Linking Heterochromatin Protein 1 (HP1) to cancer progression

被引：105

作者：

Dialynas, George K. ^{[1
]}

Vitalini, Michael W. ^{[1
]}

Wallrath, Lori L. ^{[1
]}

机构：

[1] Univ Iowa, Dept Biochem, Iowa City, IA 52242 USA

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2008年 / 647卷 / 1-2期

关键词：

Cancer; Chromatin; Epigenetics; Gene regulation; Heterochromatin; Histone modifications;

D O I：

10.1016/j.mrfmmm.2008.09.007

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

All cells of a given organism contain nearly identical genetic information, yet tissues display unique gene expression profiles. This specificity is in part due to transcriptional control by epigenetic mechanisms that involve post-translational modifications of histones. These modifications affect the folding of the chromatin fiber and serve as binding sites for non-histone chromosomal proteins. Here we discuss functions of the Heterochromatin Protein 1 (HP1) family of proteins that recognize H3K9me, an epigenetic mark generated by the histone methyltransferases SU(VAR)3-9 and orthologues. Loss of HP1 proteins causes chromosome segregation defects and lethality in some organisms; a reduction in levels of HP1 family members is associated with cancer progression in humans. These consequences are likely due to the role of HP1 in centromere stability, telomere capping and the regulation of euchromatic and heterochromatic gene expression. (c) 2008 Elsevier B.V. All rights reserved.

引用

页码：13 / 20

页数：8

共 94 条

[31] M32, a murine homologue of Drosophila heterochromatin protein 1 (HP1), localises to euchromatin within interphase nuclei and is largely excluded from constitutive heterochromatin [J].