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Downstream activation of a TATA-less promoter by Oct-2, Bob1, and NF-κB directs expression of the homing receptor BLR1 to mature B cells

Item Type:Article
Title:Downstream activation of a TATA-less promoter by Oct-2, Bob1, and NF-κB directs expression of the homing receptor BLR1 to mature B cells
Creators Name:Wolf, I. and Pevzner, V. and Kaiser, E. and Bernhardt, G. and Claudio, E. and Siebenlist, U. and Foerster, R. and Lipp, M.
Abstract:The chemokine receptor, BLR1, is a major regulator of the microenvironmental homing of B cells in lymphoid organs. In vitro studies identify three essential elements of the TATA-less blr1 core promoter that confer cell type- and differentiation-specific expression in the B cells of both humans and mice, a functional promoter region (-36 with respect to the transcription start site), a NF-kappaB motif (+44), and a noncanonical octamer motif (+157). The importance of these sites was confirmed by in vivo studies in gene-targeted mice deficient of either Oct-2, Bob1, or both NF-kappaB subunits p50 and p52. In all of these animals, the expression of BLR1 was reduced or absent. In mice deficient only of p52/NF-kappaB, BLR1 expression was unaffected. Thus our data demonstrate that BLR1 is a target gene for Oct-2, Bob1, and members of the NF-kappaB/Rel family and provides a link to the impaired B cell functions in mice deficient for these factors.
Keywords:B-Lymphocytes, Base Sequence, Cell Differentiation, Chemokine Receptors, Cultured Tumor Cells, CXCR5 Receptors, Cytokine Receptors, DNA-Binding Proteins, Genetic Promoter Regions, GTP-Binding Proteins, Lymphoid Tissue, Molecular Sequence Data, NF-kappa B, Octamer Transcription Factor-2, TATA Box, Trans-Activators, Transcription Factors, Animals, Mice
Source:Journal of Biological Chemistry
ISSN:0021-9258
Publisher:American Society for Biochemistry and Molecular Biology (U.S.A.)
Volume:273
Number:44
Page Range:28831-28836
Date:30 October 1998
Official Publication:http://www.jbc.org/cgi/content/abstract/273/44/28831
PubMed:View item in PubMed

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