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Targeting cardiac hypertrophy through a nuclear co-repressor.
EMBO Molecular Medicine ( IF 9.0 ) Pub Date : 2019-10-17 , DOI: 10.15252/emmm.201911297 Andrea Grund 1 , Joerg Heineke 1, 2
EMBO Molecular Medicine ( IF 9.0 ) Pub Date : 2019-10-17 , DOI: 10.15252/emmm.201911297 Andrea Grund 1 , Joerg Heineke 1, 2
Affiliation
Heart failure entails the inability of the heart to pump blood to vital organs. One of the main risk factors for heart failure is the development of pathological hypertrophy. In this issue of EMBO Molecular Medicine, Li and coworkers show that NCoR1, a co-repressor of transcription factors, inhibits the transcriptional activity of MEF2 by stabilizing its complex with class II HDACs. By this mechanism, NCoR1 was identified as potent inhibitor of pathological cardiac hypertrophy and dysfunction.
中文翻译:
通过核协同阻遏物靶向心脏肥大。
心力衰竭导致心脏无法将血液泵送到重要器官。心力衰竭的主要危险因素之一是病理性肥大的发展。Li及其同事在本期《 EMBO分子医学》中表明,转录因子的共阻遏物NCoR1通过稳定其与II类HDAC的复合物来抑制MEF2的转录活性。通过这种机制,NCoR1被确定为病理性心脏肥大和功能障碍的有效抑制剂。
更新日期:2019-11-07
中文翻译:
通过核协同阻遏物靶向心脏肥大。
心力衰竭导致心脏无法将血液泵送到重要器官。心力衰竭的主要危险因素之一是病理性肥大的发展。Li及其同事在本期《 EMBO分子医学》中表明,转录因子的共阻遏物NCoR1通过稳定其与II类HDAC的复合物来抑制MEF2的转录活性。通过这种机制,NCoR1被确定为病理性心脏肥大和功能障碍的有效抑制剂。