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Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()

ETO2 is a component of a protein complex containing master regulators of hematopoiesis, including GATA-1 and SCL/TAL1, and also has RNA binding properties. Although ETO2 has been reported to repress GATA-1 target genes through histone deacetylation of the target gene loci in erythroid cells, little...

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Autores principales: Fujiwara, Tohru, Okitsu, Yoko, Katsuoka, Yuna, Fukuhara, Noriko, Onishi, Yasushi, Ishizawa, Kenichi, Harigae, Hideo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821025/
https://www.ncbi.nlm.nih.gov/pubmed/24251106
http://dx.doi.org/10.1016/j.fob.2013.10.004
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author Fujiwara, Tohru
Okitsu, Yoko
Katsuoka, Yuna
Fukuhara, Noriko
Onishi, Yasushi
Ishizawa, Kenichi
Harigae, Hideo
author_facet Fujiwara, Tohru
Okitsu, Yoko
Katsuoka, Yuna
Fukuhara, Noriko
Onishi, Yasushi
Ishizawa, Kenichi
Harigae, Hideo
author_sort Fujiwara, Tohru
collection PubMed
description ETO2 is a component of a protein complex containing master regulators of hematopoiesis, including GATA-1 and SCL/TAL1, and also has RNA binding properties. Although ETO2 has been reported to repress GATA-1 target genes through histone deacetylation of the target gene loci in erythroid cells, little is known about the contribution of ETO2 to microRNA (miRNA) regulation. Here, we conducted miRNA profiling in ETO2-overexpressing and ETO2-silenced K562 cells. The analysis suggests that ETO2 positively regulates the abundance of mature miRNAs, including miR-21, miR-29b and let-7e. Our data suggest a novel mode of ETO2-mediated target gene repression via effects on miRNA expression.
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spelling pubmed-38210252013-11-18 Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance() Fujiwara, Tohru Okitsu, Yoko Katsuoka, Yuna Fukuhara, Noriko Onishi, Yasushi Ishizawa, Kenichi Harigae, Hideo FEBS Open Bio Article ETO2 is a component of a protein complex containing master regulators of hematopoiesis, including GATA-1 and SCL/TAL1, and also has RNA binding properties. Although ETO2 has been reported to repress GATA-1 target genes through histone deacetylation of the target gene loci in erythroid cells, little is known about the contribution of ETO2 to microRNA (miRNA) regulation. Here, we conducted miRNA profiling in ETO2-overexpressing and ETO2-silenced K562 cells. The analysis suggests that ETO2 positively regulates the abundance of mature miRNAs, including miR-21, miR-29b and let-7e. Our data suggest a novel mode of ETO2-mediated target gene repression via effects on miRNA expression. Elsevier 2013-10-11 /pmc/articles/PMC3821025/ /pubmed/24251106 http://dx.doi.org/10.1016/j.fob.2013.10.004 Text en © 2013 The Authors http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
spellingShingle Article
Fujiwara, Tohru
Okitsu, Yoko
Katsuoka, Yuna
Fukuhara, Noriko
Onishi, Yasushi
Ishizawa, Kenichi
Harigae, Hideo
Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title_full Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title_fullStr Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title_full_unstemmed Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title_short Expression profiling of ETO2-regulated miRNAs in erythroid cells: Possible influence on miRNA abundance()
title_sort expression profiling of eto2-regulated mirnas in erythroid cells: possible influence on mirna abundance()
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821025/
https://www.ncbi.nlm.nih.gov/pubmed/24251106
http://dx.doi.org/10.1016/j.fob.2013.10.004
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