Abstract
The murine Ly6-E gene is transcriptionally induced by interferon-α/β (IFN-α/β) and IFN-γ in a variety of distinct cell types. The mechanism of IFN inducibility in B-cell lines was investigated by deletion analysis of the promoter and by identifying DNA binding proteins in mobility shift assays. A region located in the distal part of the promoter at -2.3 kb contributed to inducibility by both types of IFNs. This region contains a novel element in addition to the previously well-characterized IFN-stimulated response element (ISRE). The probes containing ISRE detected IFN-inducible complexes in mobility shift assays and the signal transducer and activator of transcription-1 was found to be in these complexes from cells treated with either type of IFN. An additional element present in the proximal part of the promoter at position -109 is also required for IFN-α/β-mediated induction. These data suggested a cooperative interaction between these physically disparate regulatory regions. A crucial role for HMGI(Y) protein in this cooperative multiprotein complex is supported by the evidence that inhibition of HMGI(Y) expression via antisense RNA results in the loss of IFN-α/β- mediated induction of the Ly6-E gene. These results show the complexity involved in achieving cell-type specificity in IFN-mediated gene regulation.
Original language | English (US) |
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Pages (from-to) | 2399-2409 |
Number of pages | 11 |
Journal | Blood |
Volume | 92 |
Issue number | 7 |
DOIs | |
State | Published - Oct 1 1998 |
Externally published | Yes |
ASJC Scopus subject areas
- Biochemistry
- Immunology
- Hematology
- Cell Biology