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Nucleic Acids Research, 2000, Vol. 28, No. 21 4219-4224
© 2000 Oxford University Press

Cloning of an interferon regulatory factor 2 isoform with different regulatory ability

Sven A. Koenig Merediz, Manuel Schmidt1,*, Georg J. Hoppe, Jens Alfken, David Meraro2, Ben-Zion Levi2, Andreas Neubauer1 and Burghardt Wittig

Abteilung für Molekularbiologie, Biochemie und Bioinformatik, Fachbereich Humanmedizin, Freie Universität Berlin, 14195 Berlin, Germany, 1Abteilung für Hämatologie, Onkologie und Immunologie, Zentrum Innere Medizin, Klinikum der Philipps-Universität, Baldingerstrasse, 35043 Marburg, Germany and 2Department of Food Engineering and Biotechnology, Technion–Israel Institute for Technology, Haifa 32000, Israel

Interferons (IFNs) are a family of multifunctional proteins involved in immune activation, regulation of cell growth and antiviral response. They exert their functions by induction of several IFN-stimulated genes, including IFN regulatory factors (IRFs), a family of transcriptional regulators. One of these factors, IRF-2, was initially cloned as an antagonistic counterpart to IRF-1 with oncogenic potential. Here we describe a second isoform of IRF-2, termed IRF-2s, cloned from human and murine cells. This isoform lacks two amino acids located C-terminal of the DNA-binding domain, which is conserved in all IRF family members, leading to a change in the predicted secondary structure. Both isoforms have similar binding affinities to known target sequences in electrophoretic mobility shift assays. Using reporter gene constructs with the type IV promoter region of the MHC class II transactivator (CIITA), which is the essential factor for IFN-{gamma}-induced MHC class II expression, we show that the short isoform IRF-2s exhibits a weaker activation ability compared to IRF-2. Thus, our data present the first evidence of two IRF-2 isoforms with different regulatory ability.

* To whom correspondence should be addressed. Tel: +49 6421 2865061; Fax: +49 6421 2865062; Email: manuel.schmidt@mailer.uni-marburg.de Present address: Georg J. Hoppe, Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors


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