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Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells

Epigenetic mechanisms are fundamental to understanding the regulatory networks of gene expression that govern stem cell maintenance and differentiation. Methylated histone H3 lysine 4 (H3K4) has emerged as a key epigenetic signal for gene transcription; it is dynamically modulated by several specifi...

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Detalles Bibliográficos
Autores principales: Gu, Bingnan, Lee, Min Gyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953348/
https://www.ncbi.nlm.nih.gov/pubmed/24172249
http://dx.doi.org/10.1186/2045-3701-3-39
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author Gu, Bingnan
Lee, Min Gyu
author_facet Gu, Bingnan
Lee, Min Gyu
author_sort Gu, Bingnan
collection PubMed
description Epigenetic mechanisms are fundamental to understanding the regulatory networks of gene expression that govern stem cell maintenance and differentiation. Methylated histone H3 lysine 4 (H3K4) has emerged as a key epigenetic signal for gene transcription; it is dynamically modulated by several specific H3K4 methyltransferases and demethylases. Recent studies have described new epigenetic mechanisms by which H3K4 methylation modifiers control self-renewal and lineage commitments of stem cells. Such advances in stem cell biology would have a high impact on the research fields of cancer stem cell and regenerative medicine. In this review, we discuss the recent progress in understanding the roles of H3K4 methylation modifiers in regulating embryonic and adult stem cells’ fates.
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spelling pubmed-39533482014-03-15 Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells Gu, Bingnan Lee, Min Gyu Cell Biosci Review Epigenetic mechanisms are fundamental to understanding the regulatory networks of gene expression that govern stem cell maintenance and differentiation. Methylated histone H3 lysine 4 (H3K4) has emerged as a key epigenetic signal for gene transcription; it is dynamically modulated by several specific H3K4 methyltransferases and demethylases. Recent studies have described new epigenetic mechanisms by which H3K4 methylation modifiers control self-renewal and lineage commitments of stem cells. Such advances in stem cell biology would have a high impact on the research fields of cancer stem cell and regenerative medicine. In this review, we discuss the recent progress in understanding the roles of H3K4 methylation modifiers in regulating embryonic and adult stem cells’ fates. BioMed Central 2013-10-09 /pmc/articles/PMC3953348/ /pubmed/24172249 http://dx.doi.org/10.1186/2045-3701-3-39 Text en Copyright © 2013 Gu and Lee; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Gu, Bingnan
Lee, Min Gyu
Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title_full Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title_fullStr Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title_full_unstemmed Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title_short Histone H3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
title_sort histone h3 lysine 4 methyltransferases and demethylases in self-renewal and differentiation of stem cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953348/
https://www.ncbi.nlm.nih.gov/pubmed/24172249
http://dx.doi.org/10.1186/2045-3701-3-39
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