We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
Cross-talk between regulators of myeloid development: C/EBPalpha binds and activates the promoter of the PU.1 gene.
Journal of Leukocyte Biology 2003 September
CCAAT/enhancer-binding protein (C/EBP)alpha and PU.1 are required for myelopoiesis. Examination of the murine PU.1 promoter revealed several potential C/EBP-binding sites. Gel-shift assay demonstrated that C/EBPalpha expressed in 293T cells bound the site centered at -68 most potently. C/EBPalpha from 32D cl3 myeloid cell nuclear extracts also bound this site strongly, and endogenous C/EBPbeta did so to a lesser extent, whereas these C/EBP isoforms bound the neutrophil elastase promoter with equal affinity. The -68 site in the murine PU.1 promoter is conserved in the human PU.1 promoter. Mutation of the -68 C/EBP-binding site in a -85/+152 promoter segment linked to the luciferase cDNA reduced promoter activity fourfold in 293T cells in the presence of cotransfected C/EBPalpha and twofold in 32D cl3 myeloid cells. Induction of endogenous PU.1 RNA by C/EBPalpha-estradiol receptor (ER) in the presence of cycloheximide is obviated by mutation of the C/EBPalpha DNA-binding domain, and chromosomal immunoprecipitation demonstrated specific interaction of C/EBPalpha and C/EBPalpha-ER with the PU.1 promoter. Finally, PU.1 RNA is reduced several-fold in immortalized C/EBPalpha (-/-) compared with (+/-) cells. Together, these findings indicate that C/EBPalpha binds and activates the endogenous PU.1 gene in myeloid cells. Induction of PU.1 by C/EBPalpha may account for increased levels of PU.1 in myeloid as compared with B lymphoid cells and in this way, may contribute to the specification of myeloid progenitors.
Full text links
Related Resources
Trending Papers
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app