DiffBind

DiffBind performs differential binding analysis of ChIP-seq data to identify genomic regions with altered protein-DNA binding across multiple experimental conditions, enabling studies of transcriptional regulation and epigenetic modifications.


Key Features:

  • Differential Binding Analysis: Computes differential binding sites from ChIP-seq datasets to identify genomic regions with significant changes in binding affinity.
  • Quantitative Affinity Integration: Integrates quantitative affinity (binding occupancy) data across multiple ChIP-seq experiments to support direct comparison between conditions.
  • Occupancy and Overlap Assessment: Assesses occupancy and overlap of binding site coverage across datasets to evaluate shared and condition-specific binding events.
  • Visualization Capabilities: Provides plotting functions to visualize differential binding results and underlying data patterns.

Scientific Applications:

  • Transcriptional Regulation: Examines transcription factor binding dynamics and their impact on gene regulation using ChIP-seq comparisons.
  • Epigenetic Modification Studies: Investigates chromatin accessibility and epigenetic modification-associated changes in protein-DNA binding.
  • Breast Cancer and Therapeutic Resistance: Applied to ERα-mediated transcriptional regulatory plasticity in breast cancer, including identification of VAV3 involvement and assessment of effects of compounds such as YC-1.

Methodology:

Performs statistical analysis of ChIP-seq data to identify regions with significant differences in binding affinity by comparing quantitative binding (occupancy) across conditions (e.g., treated vs untreated or resistant vs sensitive), assesses overlap of binding sites, and generates plots of results.

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Details

License:
Artistic-2.0
Tool Type:
command-line tool, library
Operating Systems:
Linux, Windows, Mac
Programming Languages:
R
Added:
1/17/2017
Last Updated:
6/30/2021

Operations

Publications

Aguilar H, Urruticoechea A, Halonen P, Kiyotani K, Mushiroda T, Barril X, Serra-Musach J, Islam A, Caizzi L, Di Croce L, Nevedomskaya E, Zwart W, Bostner J, Karlsson E, Pérez Tenorio G, Fornander T, Sgroi DC, Garcia-Mata R, Jansen MP, García N, Bonifaci N, Climent F, Soler MT, Rodríguez-Vida A, Gil M, Brunet J, Martrat G, Gómez-Baldó L, Extremera AI, Figueras A, Balart J, Clarke R, Burnstein KL, Carlson KE, Katzenellenbogen JA, Vizoso M, Esteller M, Villanueva A, Rodríguez-Peña AB, Bustelo XR, Nakamura Y, Zembutsu H, Stål O, Beijersbergen RL, Pujana MA. VAV3 mediates resistance to breast cancer endocrine therapy. Breast Cancer Research. 2014;16(3). doi:10.1186/bcr3664. PMID:24886537. PMCID:PMC4076632.

Documentation

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