返回
Computational analysis of CLIP-seq data
DOI:10.1016/j.ymeth.2017.02.006.png)
摘要
En 中文
CLIP-seq experiments are currently the most important means for determining the binding sites of RNA binding proteins on a genome-wide level. The computational analysis can be divided into three steps. In the first pre-processing stage, raw reads have to be trimmed and mapped to the genome. This step has to be specifically adapted for each CLIP-seq protocol. The next step is peak calling, which is required to remove unspecific signals and to determine bona fide protein binding sites on target RNAs. Here, both protocol-specific approaches as well as generic peak callers are available. Despite some peak callers being more widely used, each peak caller has its specific assets and drawbacks, and it might be advantageous to compare the results of several methods. Although peak calling is often the final step in many CLIP-seq publications, an important follow-up task is the determination of binding models from CLIP-seq data. This is central because CLIP-seq experiments are highly dependent on the transcriptional state of the cell in which the experiment was performed. Thus, relying solely on binding sites determined by CLIP-seq from different cells or conditions can lead to a high false negative rate. This shortcoming can, however, be circumvented by applying models that predict additional putative binding sites. (C) 2017 Published by Elsevier Inc.
Keyword:
CLIP-seq data analysis
Peak calling
RBP binding models
RBP binding site prediction
AI总结
对已上传原文的论文进行重点信息的提取,主要内容包括:简要概述、研究摘要、背景介绍、关键亮点、图文解析、展望与总结。
期刊
IF:
4.3
论文数:
4.9K
被引数:
2.4W
机构
引用论文
Reduced graphene oxide–CdS nanocomposites with enhanced visible-light photoactivity synthesized using ionic-liquid precursors使用离子液体前体合成的具有增强的可见光光活性的还原氧化石墨烯-CdS纳米复合材料
New J. Chem.
IF0
The mRNA-Bound Proteome and Its Global Occupancy Profile on Protein-Coding Transcripts
MOLECULAR CELL
IF16.6
Antiviral proinflammatory phenotype of monocytes in anti-MDA5 antibody-associated interstitial lung disease
Rheumatology
IF0

