Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.

Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.
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在补体蛋白 C1q 存在或不存在的情况下摄取修饰脂蛋白的人巨噬细胞的转录组数据和基因本体分析。

DOI:
10.1016/j.dib.2016.09.008
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发表时间:
2016
期刊:
影响因子:
1.2
通讯作者:
Fraser,DeborahA
Fraser,DeborahA
中科院分区:
--
文献类型:
--
作者:
Ho,Minh-Minh;Fraser,DeborahA

文献摘要

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我们表征了补体调理作用对人单核细胞源性巨噬细胞 (HMDM) 泡沫细胞形成的转录效应。 RNA 测序用于鉴定 HMDM 摄入致动脉粥样硬化脂蛋白氧化低密度脂蛋白 (oxLDL) 和乙酰化低密度脂蛋白 (acLDL) 期间补体蛋白 C1q 调节的途径。所有原始数据均提交至符合 MIAME 标准的数据库 Gene Expression Omnibus(登录号 GEO:GSE80442;http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80442)。这里提供的数据包括每种测试条件的上调和下调基因的维恩图概述、生物过程的基因本体分析、分子功能和细胞成分以及 KEGG 通路分析。对摄入致动脉粥样化脂蛋白期间 HMDM 中 C1q 调节的途径及其功能相关性的进一步研究描述于“摄入致动脉粥样化脂蛋白期间的巨噬细胞分子信号传导和炎症反应由补体蛋白 C1q 调节”(M.M. Ho、A. Manughian-Peter、W.R. Spivia、A. Taylor、D.A. Fraser,2016)[1]。
We characterized the transcriptional effects of complement opsonization on foam cell formation in human monocyte-derived macrophages (HMDM). RNA-sequencing was used to identify the pathways modulated by complement protein C1q during HMDM ingestion of the atherogenic lipoproteins oxidized low density lipoprotein (oxLDL) and acetylated low density lipoprotein (acLDL). All raw data were submitted to the MIAME-compliant database Gene Expression Omnibus (accession number GEO: GSE80442; http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80442). Data presented here include Venn diagram overviews of up- and down-regulated genes for each condition tested, gene ontology analyses of biological processes, molecular functions and cellular components and KEGG pathway analysis. Further investigation of the pathways modulated by C1q in HMDM during ingestion of atherogenic lipoproteins and their functional relevance are described in “Macrophage molecular signaling and inflammatory responses during ingestion of atherogenic lipoproteins are modulated by complement protein C1q” (M.M. Ho, A. Manughian-Peter, W.R. Spivia, A. Taylor, D.A. Fraser, 2016) [1].