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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), p.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:
DNA
Publisher: United States: Elsevier Inc
ID: ISSN: 1535-6108
Link: https://www.ncbi.nlm.nih.gov/pubmed/21075309
Zum Text:
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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:
  • Acetylation
  • Animals
  • Article
  • Cancer Research
  • Carcinoma, Hepatocellular - genetics
  • Carcinoma, Hepatocellular - pathology
  • Cell Biology
  • Cell Line, Tumor
  • Chromatin
  • Chromatin - ultrastructure
  • Chromatin Assembly and Disassembly
  • DNA
  • DNA Damage
  • DNA Repair
  • DNA Replication
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic
  • Genomic Instability
  • Genomics
  • Histone Deacetylases - physiology
  • Histones - metabolism
  • Humans
  • Liver cancer
  • Liver Neoplasms, Experimental - genetics
  • Liver Neoplasms, Experimental - pathology
  • Messenger RNA
  • Mice
  • Nuclear Receptor Co-Repressor 1 - metabolism
  • Nuclear Receptor Co-Repressor 2 - metabolism
  • Oncology
  • Radiation
  • RNA Interference
  • RNA, Messenger - metabolism
  • S Phase
  • Wetlands
  • Yuan (China)
ispartof: Cancer cell, 2010, Vol.18 (5), p.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
fulltext: no_fulltext
issn:
  • 1535-6108
  • 1878-3686
url: Link


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titleHdac3 Is Essential for the Maintenance of Chromatin Structure and Genome Stability
creatorBhaskara, 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
creatorcontribBhaskara, 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
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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subjectAcetylation ; Animals ; Article ; Cancer Research ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell Biology ; Cell Line, Tumor ; Chromatin ; Chromatin - ultrastructure ; Chromatin Assembly and Disassembly ; DNA ; DNA Damage ; DNA Repair ; DNA Replication ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Genomic Instability ; Genomics ; Histone Deacetylases - physiology ; Histones - metabolism ; Humans ; Liver cancer ; Liver Neoplasms, Experimental - genetics ; Liver Neoplasms, Experimental - pathology ; Messenger RNA ; Mice ; Nuclear Receptor Co-Repressor 1 - metabolism ; Nuclear Receptor Co-Repressor 2 - metabolism ; Oncology ; Radiation ; RNA Interference ; RNA, Messenger - metabolism ; S Phase ; Wetlands ; Yuan (China)
ispartofCancer cell, 2010, Vol.18 (5), p.436-447
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8Yuan, Jia-ling
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10Wells, Christina E
11Kaiser, Jonathan F
12Washington, M. Kay
13Zhao, Zhongming
14Wagner, Florence F
15Sun, Zu-Wen
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17Holson, Edward B
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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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3Cancer Research
4Carcinoma, Hepatocellular - genetics
5Carcinoma, Hepatocellular - pathology
6Cell Biology
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11DNA
12DNA Damage
13DNA Repair
14DNA Replication
15Down-Regulation
16Gene Expression Regulation, Neoplastic
17Genomic Instability
18Genomics
19Histone Deacetylases - physiology
20Histones - metabolism
21Humans
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23Liver Neoplasms, Experimental - genetics
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25Messenger RNA
26Mice
27Nuclear Receptor Co-Repressor 1 - metabolism
28Nuclear Receptor Co-Repressor 2 - metabolism
29Oncology
30Radiation
31RNA Interference
32RNA, Messenger - metabolism
33S Phase
34Wetlands
35Yuan (China)
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titleHdac3 Is Essential for the Maintenance of Chromatin Structure and Genome Stability
authorBhaskara, 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
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issn1535-6108
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abstractHdac3 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.
copUnited States
pubElsevier Inc
pmid21075309
doi10.1016/j.ccr.2010.10.022
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