Groenendyk Jody, Fan Xiao, Peng Zhenling, Ilnytskyy Yaroslav, Kurgan Lukasz, Michalak Marek
Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2S7, Canada.
Department of Electrical and Computer Engineering, University of Alberta, Edmonton, Alberta T6G 2V4, Canada.
Genom Data. 2014 Oct 7;2:325-7. doi: 10.1016/j.gdata.2014.10.002. eCollection 2014 Dec.
Disruption of the endoplasmic reticulum (ER) homeostasis is the cause of ER stress. We performed microRNA (miRNA) analysis (deep sequencing) to search for coping responses (including signaling pathways) induced by disrupted ER Ca(2 +) homeostasis. Our focus was on a specific branch of UPR namely the bi-functional protein kinase/endoribonuclease inositol-requiring element 1α (IRE1α). Activated IRE1α undergoes autophosphorylation and oligomerization, leading to the activation of the endoribonuclease domain and splicing of the mRNA encoding XBP1 specific transcription factor. This processing changes the coding reading frame, producing a potent transcription factor termed XBP1s. We utilized the XBP1 splicing luciferase reporter to screen for modulators of the IRE1α branch of the unfolded protein response (UPR). Here, we describe a detailed experimental design and bioinformatics analysis of ER Ca(2 +) depletion (thapsigargin treated)-induced microRNA (deep sequencing) profile. The data can be access at the Gene Expression Omnibus (GEO), the National Center for Biotechnology Information (NCBI), reference number GSE57138.
内质网（ER）稳态的破坏是内质网应激的原因。我们进行了微小RNA（miRNA）分析（深度测序），以寻找由内质网Ca(2+)稳态破坏诱导的应对反应（包括信号通路）。我们关注的是未折叠蛋白反应（UPR）的一个特定分支，即双功能蛋白激酶/核糖核酸内切酶肌醇需求酶1α（IRE1α）。激活的IRE1α会发生自磷酸化和寡聚化，导致核糖核酸内切酶结构域的激活以及编码XBP1特异性转录因子的mRNA的剪接。这种加工改变了编码阅读框，产生了一种称为XBP1s的强效转录因子。我们利用XBP1剪接荧光素酶报告基因来筛选未折叠蛋白反应（UPR）的IRE1α分支的调节剂。在这里，我们描述了内质网Ca(2+)耗竭（毒胡萝卜素处理）诱导的微小RNA（深度测序）谱的详细实验设计和生物信息学分析。这些数据可在国家生物技术信息中心（NCBI）的基因表达综合数据库（GEO）中获取，参考编号为GSE57138。
