心力衰竭
生物
基因敲除
染色质免疫沉淀
扩张型心肌病
转录因子
染色质重塑
转基因小鼠
内科学
染色质
发起人
表观遗传学
细胞生物学
小干扰RNA
转基因
转录调控
分子生物学
组蛋白H2B
医学
心肌病
泛素
核糖核酸
基因
基因表达
遗传学
作者
Maria Areli Lorenzana‐Carrillo,Saymon Tejay,Joseph Nanoa,Guocheng Huang,Бо Лю,Alois Haromy,Yuan Zhao,Michelle Mendiola,Dawn E. Bowles,Adam Kinnaird,Evangelos D. Michelakis,Gopinath Sutendra
出处
期刊:Circulation Research
[Ovid Technologies (Wolters Kluwer)]
日期:2024-07-05
卷期号:135 (2): 301-313
被引量:1
标识
DOI:10.1161/circresaha.123.324202
摘要
The tumor suppressor and proapoptotic transcription factor P53 is induced (and activated) in several forms of heart failure, including cardiotoxicity and dilated cardiomyopathy; however, the precise mechanism that coordinates its induction with accessibility to its transcriptional promoter sites remains unresolved, especially in the setting of mature terminally differentiated (nonreplicative) cardiomyocytes.
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