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Ko, Myunggon
Molecular Immunology & Cancer Epigenetics
Research Interests
  • TET proteins, DNA hydroxymethylation, oncogenesis, cancer stem cells, cancer therapy

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Chromatin remodeling, development and disease

Cited 27 times inthomson ciCited 27 times inthomson ci
Title
Chromatin remodeling, development and disease
Author
Ko, Myung GonSohn, Dong HChung, HeekyoungSeong, Rho H
Keywords
Chromatin remodeling; Development; Embryo; SWI/SNF; T-cell; Tumor suppression
Issue Date
2008-12
Publisher
ELSEVIER SCIENCE BV
Citation
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, v.647, no.1-2, pp.59 - 67
Abstract
Development is a stepwise process in which multi-potent progenitor cells undergo lineage commitment, differentiation, proliferation and maturation to produce mature cells with restricted developmental potentials. This process is directed by spatiotemporally distinct gene expression programs that allow cells to stringently orchestrate intricate transcriptional activation or silencing events. In eukaryotes, chromatin structure contributes to developmental progression as a blueprint for coordinated gene expression by actively participating in the regulation of gene expression. Changes in higher order chromatin structure or covalent modification of its components are considered to be critical events in dictating lineage-specific gene expression during development. Mammalian cells utilize multi-subunit nuclear complexes to alter chromatin structure. Histone-modifying complex catalyzes covalent modifications of histone tails including acetylation, methylation, phosphorylation and ubiquitination. ATP-dependent chromatin remodeling complex, which disrupts histone-DNA contacts and induces nucleosome mobilization, requires energy from ATP hydrolysis for its catalytic activity. Here, we discuss the diverse functions of ATP-dependent chromatin remodeling complexes during mammalian development. In particular, the roles of these complexes during embryonic and hematopoietic development are reviewed in depth. In addition, pathological conditions such as tumor development that are induced by mutation of several key subunits of the chromatin remodeling complex are discussed, together with possible mechanisms that underlie tumor suppression by the complex. © 2008 Elsevier B.V. All rights reserved.
URI
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DOI
10.1016/j.mrfmmm.2008.08.004
ISSN
0027-5107
Appears in Collections:
PHY_Journal Papers
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