Activation of β-catenin signaling pathways by classical G-protein-coupled receptors:: Mechanisms and consequences in cycling and non-cycling cells
Activation of β-catenin signaling pathways by classical G-protein-coupled receptors:: Mechanisms and consequences in cycling and non-cycling cells
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DOI：
10.4161/cc.5.20.3357
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发表时间：
2006-10-15
期刊：
影响因子：
4.3
通讯作者：
Force, Thomas
中科院分区：
文献类型：
--
作者：
Shevtsov, Sergey P.;Haq, Syed;Force, Thomas
Wnt 信号通路是所有生物学领域最深入的研究之一。最近，许多经典的异三聚体 G 蛋白偶联受体 (GPCR) 已被证明可以激活经典的 Wnt 通路，最终稳定 β-连环蛋白并诱导受 Tcf/Lef 反式激活因子家族调控的基因转录。然而，这些 GPCR 实现这一目标的机制在关键方面有所不同，并且在某些情况下，产生的表型是新颖的。在此，我们将研究经典 GPCR 与经典 Wnt 通路相互作用的机制，最终导致其激活，并描述这种激活的后果，重点关注心脏。在心脏中，收缩细胞或心肌细胞进行终末分化，并且几乎完全通过增加细胞大小（肥大）而不是细胞数量来生长，我们将描述 GPCR 介导的经典途径激活如何驱动这一过程。
Wnt signaling pathways are some of the most intensely studies in all of biology. Recently, a number of classical heterotrimeric G protein coupled receptors (GPCRs) have been shown to activate the canonical Wnt pathway, culminating in the stabilization of beta-catenin and induction of transcription of genes regulated by the Tcf/Lef family of transactivators. However, mechanisms by which these GPCRs accomplish this differ in key ways, and in some circumstances, the phenotypes produced are novel. Herein, we will examine mechanisms by which classical GPCRs interact with the canonical Wnt pathway, culminating in its activation, and describe the consequences of this activation, focusing on the heart. In the heart, the contractile cells, or cardiomyocytes, are terminally differentiated and virtually exclusively grow by increasing cell size (hypertrophy) rather than cell number, and we will describe how GPCR-mediated activation of the canonical pathway can drive this process.