Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 11, Issue 1, Pages 73-80Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb713
Keywords
-
Funding
- NHLBI NIH HHS [N01-HV-28179, HL57620] Funding Source: Medline
- NIDDK NIH HHS [DK44746] Funding Source: Medline
- DIVISION OF HEART AND VASCULAR DISEASES [N01HV028179] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL057620] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R37DK044746, R01DK044746] Funding Source: NIH RePORTER
Ask authors/readers for more resources
During erythroid differentiation, beta-globin gene expression is regulated by the locus control region (LCR). The transcription factor NF-E2p18/MafK binds within this region and is essential for beta-globin expression in murine erythroleukemia (MEL) cells. Here we use the isotope-coded affinity tag (ICAT) technique of quantitative mass spectrometry to compare proteins interacting with NF-E2p18/MafK during differentiation. Our results define MafK as a 'dual-function' molecule that shifts from a repressive to an activating mode during erythroid differentiation. The exchange of MafK dimerization partner from Bach1 to NF-E2p45 is a key step in the switch from the repressed to the active state. This shift is associated with changes in the interaction of MafK with co-repressors and co-activators. Thus, our results suggest that in addition to its role as a cis-acting activator of beta-globin gene expression in differentiated erythroid cells, the LCR also promotes an active repression of beta-globin transcription in committed cells before terminal differentiation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available