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

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
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DOI:
10.1074/jbc.273.44.28831
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发表时间:
1998-10-30
影响因子:
4.8
通讯作者:
Lipp, M
Lipp, M
中科院分区:
生物学2区
文献类型:
--
作者:
Wolf, I;Pevzner, V;Lipp, M

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趋化因子受体BLR1是B细胞在淋巴器官微环境归巢的主要调节因子。体外研究确定的三个基本要素TATA-less blr1核心启动子,赋予细胞类型和differentiation-specific表达在人类和小鼠的B细胞功能启动子区域(-36对转录起始站点),nf -κB主题(+ 44),和一个不在经典里的八聚物图案(+ 157),证实了这些网站的重要性在活体内研究基因的老鼠缺乏Oct-2, Bob1,或两者nf -κB亚基p50 p52,在所有这些动物中,BLR1的表达都减少或缺失。在仅缺乏p52/NF-KB的小鼠中,BLR1的表达不受影响。因此,我们的数据表明,BLR1是Oct-2、Bob1和NF-kappa B/Rel家族成员的靶基因,并与缺乏这些因子的小鼠的B细胞功能受损有关。
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-kappa B 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-kappa B subunits p50 and p52, In all of these animals, the expression of BLR1 was reduced or absent. In mice deficient only of p52/NF-KB, BLR1 expression was unaffected. Thus our data demonstrate that BLR1 is a target gene for Oct-2, Bob1, and members of the NF-kappa B/Rel family and provides a link to the impaired B cell functions in mice deficient for these factors.