechanisms lead to upregulation of Sp100 gene expression and whether IFNs also increase expression of the promyelocytic leukemia (PML) gene. We found that both mRNA and protein levels of PML are also strongly upregulated by IFNs. In addition, new Sp100 and PML proteins were detected immunologically after IFN treatment of cells. Nuclear run‐on analysis revealed protein‐synthesis‐independent, rapid IFN‐enhanced transcription rates as well as synergistic activation of the Sp100 and PML genes by type‐I and type‐II IFNs. These data demonstrate that PML and Sp100 belong to the growing family of IFN‐stimulated genes (ISGs) upregulated most likely by the transcription factor ISGF3, and indicate that IFNs also qualitatively alter the expression of these two genes.