http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Synaptic removal of diacylglycerol by DGKzeta and PSD-95 regulates dendritic spine maintenance.
Kim, Karam,Yang, Jinhee,Zhong, Xiao-Ping,Kim, Myoung-Hwan,Kim, Yun Sook,Lee, Hyun Woo,Han, Seungnam,Choi, Jeonghoon,Han, Kihoon,Seo, Jinsoo,Prescott, Stephen M,Topham, Matthew K,Bae, Yong Chul,Koretzk Published for the European Molecular Biology Organ 2009 The EMBO journal Vol.28 No.8
<P>Diacylglycerol (DAG) is an important lipid signalling molecule that exerts an effect on various effector proteins including protein kinase C. A main mechanism for DAG removal is to convert it to phosphatidic acid (PA) by DAG kinases (DGKs). However, it is not well understood how DGKs are targeted to specific subcellular sites and tightly regulates DAG levels. The neuronal synapse is a prominent site of DAG production. Here, we show that DGKzeta is targeted to excitatory synapses through its direct interaction with the postsynaptic PDZ scaffold PSD-95. Overexpression of DGKzeta in cultured neurons increases the number of dendritic spines, which receive the majority of excitatory synaptic inputs, in a manner requiring its catalytic activity and PSD-95 binding. Conversely, DGKzeta knockdown reduces spine density. Mice deficient in DGKzeta expression show reduced spine density and excitatory synaptic transmission. Time-lapse imaging indicates that DGKzeta is required for spine maintenance but not formation. We propose that PSD-95 targets DGKzeta to synaptic DAG-producing receptors to tightly couple synaptic DAG production to its conversion to PA for the maintenance of spine density.</P>