GATA-1, but Not GATA-2, Antagonizes PU.1 Mediated Transcriptional Activity at the CBFA2T3 (ETO2, MTG16) Promoter through a Mechanism Dependent on GATA DNA Binding
العنوان: | GATA-1, but Not GATA-2, Antagonizes PU.1 Mediated Transcriptional Activity at the CBFA2T3 (ETO2, MTG16) Promoter through a Mechanism Dependent on GATA DNA Binding |
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المؤلفون: | Vinzon Ibanez, Shrihari S. Kadkol, SiJun Yang, Marie K. Baraoidan, Yogenthiran Saunthararajah, Fariborz Mortazavi |
المصدر: | Blood. 106:1749-1749 |
بيانات النشر: | American Society of Hematology, 2005. |
سنة النشر: | 2005 |
مصطلحات موضوعية: | Mutation, Immunology, Myeloid leukemia, Cell Biology, Hematology, medicine.disease_cause, Biochemistry, Chromatin, Cell biology, DNA binding site, chemistry.chemical_compound, Haematopoiesis, chemistry, Cell culture, embryonic structures, medicine, Transcription factor, DNA |
الوصف: | CBFA2T3 (ETO2, MTG16), a target of chromosomal translocation in acute myeloid leukemia, has its highest expression in hematopoietic cells compared to other tissues. This suggests that its expression is regulated by major hematopoietic transcription factors. The proximal promoter from −171 to −65 bp has greater than 90% identity between mouse and human and contains recognition sites for major hematopoietic transcription factors PU.1, GATA-1 and GATA-2. Using chromatin immuno-precipitation and the MPD hematopoietic cell-line, this segment was pulled down with endogenous PU.1, GATA-1 and GATA-2. In luciferase reporter gene assays, PU.1 and GATA-2, but not GATA-1, activated the promoter. As would be expected from these findings, CBFA2T3 levels declined during terminal erythroid differentiation of primary hematopoietic cells. GATA-1, but not GATA-2, antagonized PU.1 mediated activation but this effect of GATA-1 was abrogated by mutation of the GATA DNA binding sites. Both GATA-1 and GATA-2 have been reported to antagonize PU.1 transcriptional activity by antagonizing PU.1 interactions with c-Jun (Zhang et al, Proc Natl Acad Sci USA1999;96:8705–8710); however, the DNA binding dependent mechanism reported here allows GATA-2 and GATA-1 to have contrasting relationships with PU.1 and may be the basis for the co-operation of GATA proteins with PU.1 in some contexts yet antagonism of PU.1 activity in others. |
تدمد: | 1528-0020 0006-4971 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_________::8541ea023cd9e1e18cfff553a3a9de6bTest https://doi.org/10.1182/blood.v106.11.1749.1749Test |
رقم الانضمام: | edsair.doi...........8541ea023cd9e1e18cfff553a3a9de6b |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15280020 00064971 |
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