Characterization of the promoter of the human gene encoding the high-affinity IgG receptor: Transcriptional induction by γ-interferon is mediated through common DNA response elements Journal Article
| Authors: | Pearse, R. N.; Feinman, R.; Ravetch, J. V. |
| Article Title: | Characterization of the promoter of the human gene encoding the high-affinity IgG receptor: Transcriptional induction by γ-interferon is mediated through common DNA response elements |
| Abstract: | Expression of the high-affinity receptor for IgG (Fc(γ)RI) is restricted to cells of myeloid lineage and is induced by γ-interferon (IFN-γ) but not by IFN-α/β. The organization of the human Fc(γ)RI gene has been determined and the DNA elements governing its cell type-restricted transcription and IFN-γ induction are reported here. A 39-nucleotide sequence (IFN-γ response region, or GRR) is defined that is both necessary and sufficient for IFN-γ inducibility. Sequence analysis of the GRR reveals the presence of promoter elements initially defined for the major histocompatibility complex class II genes: i.e., X, H, and γ-IRE sequences. Comparison of a number of genes whose expression is induced selectively by IFN-γ indicates that the presence of these elements is a general feature of IFN-γ-responsive genes. Our studies suggest that the combination of X, H, and γ-IRE elements is a common motif in the pathway of transcriptional induction by this lymphokine. |
| Keywords: | promoter region; nonhuman; mouse; transcription regulation; gamma interferon; immunoglobulin g; dna responsive element; immunoglobulin receptor; human; priority journal; article |
| Journal Title: | Proceedings of the National Academy of Sciences of the United States of America |
| Volume: | 88 |
| Issue: | 24 |
| ISSN: | 0027-8424 |
| Publisher: | National Academy of Sciences |
| Date Published: | 1991-12-15 |
| Start Page: | 11305 |
| End Page: | 11309 |
| Language: | English |
| DOI: | 10.1073/pnas.88.24.11305 |
| PUBMED: | 1837149 |
| PROVIDER: | scopus |
| PMCID: | PMC53123 |
| DOI/URL: | |
| Notes: | Source: Scopus |
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