Cardiac deletion of Smyd2 is dispensable for mouse heart development.
Cardiac deletion of Smyd2 is dispensable for mouse heart development.
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DOI:
10.1371/journal.pone.0009748
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发表时间:
2010-03-17
期刊:
影响因子:
3.7
通讯作者:
Engel FB
中科院分区:
文献类型:
--
作者:
Diehl F;Brown MA;van Amerongen MJ;Novoyatleva T;Wietelmann A;Harriss J;Ferrazzi F;Böttger T;Harvey RP;Tucker PW;Engel FB
Chromatin modifying enzymes play a critical role in cardiac differentiation. Previously, it has been shown that the targeted deletion of the histone methyltransferase, Smyd1, the founding member of the SET and MYND domain containing (Smyd) family, interferes with cardiomyocyte maturation and proper formation of the right heart ventricle. The highly related paralogue, Smyd2 is a histone 3 lysine 4- and lysine 36-specific methyltransferase expressed in heart and brain. Here, we report that Smyd2 is differentially expressed during cardiac development with highest expression in the neonatal heart. To elucidate the functional role of Smyd2 in the heart, we generated conditional knockout (cKO) mice harboring a cardiomyocyte-specific deletion of Smyd2 and performed histological, functional and molecular analyses. Unexpectedly, cardiac deletion of Smyd2 was dispensable for proper morphological and functional development of the murine heart and had no effect on global histone 3 lysine 4 or 36 methylation. However, we provide evidence for a potential role of Smyd2 in the transcriptional regulation of genes associated with translation and reveal that Smyd2, similar to Smyd3, interacts with RNA Polymerase II as well as to the RNA helicase, HELZ.
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影响因子:
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通讯作者:
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DOI:
10.1152/ajpheart.00514.2007
发表时间:
2007-09-01
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影响因子:
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作者:
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