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摘要
En 中文
The accumulation of SIRT4 in the nuclei of kidney cells drives kidney fibrosis, so blocking the movement of this protein could be a potential therapeutic strategy against fibrosis.
Keyword:
kidney fibrosis
sirtuin 4
TGF-beta 1
splicing
nuclear translocation
CCN2
Mouse
Other
期刊
IF:
0
论文数:
1.8W
被引数:
16
机构
引用论文
Nuclear translocation of SIRT4 mediates deacetylation of U2AF2 to modulate renal fibrosis through alternative splicing-mediated upregulation of CCN2SIRT4的核转位介导U2AF2的去乙酰化通过选择性剪接介导的CCN2上调调节肾纤维化.png)
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OAAI
ELIFEIF0
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收藏An extended U2AF65-RNA-binding domain recognizes the 3′ splice site signalNATURE COMMUNICATIONS
OAAI
NATURE COMMUNICATIONSIF15.7
OAAI分享收藏SIRT4 is essential for metabolic control and meiotic structure during mouse oocyte maturationAGING CELLOAAI
AGING CELLIF7.1
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