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

التفاصيل البيبلوغرافية
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
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