Isogenic human pluripotent stem cell disease models reveal ABRA deficiency underlies cTnT mutation-induced familial dilated cardiomyopathy.

Author: Bin LI ¹ ; Yongkun ZHAN ¹ ; Qianqian LIANG ¹ ; Chen XU ¹ ; Xinyan ZHOU ¹ ; Huanhuan CAI ¹ ; Yufan ZHENG ¹ ; Yifan GUO ¹ ; Lei WANG ² ; Wenqing QIU ² ; Baiping CUI ¹ ; Chao LU ¹ ; Ruizhe QIAN ¹ ; Ping ZHOU ¹ ; Haiyan CHEN ³ ; Yun LIU ² ; Sifeng CHEN ¹ ; Xiaobo LI ¹ ; Ning SUN ⁴
Author Information

1. Department of Physiology and Pathophysiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
2. Department of Biochemistry, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
3. Department of Echocardiography, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
4. Department of Physiology and Pathophysiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. sunning@fudan.edu.cn.
Publication Type:Research Support, Non-U.S. Gov't
MeSH: Cardiomyopathy, Dilated/metabolism*; Humans; Microfilament Proteins/metabolism*; Models, Cardiovascular; Mutation; Myocytes, Cardiac; Pluripotent Stem Cells/metabolism*; Transcription Factors/metabolism*; Troponin T/metabolism*
From: Protein & Cell 2022;13(1):65-71
CountryChina
Language:English