CARIP-/- (KO) 和野生型 (WT) 小鼠组织的RNA-seq以及RIP-Seq数据

利用CaMKIIβ 的RNA 免疫沉降技术（RIP-seq）发现了一条未被报道的lncRNA，Carip。Carip 可以直接和CaMKIIβ 蛋白结合并调控下游AMPAR 和NMDAR 的亚基的磷酸化水平。Carip 的缺失会导致海马神经元中的LTP 减弱，小鼠的空间学习记忆能力也有明显下降。CARIP是一种在小鼠大脑中高表达的lncRNA。 为了更好地理解 lncRNA 的功能，我们对 CARIP-/- (KO) 和野生型 (WT) 小鼠的组织进行了 RNA-seq 分析，并对两组之间的差异表达基因进行了分析。收集小鼠脑组织，提取RNA，通过建库、二代测序，分析表达差异。数据进行严格质控，使用 Trim Galore和 Cutadapt处理原始数据，然后使用 STAR比对到小鼠基因组（GRCm38.p6）。 使用软件 featureCounts进行基因量化，以计算每个基因的读数和每百万计数（CPM）水平。 使用 edgeR 包（版本 3.30.3）分析差异表达基因（DEG）。

A previously unreported lncRNA, Carip, was discovered via RNA immunoprecipitation sequencing (RIP-seq) targeting CaMKIIβ. Carip directly binds to CaMKIIβ protein and regulates the phosphorylation levels of downstream AMPAR and NMDAR subunits. Loss of Carip leads to attenuated long-term potentiation (LTP) in hippocampal neurons and a significant decline in spatial learning and memory abilities of mice. CARIP is a lncRNA highly expressed in the mouse brain. To better understand the functions of lncRNAs, we conducted RNA-seq analysis on tissues from CARIP knockout (KO) and wild-type (WT) mice, and performed differential expression gene analysis between the two groups. Mouse brain tissues were collected, RNA was extracted, and expression differences were analyzed following library construction and next-generation sequencing (NGS). Raw data underwent rigorous quality control, were processed using Trim Galore! and Cutadapt, and then aligned to the mouse genome (GRCm38.p6) using STAR. Gene quantification was carried out with featureCounts software to calculate the read counts and counts per million (CPM) values for each gene. Differentially expressed genes (DEGs) were analyzed using the edgeR package (version 3.30.3).

搜集汇总

背景与挑战

背景概述

该数据集包含CARIP敲除（KO）和野生型（WT）小鼠组织的RNA-seq和RIP-Seq数据，旨在研究lncRNA Carip在调控海马神经元功能和空间学习记忆中的作用。数据通过二代测序生成，经过严格质控和生物信息学分析，包括差异表达基因鉴定，总大小为87.67 GB，覆盖2019年至2020年的时间范围。数据集支持神经科学领域对非编码RNA功能机制的探索，并附有相关研究文章的引用。