c-Jun inhibits NF-E2 transcriptional activity in association with p18/maf in Friend erythroleukemia cells
| Autor: | Michel Prenant, Mark C. Walters, David I. K. Martin, Claire Francastel, Yvette Augery-Bourget, J Robert-Lézénès |
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| Rok vydání: | 1997 |
| Předmět: |
Cancer Research
NF-E2 Transcription Factor Cellular differentiation Repressor Biology 3T3 cells Mice Genes jun Proto-Oncogene Proteins hemic and lymphatic diseases Genetics medicine Animals Molecular Biology MafK Transcription Factor Erythroid-Specific DNA-Binding Factors GATA1 3T3 Cells Friend murine leukemia virus Cell biology DNA-Binding Proteins Transcription Factor AP-1 medicine.anatomical_structure NF-E2 Transcription Factor p45 Subunit Proto-Oncogene Proteins c-maf Leukemia Erythroblastic Acute Transcription Factors |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1476-5594 0950-9232 |
| DOI: | 10.1038/sj.onc.1200902 |
| Popis: | We have reported previously that antisense c-jun overcomes a block of Friend erythroleukemia cells to differentiation suggesting that the factor c-Jun may be an important negative regulator of erythroid differentiation. The recently described erythroid transcription factor NF-E2 plays an important role in the regulation of the transcription of globin genes and recognizes a sequence containing an AP-1 site. NF-E2 is a complex of two bZip proteins, p45 and p18/Maf. In order to determine whether c-Jun can interact with NF-E2/AP-1 sites to regulate transcriptional activation from them, we have compared the activity of AP-1 and NF-E2 in transient transcriptional assays, in erythroid and nonerythroid cells in the presence of c-jun sense and antisense expression vectors. In non-erythroid cells, c-Jun activates and NF-E2p18 inhibits both AP-1 and NF-E2 activities, suggesting that NF-E2/AP-1 sites function as AP-1 binding sites in these cells. In contrast, NF-E2p18 is a positive regulator of NF-E2 activity in erythroid cells. c-Jun alone is also a positive regulator of NF-E2 activity in erythroid cells but in association with NF-E2p18 inhibits this activity. Moreover antisense c-jun increases endogenous NF-E2 activity in erythroid cells. These results suggest that c-Jun could act as a repressor of NF-E2 transcriptional activity by forming inactive c-Jun/NF-E2p18 heterocomplexes which interfer with the transcription of globin genes in Friend erythroleukemia cells. |
| Databáze: | OpenAIRE |
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