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International Immunology, Vol. 15, No. 7, pp. 807-815, July 2003
© 2003 Japanese Society for Immunology

A truncated IFN-regulatory factor-8\IFN consensus sequence-binding protein acts as dominant-negative, interferes with endogenous protein–protein interactions and leads to apoptosis of immune cells

Sharon Hashmueli1, Merav Gleit-Kielmanowicz1, David Meraro1, Aviva Azriel1, Doron Melamed2 and Ben-Zion Levi1

Departments of 1 Food Engineering and Biotechnology and 2 Medicine, Technion, Haifa 3200, Israel

The first two authors contributed equally to this work
Correspondence to: B.-Z. Levi; E-mail: blevi{at}tx.technion.ac.il
Transmitting editor: D. Wallach

IFN consensus sequence-binding protein (ICSBP) is a member of the IFN-regulatory factors (IRF) and is thus also called IRF-8. Its expression is restricted to hematopoietic cells and IRF-8\ICSBP–/– mice are defective in myeloid cell differentiation. This factor exerts its transcriptional activity through interaction with other transcription factors, which leads to either repression or activation. In this paper, we describe the use of a dominant-negative (DN) mutant of IRF-8\ICSBP designed to serve as a molecular tool to dissociate the role of the various protein–protein interactions. This DN-ICSBP is truncated at the DNA-binding domain and can still associate with other factors, but the heterocomplexes produced are incapable of binding to the DNA. We show that the DN-ICSBP is able to compete for the interaction of IRF-8\ICSBP with either IRF or non-IRF members such as PU.1. Accordingly, this DN construct was able to inhibit the PU.1-dependent expression of the IgL{lambda} in the plasmacytoma cell line J558L. However, stable expression of this DN-ICSBP led to apoptosis of only hematopoietic cells. The data suggests that DN-ICSBP can form heterocomplexes with an as-yet unidentified survival factor for hematopoietic cells.

Keywords: IFN-regulatory factor, PU.1, transcriptional regulation


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