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

作者信息

Wolf I, Pevzner V, Kaiser E, Bernhardt G, Claudio E, Siebenlist U, Förster R, Lipp M

机构信息

Department of Tumorgenetics and Immunogenetics, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10, D-13122, Berlin-Buch, Germany.

出版信息

J Biol Chem. 1998 Oct 30;273(44):28831-6. doi: 10.1074/jbc.273.44.28831.

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.

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