FOXO1通过结合共识FOXO1 Motif上调人类l -选择素表达。

Gene regulation and systems biology Pub Date : 2012-01-01 Epub Date: 2012-10-29 DOI:10.4137/GRSB.S10343
Yuefen Lou, Xiaojiong Lu, Xitong Dang
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引用次数: 13

摘要

l -选择素在淋巴细胞归巢和白细胞滚动中起重要作用。越来越多的证据表明,它参与许多疾病实体,包括糖尿病、缺血/再灌注损伤、炎症性疾病和肿瘤转移。l -选择素在蛋白水平上的调控已被很好地表征。然而,人类l -选择素转录的调控在很大程度上仍然未知。为了解决l -选择素的转录调控,我们克隆了起始密码子ATG的1088 bp 5'。荧光素酶分析发现,序列5'缺失突变体的核心启动子区域位于-288/-1。5'RACE在-115位点定位了一个主要的转录起始位点。转录因子Sp1, Ets1, Mzf1, Klf2和Irf1结合并反激活l -选择素启动子。值得注意的是,fox01与fox01基序CCCTTTGG结合在-87/-80的位置,并以剂量依赖的方式激活l -选择素启动子。在Jurkat细胞中,过表达构成活性FOXO1增加内源性l -选择素的表达。我们认为FOXO1通过靶向启动子调控l -选择素的表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

FOXO1 Up-Regulates Human L-selectin Expression Through Binding to a Consensus FOXO1 Motif.

FOXO1 Up-Regulates Human L-selectin Expression Through Binding to a Consensus FOXO1 Motif.

FOXO1 Up-Regulates Human L-selectin Expression Through Binding to a Consensus FOXO1 Motif.

FOXO1 Up-Regulates Human L-selectin Expression Through Binding to a Consensus FOXO1 Motif.

L-selectin plays important roles in lymphocyte homing and leukocyte rolling. Mounting evidence shows that it is involved in many disease entities including diabetes, ischemia/reperfusion injuries, inflammatory diseases, and tumor metastasis. Regulation of L-selectin at protein level has been well characterized. However, the regulation of human L-selectin transcription remains largely unknown. To address transcriptional regulation of L-selectin, we cloned 1088 bp 5' of the start codon ATG. Luciferase analysis of the serial 5' deletion mutants located the core promoter region at -288/-1. A major transcription initiation site was mapped at -115 by 5'RACE. Transcription factors Sp1, Ets1, Mzf1, Klf2, and Irf1 bind to and transactivate the L-selectin promoter. Significantly, FOXO1 binds to a FOXO1 motif, CCCTTTGG, at -87/-80, and transactivates the L-selectin promoter in a dose-dependent manner. Over-expression of a constitutive-active FOXO1 increased the endogenous L-selectin expression in Jurkat cells. We conclude that FOXO1 regulates L-selectin expression through targeting its promoter.

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