Divergent signalling pathways regulate lipopolysaccharide-induced eRNA expression in human monocytic THP1 cells.
Divergent signalling pathways regulate lipopolysaccharide-induced eRNA expression in human monocytic THP1 cells.
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DOI：
10.1016/j.febslet.2014.12.026
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发表时间：
2015-01-30
期刊：
影响因子：
3.5
通讯作者：
Lindsay MA
中科院分区：
文献类型：
--
作者：
Heward JA;Roux BT;Lindsay MA
erna由增强子表达，并已被证明可调节基因表达。erna的表达在先天免疫反应激活时广泛存在。我们发现NF-κB信号通路调节lps诱导的erna。单个erna的表达也依赖于ERK-1/2和p38。近年来的研究表明，从增强子区域转录的非编码rna是增强子功能和基因表达的重要调节因子。在本报告中，我们描述了脂多糖（LPS）激活先天免疫反应后，在人单核THP1细胞中诱导的六种增强子rna （eRNAs）的表达。具体来说，我们已经证明了lps诱导的单个erna的表达是通过不同的细胞内信号通路介导的，包括NF-κB和丝裂原活化蛋白激酶、细胞外调节激酶1/2和p38。
eRNAs are expressed from enhancers and have been shown to regulate gene expression. Expression of eRNAs is widespread upon activation of the innate immune response. We show that the NF-κB signalling pathway regulates LPS-induced eRNAs. Expression of individual eRNAs is also dependent on ERK-1/2 and p38. Recent studies have indicated that non-coding RNAs transcribed from enhancer regions are important regulators of enhancer function and gene expression. In this report, we have characterised the expression of six enhancer RNAs (eRNAs) induced in human monocytic THP1 cells following activation of the innate immune response by lipopolysaccharide (LPS). Specifically, we have demonstrated that LPS-induced expression of individual eRNAs is mediated through divergent intracellular signalling pathways that includes NF-κB and the mitogen activated protein kinases, extracellular regulated kinase-1/2 and p38.
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DOI：
10.1152/ajpcell.1998.275.3.c740
发表时间：
1998-09-01
影响因子：
5.5
作者：
Tian, LC;White, JE;Tsan, MF
通讯作者：
Tsan, MF
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
16
作者：
Kaikkonen, Minna U.;Spann, Nathanael J.;Heinz, Sven;Romanoski, Casey E.;Allison, Karmel A.;Stender, Joshua D.;Chun, Hyun B.;Tough, David F.;Prinjha, Rab K.;Benner, Christopher;Glass, Christopher K.
通讯作者：
Glass, Christopher K.
影响因子：
16.8
作者：
Heward JA;Lindsay MA
通讯作者：
Lindsay MA
影响因子：
5.3
作者：
Teferedegne, Belete;Green, Myesha R.;Boss, Jeremy M.
通讯作者：
Boss, Jeremy M.