4.8 Article

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

期刊

CANCER CELL
卷 18, 期 5, 页码 436-447

出版社

CELL PRESS
DOI: 10.1016/j.ccr.2010.10.022

关键词

-

资金

  1. Vanderbilt Imaging
  2. Human Tissue Acquisition and Pathology
  3. Functional Genomics Shared Resources
  4. T.J. Martell Foundation
  5. Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation
  6. National Institutes of Health [R01-CA64140, R01-CA77274, R01-CA109355]
  7. NIDDK [P30DK58404]
  8. NCI [P30CA68485, 1F32CA138091-01]

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据