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Translating the histone code into leukemia
Author(s) -
Linggi Bryan E.,
Brandt Stephen J.,
Sun ZuWen,
Hiebert Scott W.
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20604
Subject(s) - histone code , histone methylation , histone methyltransferase , histone h2a , epigenomics , histone , histone modifying enzymes , biology , histone h1 , histone octamer , microbiology and biotechnology , genetics , gene , gene expression , nucleosome , dna methylation
Abstract The “histone code” is comprised of the covalent modifications of histone tails that function to regulate gene transcription. The post‐translational modifications that occur in histones within the regulatory regions of genes include acetylation, methylation, phosphorylation, ubiquitination, sumoylation, and ADP‐ribosylation. These modifications serve to alter chromatin structure and accessibility, and to act as docking sites for transcription factors or other histone modifying enzymes. Several of the factors that are disrupted by chromosomal translocations associated with hematological malignancies can alter the histone code in a gene‐specific manner. Here, we discuss how the histone code may be disrupted by chromosomal translocations, either directly by altering the activity of histone modifying enzymes, or indirectly by recruitment of this type of enzyme by oncogenic transcription factors. These alterations in the histone code may alter gene expression pattern to set the stage for leukemogenesis. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.