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Histone Modification

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...

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Related Experiment Video

Updated: Apr 17, 2026

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

Integrative analysis of 111 reference human epigenomes.

, Anshul Kundaje¹, Wouter Meuleman²

¹1] Computer Science and Artificial Intelligence Lab, Massachusetts Institute of Technology, 32 Vassar St, Cambridge, Massachusetts 02139, USA. [2] The Broad Institute of Harvard and MIT, 415 Main Street, Cambridge, Massachusetts 02142, USA. [3] Department of Genetics, Department of Computer Science, 300 Pasteur Dr., Lane Building, L301, Stanford, California 94305-5120, USA.

|February 20, 2015

Summary

This study created the largest collection of human epigenomes, mapping regulatory elements and revealing how genetic variants link to traits and diseases by analyzing epigenomic marks in specific tissues.

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Area of Science:

Genomics
Epigenetics
Molecular Biology

Background:

The human genome sequence is a foundational resource, but a similar reference for epigenomic studies is lacking.
Epigenomic information is crucial for understanding gene regulation, cellular differentiation, and human disease.

Purpose of the Study:

To generate and analyze a comprehensive collection of human epigenomes.
To create global maps of regulatory elements and define their associated regulatory modules.
To investigate the relationship between genetic variants, epigenomic marks, and human traits/diseases.

Main Methods:

Integrative analysis of 111 reference human epigenomes.
Profiling histone modification patterns, DNA accessibility, DNA methylation, and RNA expression.
Mapping regulatory elements and identifying coordinated regulatory modules.

Main Results:

Established global maps of regulatory elements and defined regulatory modules.
Demonstrated enrichment of disease- and trait-associated genetic variants in tissue-specific epigenomic marks.
Identified biologically relevant cell types for diverse human traits.

Conclusions:

Epigenomic data provides a critical resource for interpreting the molecular basis of human disease.
Epigenomic information is central to understanding gene regulation, cellular differentiation, and disease.
This work highlights the importance of epigenomic context in genetic association studies.