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Hdac3 Is Essential for the Maintenance of Chromatin Structure and Genome Stability

Hdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, a... Full description

Journal Title: Cancer Cell 2010, Vol.18(5), pp.436-447
Main Author: Bhaskara, Srividya
Other Authors: Knutson, Sarah K , Jiang, Guochun , Chandrasekharan, Mahesh B , Wilson, Andrew J , Zheng, Siyuan , Yenamandra, Ashwini , Locke, Kimberly , Yuan, Jia-Ling , Bonine-Summers, Alyssa R , Wells, Christina E , Kaiser, Jonathan F , Washington, M. Kay , Zhao, Zhongming , Wagner, Florence F , Sun, Zu-Wen , Xia, Fen , Holson, Edward B , Khabele, Dineo , Hiebert, Scott W
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1535-6108 ; E-ISSN: 1878-3686 ; DOI: 10.1016/j.ccr.2010.10.022
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recordid: elsevier_sdoi_10_1016_j_ccr_2010_10_022
title: Hdac3 Is Essential for the Maintenance of Chromatin Structure and Genome Stability
format: Article
creator:
  • Bhaskara, Srividya
  • Knutson, Sarah K
  • Jiang, Guochun
  • Chandrasekharan, Mahesh B
  • Wilson, Andrew J
  • Zheng, Siyuan
  • Yenamandra, Ashwini
  • Locke, Kimberly
  • Yuan, Jia-Ling
  • Bonine-Summers, Alyssa R
  • Wells, Christina E
  • Kaiser, Jonathan F
  • Washington, M. Kay
  • Zhao, Zhongming
  • Wagner, Florence F
  • Sun, Zu-Wen
  • Xia, Fen
  • Holson, Edward B
  • Khabele, Dineo
  • Hiebert, Scott W
subjects:
  • Medicine
ispartof: Cancer Cell, 2010, Vol.18(5), pp.436-447
description: Hdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, and histone deposition marks were retained in quiescent Hdac3-null cells. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. Whereas HDAC3 expression was downregulated in only a small number of human liver cancers, the mRNA levels of the HDAC3 cofactor NCOR1 were reduced in one-third of these cases. siRNA targeting of NCOR1 and SMRT ( NCOR2) increased H4K5ac and caused DNA damage, indicating that the HDAC3/NCOR/SMRT axis is critical for maintaining chromatin structure and genomic stability.
language: eng
source:
identifier: ISSN: 1535-6108 ; E-ISSN: 1878-3686 ; DOI: 10.1016/j.ccr.2010.10.022
fulltext: fulltext
issn:
  • 1535-6108
  • 15356108
  • 1878-3686
  • 18783686
url: Link


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descriptionHdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, and histone deposition marks were retained in quiescent Hdac3-null cells. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. Whereas HDAC3 expression was downregulated in only a small number of human liver cancers, the mRNA levels of the HDAC3 cofactor NCOR1 were reduced in one-third of these cases. siRNA targeting of NCOR1 and SMRT ( NCOR2) increased H4K5ac and caused DNA damage, indicating that the HDAC3/NCOR/SMRT axis is critical for maintaining chromatin structure and genomic stability.
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Hdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, and histone deposition marks were retained in quiescent Hdac3-null cells. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. Whereas HDAC3 expression was downregulated in only a small number of human liver cancers, the mRNA levels of the HDAC3 cofactor NCOR1 were reduced in one-third of these cases. siRNA targeting of NCOR1 and SMRT ( NCOR2) increased H4K5ac and caused DNA damage, indicating that the HDAC3/NCOR/SMRT axis is critical for maintaining chromatin structure and genomic stability.

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abstract

Hdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, and histone deposition marks were retained in quiescent Hdac3-null cells. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. Whereas HDAC3 expression was downregulated in only a small number of human liver cancers, the mRNA levels of the HDAC3 cofactor NCOR1 were reduced in one-third of these cases. siRNA targeting of NCOR1 and SMRT ( NCOR2) increased H4K5ac and caused DNA damage, indicating that the HDAC3/NCOR/SMRT axis is critical for maintaining chromatin structure and genomic stability.

pubElsevier Inc
doi10.1016/j.ccr.2010.10.022
lad01Cancer Cell
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