Shaping the cellular landscape with Set2/SETD2 methylation.
Shaping the cellular landscape with Set2/SETD2 methylation.
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DOI：
10.1007/s00018-017-2517-x
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发表时间：
2017-09
期刊：
影响因子：
--
通讯作者：
Strahl BD
中科院分区：
文献类型：
--
作者：
McDaniel SL;Strahl BD
染色质结构是基因转录的主要障碍，在每一轮转录过程中必须被破坏和重置。该过程的核心是Set 2/SETD 2甲基转移酶，其介导组蛋白H3在赖氨酸36（H3 K36 me）处的共转录甲基化。研究表明，H3 K36 me不仅可以防止基因体内出现不适当的转录起始，而且还具有其他保守功能，包括修复受损DNA和调节前体mRNA剪接。与Set 2/SETD 2在染色质生物学中的重要性一致，最近发现SETD 2的突变或H3.3中H3 K36处或附近的突变是癌症发展的基础。本文就Set 2/SETD 2在基因组调控和肿瘤发生发展中的作用作一综述。
Chromatin structure is a major barrier to gene transcription that must be disrupted and re-set during each round of transcription. Central to this process is the Set2/SETD2 methyltransferase that mediates co-transcriptional methylation to histone H3 at lysine 36 (H3K36me). Studies reveal that H3K36me not only prevents inappropriate transcriptional initiation from arising within gene bodies, but that it has other conserved functions that include the repair of damaged DNA and regulation of pre-mRNA splicing. Consistent with the importance of Set2/SETD2 in chromatin biology, mutations of SETD2, or mutations at or near H3K36 in H3.3, have recently been found to underlie cancer development. This review will summarize the latest insights into the functions of Set2/SETD2 in genome regulation and cancer development.
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