Ehrnsperger, Achim and Rehli, Michael and Thu-Hang, Pham and Kreutz, Marina (2005) Epigenetic regulation of the dendritic cell-marker gene ADAM19. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 332 (2). pp. 456-464. ISSN 0006-291X, 1090-2104
Full text not available from this repository. (Request a copy)Abstract
Human ADAM 19 (MADDAM) is a molecular marker for human dendritic cells and not expressed in macrophages. To investigate its cell-type-specific expression, we defined the transcriptional start site and the proximal promoter. Sequence analysis of the promoter revealed putative binding sites for several transcription factors including Sp1, Sp3, NF-kappa B, and VDR. A minimal promoter construct of 150 bp showed little difference in reporter activity between macrophages and dendritic cells. Transfection of monocytic THP-1 with the 150-bp fragment also resulted in significant reporter activity, despite the lack of endogenous MADDAM expression. TSA, a known inhibitor of histone deacetylation, led to a dose-dependent induction of MADDAM mRNA in THP-1. ChIP assays demonstrated high levels of acetylated histone H3 in the proximal promoter region of the MADDAM gene in TSA-treated THP-1 cells and dendritic cells as compared to macrophages, indicating an important role of histone acetylation in the regulation of the MADDAM gene. (C) 2005 Elsevier Inc. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | NF-KAPPA-B; MELTRIN-BETA; TRANSCRIPTION FACTOR; HISTONE ACETYLATION; ACCESSORY CELLS; BLOOD MONOCYTES; DC-SIGN; DIFFERENTIATION; PROMOTER; MACROPHAGES; monocyte; dendritic cell; macrophage; differentiation; ADAM; transcriptional regulation; histone; epigenetic |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin III (Hämatologie und Internistische Onkologie) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 07 May 2021 04:50 |
| Last Modified: | 07 May 2021 04:50 |
| URI: | https://pred.uni-regensburg.de/id/eprint/35899 |
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