| First Author | Khodadoust MM | Year | 1998 |
| Journal | Blood | Volume | 92 |
| Issue | 7 | Pages | 2399-409 |
| PubMed ID | 9746780 | Mgi Jnum | J:50213 |
| Mgi Id | MGI:1290034 | Doi | 10.1182/blood.v92.7.2399.2399_2399_2409 |
| Citation | Khodadoust MM, et al. (1998) Distinct regulatory mechanisms for interferon-alpha/beta (IFN-alpha/beta)- and IFN-gamma-mediated induction of Ly-6E gene in B cells. Blood 92(7):2399-409 |
| abstractText | The murine Ly6-E gene is transcriptionally induced by interferon-alpha/beta (IFN-alpha/beta) and IFN-gamma 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 transcripition-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-alpha/beta-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-alpha/beta-mediated induction of the Ly6-E gene. These results show the complexity involved in achieving cell-type specificity in IFN-mediated gene regulation. |
