ChIP-seq Analysis of Human Chronic Myeloid Leukemia Cells

Methods Mol Biol. 2016:1465:129-38. doi: 10.1007/978-1-4939-4011-0_11.

Abstract

Many transcription factors, chromatin-associated proteins and regulatory DNA elements are genetically and/or epigenetically altered in cancer, including Chronic Myeloid Leukemia (CML). This leads to deregulation of transcription that is often causally linked to the tumorigenic state. Chromatin-immunoprecipitation coupled with massively parallel DNA sequencing (ChIP-seq) is the key technology to study transcription as it allows in vivo whole-genome mapping of epigenetic modifications and interactions of proteins with DNA or chromatin. However, numerous DNA/chromatin-binding proteins, including EZH2, remain difficult to "ChIP," thus yielding genome-wide binding maps of only suboptimal quality. Here, we describe a ChIP-seq protocol optimized for high-quality protein-genome binding maps that have proven especially useful for studying difficult to 'ChIP' transcription regulatory factors in Chronic Myeloid Leukemia (CML) and related malignancies.

Keywords: ChIP-seq; Chronic myeloid leukemia; Immunoprecipitation; Sequencing; Sonication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromatin Immunoprecipitation / methods*
  • DNA, Neoplasm / genetics
  • DNA, Neoplasm / metabolism
  • DNA-Binding Proteins / metabolism*
  • Epigenesis, Genetic
  • Gene Expression Profiling
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Protein Binding
  • Protein Interaction Mapping
  • Sequence Analysis, DNA / methods*

Substances

  • DNA, Neoplasm
  • DNA-Binding Proteins