心脏中一条新的由G(q)启动的丝裂原活化蛋白激酶信号通路。
A new G(q)-initiated MAPK signaling pathway in the heart.
作者信息
Gutkind J Silvio, Offermanns Stefan
出版信息
Dev Cell. 2009 Feb;16(2):163-4. doi: 10.1016/j.devcel.2009.01.021.
PMID:19217418
Abstract
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through G(q/11)-coupled receptors. A novel signaling route stimulated by betagamma-subunits of G(q/11) results in the autophosphorylation of ERK1/2 on a new site and the nuclear retention of ERK1/2, thereby activating hypertrophic gene programs.
摘要
病理性心脏肥大涉及通过G(q/11)偶联受体起作用的自分泌/旁分泌介质。由G(q/11)的βγ亚基刺激的一条新信号通路导致ERK1/2在一个新位点上的自磷酸化以及ERK1/2在细胞核内的滞留，从而激活肥大基因程序。
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