title: ChIP-seq Analysis of Human Chronic Myeloid Leukemia Cells.
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.
authors: Whitehead Institute for Biomedical Research, Cambridge, MA, 02142, USA.
authors: Lars
authors: L
authors: Anders
authors: Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, 02215, USA. Zhaodong_Li@dfci.harvard.edu.
authors: Zhaodong
authors: Z
authors: Li
mesh_terms: D047369:Chromatin Immunoprecipitation / Q000379:methods*; D004273:DNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism*; D044127:Epigenesis, Genetic; D020869:Gene Expression Profiling; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000378:metabolism; D011485:Protein Binding; D025941:Protein Interaction Mapping; D017422:Sequence Analysis, DNA / Q000379:methods*
chemical_list: D004273:DNA, Neoplasm; D004268:DNA-Binding Proteins
keywords: ChIP-seq; Chronic myeloid leukemia; Immunoprecipitation; Sequencing; Sonication