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Diacylglycerol kinase-? restores cardiac dysfunction under chronic pressure overload: a new specific regulator of Gaq signaling cascade

机译:二酰基甘油激酶-?在慢性压力超负荷下恢复心脏功能障碍:Gaq信号级联的新特异性调节剂

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摘要

Gaq protein-coupled receptor (GPCR) signaling pathway, which includes diacylglycerol (DAG) and protein kinase C (PKC), plays a critical role in cardiac hypertrophy. DAG kinase (DGK) catalyzes DAG phosphor-ylation and controls cellular DAG levels, thus acting as a regulator of GPCR signaling. It has been reported that DGKe acts specifically on DAG produced by inositol cycling. In this study, we examined whether DGKe prevents cardiac hypertrophy and progression to heart failure under chronic pressure overload. We generated transgenic mice with cardiac-specific overexpression of DGKe (DGKe-TG) using an a-myosin heavy chain promoter.
机译:Gaq蛋白偶联受体(GPCR)信号通路包括二酰基甘油(DAG)和蛋白激酶C(PKC),在心脏肥大中起关键作用。 DAG激酶(DGK)催化DAG磷酸化并控制细胞DAG的水平,从而充当GPCR信号的调节剂。据报道,DGKe专门作用于肌醇循环产生的DAG。在这项研究中,我们检查了DGKe是否在慢性压力超负荷下预防心脏肥大和发展为心力衰竭。我们使用α-肌球蛋白重链启动子产生了具有心脏特异性DGKe(DGKe-TG)过表达的转基因小鼠。

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