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首页> 外文期刊>Data in Brief >Quantitative analysis by next generation sequencing of hematopoietic stem and progenitor cells (LSK) and of splenic B cells transcriptomes from wild-type and Usp3-knockout mice
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Quantitative analysis by next generation sequencing of hematopoietic stem and progenitor cells (LSK) and of splenic B cells transcriptomes from wild-type and Usp3-knockout mice

机译:下一代测序对野生型和 Usp3 -敲除小鼠的造血干细胞和祖细胞(LSK)以及脾脏B细胞转录组的定量分析

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摘要

The data described here provide genome-wide expression profiles of murine primitive hematopoietic stem and progenitor cells (LSK) and of B cell populations, obtained by high throughput sequencing. Cells are derived from wild-type mice and from mice deficient for the ubiquitin-specific protease 3 (USP3; Usp3Δ / Δ ). Modification of histone proteins by ubiquitin plays a crucial role in the cellular response to DNA damage (DDR) (Jackson and Durocher, 2013) . USP3 is a histone H2A deubiquitinating enzyme (DUB) that regulates ubiquitin-dependent DDR in response to DNA double-strand breaks (Nicassio et al., 2007; Doil et al., 2008) . Deletion of USP3 in mice increases the incidence of spontaneous tumors and affects hematopoiesis . In particular, Usp3 -knockout mice show progressive loss of B and T cells and decreased functional potential of hematopoietic stem cells (HSCs) during aging. USP3-deficient cells, including HSCs, display enhanced histone ubiquitination, accumulate spontaneous DNA damage and are hypersensitive to ionizing radiation (Lancini et al., 2014) . To address whether USP3 loss leads to deregulation of specific molecular pathways relevant to HSC homeostasis and/or B cell development, we have employed the RNA-sequencing technology and investigated transcriptional differences between wild-type and Usp3 Δ/Δ LSK, na?ve B cells or in vitro activated B cells. The data relate to the research article “Tight regulation of ubiquitin-mediated DNA damage response by USP3 preserves the functional integrity of hematopoietic stem cells” (Lancini et al., 2014) . The RNA-sequencing and analysis data sets have been deposited in NCBI?s Gene Expression Omnibus (Edgar et al., 2002) and are accessible through GEO Series accession number GSE58495 ( http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58495 ). With this article, we present validation of the RNA-seq data set through quantitative real-time PCR and comparative analysis.
机译:此处描述的数据提供了通过高通量测序获得的小鼠原始造血干细胞和祖细胞(LSK)以及B细胞群体的全基因组表达谱。细胞来自野生型小鼠和缺乏泛素特异性蛋白酶3(USP3;Usp3Δ/Δ)的小鼠。泛素对组蛋白的修饰在细胞对DNA损伤(DDR)的反应中起着至关重要的作用(Jackson and Durocher,2013)。 USP3是组蛋白H2A去泛素化酶(DUB),其响应DNA双链断裂而调节泛素依赖性DDR(Nicassio等,2007; Doil等,2008)。小鼠中USP3的缺失增加了自发性肿瘤的发生并影响了造血功能。特别是,Usp3基因敲除小鼠在衰老过程中表现出B和T细胞的逐渐丧失以及造血干细胞(HSC)的功能潜能降低。 USP3缺陷型细胞(包括HSC)显示出增强的组蛋白泛素化作用,积累了自发的DNA损伤,并对电离辐射过敏(Lancini等人,2014)。为了解决USP3缺失是否导致与HSC稳态和/或B细胞发育相关的特定分子途径的失调,我们采用了RNA测序技术,并研究了野生型和Usp3Δ/ΔLSK(纯天然B)之间的转录差异细胞或体外活化的B细胞。数据与研究文章“ USP3对泛素介导的DNA损伤反应的严格调节保留了造血干细胞的功能完整性”有关(Lancini等,2014)。 RNA测序和分析数据集已保存在NCBI的Gene Expression Omnibus中(Edgar等,2002),可通过GEO系列登录号GSE58495(http://www.ncbi.nlm.nih.gov/访问) geo / query / acc.cgi?acc = GSE58495)。通过本文,我们介绍了通过定量实时PCR和比较分析对RNA-seq数据集的验证。

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