1. Omics Types

chromatin remodeling

Definition

Chromatin remodeling refers to the dynamic restructuring of chromatin architecture to regulate DNA accessibility for transcription, replication, and repair. This process involves ATP-dependent chromatin remodeling complexes (such as SWI/SNF, ISWI, and CHD families) that slide, eject, or restructure nucleosomes, as well as histone-modifying enzymes that add or remove post-translational modifications. Chromatin remodeling is essential for gene expression regulation, cellular differentiation, and response to environmental signals. Dysregulation of chromatin remodeling machinery is implicated in cancer, developmental disorders, and neurological diseases, making it a critical target for epigenetic therapies and a fundamental mechanism in understanding gene regulation networks.

Visualize chromatin remodeling in Nodes Bio

Researchers can map chromatin remodeling networks in Nodes Bio by connecting remodeling complexes to their target genes, histone modifications, and downstream transcriptional outcomes. Network visualization reveals how chromatin remodelers interact with transcription factors, co-regulators, and signaling pathways, enabling identification of regulatory hubs and potential therapeutic intervention points in disease-specific chromatin landscapes.

Visualization Ideas:

  • Chromatin remodeling complex-transcription factor interaction networks
  • Gene regulatory networks showing chromatin accessibility and expression changes
  • Multi-omics integration of ChIP-seq, ATAC-seq, and RNA-seq data as causal networks
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Example Use Case

A cancer research team investigating resistance to targeted therapy discovers that SWI/SNF chromatin remodeling complexes are mutated in 20% of treatment-resistant tumors. Using ChIP-seq and RNA-seq data, they map how these mutations alter chromatin accessibility at drug resistance genes. By visualizing the network of affected transcription factors, remodeling complexes, and downstream gene targets, they identify synthetic lethal interactions and propose combination therapies targeting both the primary oncogenic pathway and compensatory chromatin remodeling mechanisms.

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