Порівняння методів

	Аналіз диференційної експресії генів методом RNA-seq	Пікове викликування ChIP-seq
Галузь	Біоінформатика	Біоінформатика
Родина	Process / pipeline	Process / pipeline
Рік появи	2008–2010 (RNA-seq DE methodology established)	2007–2008
Автор методу	Multiple groups; foundational methods from Anders & Huber (DESeq, 2010), Robinson, McCarthy & Smyth (edgeR, 2010)	Johnson et al. (ChIP-seq concept, 2007); Zhang et al. (MACS algorithm, 2008)
Тип	Quantitative genomics pipeline	Computational genomics pipeline
Основоположне джерело	Love, M. I., Huber, W., & Anders, S. (2014). Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biology, 15(12), 550.	Zhang, Y., Liu, T., Meyer, C. A., Eeckhoute, J., Johnson, D. S., Bernstein, B. E., Nusbaum, C., Myers, R. M., Brown, M., Li, W., & Liu, X. S. (2008). Model-based analysis of ChIP-seq (MACS). Genome Biology, 9(9), R137.
Інші назви	RNA-seq DE analysis, transcriptomic differential expression, bulk RNA-seq DE, DEA	ChIP-seq analysis, peak detection, MACS peak calling, ChIP peak identification
Пов'язані	6	6
Підсумок	RNA-seq differential expression (DE) analysis identifies genes whose transcript abundance differs significantly between two or more biological conditions — for example, treated versus control, or diseased versus healthy tissue. Starting from raw sequencing reads, the pipeline moves through alignment, count-based normalization, statistical modeling of count dispersion, hypothesis testing, and multiple-testing correction to produce a ranked list of differentially expressed genes accompanied by fold-change estimates and adjusted p-values.	ChIP-seq peak calling is a computational pipeline that identifies genomic regions where a protein of interest — a transcription factor or histone modification — is enriched, based on sequencing reads from chromatin immunoprecipitation experiments. It converts raw sequencing data into a set of high-confidence binding or modification sites across the genome, enabling downstream analysis of gene regulation, chromatin state, and epigenetic mechanisms.