Homer binds a novel proline-rich motif and links group 1 metabotropic glutamate receptors with IP3 receptors
Homer binds a novel proline-rich motif and links group 1 metabotropic glutamate receptors with IP3 receptors
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DOI：
10.1016/s0896-6273(00)80589-9
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发表时间：
1998-10-01
期刊：
影响因子：
16.2
通讯作者：
Worley, PF
中科院分区：
文献类型：
--
作者：
Tu, JC;Xiao, B;Worley, PF
第1组代谢型谷氨酸受体（mGluRs）激活PI周转，从而触发细胞内钙释放。先前，我们证明了mGluRs与Homer相关突触蛋白家族的成员形成天然复合物。在这里，我们提出的证据表明，荷马蛋白形成一个物理系绳连接mGluRs与三磷酸肌醇受体（IP3R）。一种新的富含脯氨酸的“荷马配体”（PPXXFr）被确定在第1组mGluRs和IP3R，这些受体共免疫沉淀作为一个复合物与荷马从大脑。缺乏交联能力的Homer的IEG形式的表达调节mGluR诱导的细胞内钙释放。这些研究确定了钙信号传导的一种新机制，并提供了证据表明，IEG的表达是由突触活动驱动的，可以直接改变特定的突触功能。
Group 1 metabotropic glutamate receptors (mGluRs) activate PI turnover and thereby trigger intracellular calcium release. Previously, we demonstrated that mGluRs form natural complexes with members of a family of Homer-related synaptic proteins. Here, we present evidence that Homer proteins form a physical tether linking mGluRs with the inositol trisphosphate receptors (IP3R). A novel proline-rich "Homer ligand" (PPXXFr) is identified in group 1 mGluRs and IP3R, and these receptors coimmunoprecipitate as a complex with Homer from brain. Expression of the IEG form of Homer, which lacks the ability to cross-link, modulates mGluR-induced intracellular calcium release. These studies identify a novel mechanism in calcium signaling and provide evidence that an IEG, whose expression is driven by synaptic activity, can directly modify a specific synaptic function.