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Additional file 1 of ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans

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DataCite Commons2024-08-14 更新2024-08-19 收录
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https://springernature.figshare.com/articles/dataset/Additional_file_1_of_ARMC5_controls_the_degradation_of_most_Pol_II_subunits_and_ARMC5_mutation_increases_neural_tube_defect_risks_in_mice_and_humans/26667849
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Additional file 1: Figure S1. Similar Rn7sk expression in WT and KO NPCs according to RNA-seq.  Table S1. Detailed parameters of differentially expressed transcripts in WT versus KO NPCs according to RNA-seq.  Table S2. GO analysis of significantly dysregulated genes in terms of biological process. Table S3. Genes with highly different Pol II peak density (FDR<0.1) between WT and KO NPCs. Table S4. RT-qPCR primer sequences.  Uncropped blots.

附加文件1:补充图S1。基于RNA测序(RNA-seq)的野生型(Wild Type, WT)与敲除型(Knock Out, KO)神经前体细胞(Neural Progenitor Cells, NPC)中Rn7sk的表达水平相似。 补充表S1。基于RNA测序的野生型与敲除型神经前体细胞间差异表达转录本的详细参数。 补充表S2。针对生物过程分类的显著差异表达基因的基因本体(Gene Ontology, GO)分析。 补充表S3。野生型与敲除型神经前体细胞间RNA聚合酶II(RNA Polymerase II, Pol II)峰密度存在显著差异(错误发现率False Discovery Rate, FDR<0.1)的基因。 补充表S4。实时定量聚合酶链式反应(RT-qPCR)引物序列。 未裁剪的免疫印迹原图。
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figshare
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2024-08-14
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