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98篇 您的检索式:作者名="Huganir"
    题名 作者 年代 出处 被引量
1Phosphorylation of amino acid neurotransmitter receptors in synaptic plasticity显示文摘RAYMOND L A BLACKSTONE C D HUGANIR R L 1993Trends Neurosci1993,16,:1
2The cell biology of synaptic plasticity: AMPA receptor trafficking显示文摘Shepherd JD Huganir RL 2007Annu Rev Cell Dev Biol2007,23,:1
3Rapid, experience dependent expression of synaptic NMDA receptors in visual cortex in vivo 显示文摘Quinlan EM Philpot BD Huganir RL Bear MF 1999Nat Neurosci1999,2,4:1
4The cell biology of synaptic plastieity:AMPA receptor trafficking显示文摘Shepherd JD Huganir RL 2007Annu Rev Cell Dev Biol2007,23,:1
5Cyclic AMP and synaptic activity-dependent phosphorylation of AMPA-preferring glutamate receptors显示文摘Blackstone C Murphy T.H Moss S.J Baraban J.M & Huganir R.L 0,,:1
6Activation of silent synapses by rapid activity-dependent synaptic recruitment of AMPA receptors显示文摘Liao D Scannevin RH Huganir R 2001J Neurosci2001,21,16:1
7Arc weakens synapses by dispersing AMPA receptors from postsynaptic density via modulating PSD phase separation显示文摘In response to stimuli,the immediate early gene product Arc can acutely down-regulate synaptic strength by removing AMPA receptors(AMPARs)from synapses and thus regulate synaptic plasticity.How Arc,a scaffold protein,can specifically facilitate synaptic removal of AMPARs is unknown.We found that Arc directly antagonizes with PSD-95 in binding to TARPs,which are the auxiliary subunits of AMPARs.Arc,in a highly concentration-sensitive manner,acutely disperses TARPs from the postsynaptic density(PSD)condensate formed via phase separation.TARPs with the Ser residue in the“P-S-Y”-motif of its tail phosphorylated are completely refractory from being dispersed by Arc,suggesting that Arc cannot displace AMPARs from PSDs in active synapses.Conversely,strengthening the interaction between Arc and TARPs enhances Arc’s capacity in weakening synapses.Thus,Arc can specifically and effectively modulate synaptic AMPAR clustering via modulating PSD phase separation.Our study further suggests that activity-dependent,bi-directional modulation of PSD condensate formation/dispersion represents a general regulatory mechanism for synaptic plasticity.Xudong Chen Bowen Jia Yoichi Araki Bian Liu Fei Ye Richard Huganir Mingjie Zhang 2022Cell Research2022,32,10:1
8RNA splicing regulates the activity of a SH2 domain-containing protein tyrosine phosphatase显示文摘Mei L Doherty CA Huganir RL 1994Biol Chem1994,269,12:1
9MAPK cascade signalling and synaptic plasticity 显示文摘Thomas GM Huganir RL 2004Nat Rev Neurosci2004,5,3:1
10Characterization of the tyrosine phosphorylation and distribution of dystro- brevin isoforms 显示文摘Balasubramanian S Fung ET Huganir RL 1998FEBS Lett1998,432,3:1
11Rapid,experience-dependent expression of synaptic NMDA receptors in visual cortex in vivo 显示文摘 PHILPOT B D HUGANIR R L 1999Nat Neurosci1999,2,4:1
12AMPARs and synaptic plasticity:the last 25years显示文摘Huganir RL Nicoll RA 2013Neuron2013,80,3:1
13Regulation of AMPA receptor trafficking and synaptic plasticity 显示文摘Anggono V Huganir RL 2012Curr Opin Neurobiol2012,22,3:1
14A dopamine/D1receptor/protein kinase A/dopamine-and cAMP-regulated phosphoprotein(Mr 32 kDa)/protein phosphatase-1 pathway regulates dephosphorylation of the NMDA receptor显示文摘Snyder GL Fienberg AA Huganir RL 1998J Neurosci1998,18,10:1
15MAPK cascade signaling and synaptic plasticity显示文摘Thomas GM Huganir RL 2004Neuroscience2004,5,:1
16AMPARs and synaptic plasticity: the last 25 years显示文摘Huganir RL Nicoll RA 2013Neuron2013,80,3:1
17受体、突触和记忆显示文摘大脑中神经元突触间的信号传递是由许多神经递质受体介导的。在过去,Richard L.Huganir实验室一直致力于神经递质受体功能调节的分子机制。而最近,该实验室又聚焦到大脑中一种最主要的兴奋性受体的研究——谷氨酸受体。谷氨酸受体主要可以分为两大类:AMPA受体和NMDA受体。AMPA受体主要介导了快速的兴奋性突触传递;而NMDA受体则在神经可塑性和发育中起到重要作用。实验发现,AMPA受体和NMDA受体都可以被一系列的蛋白激酶磷酸化,而磷酸化的水平则直接影响了这些受体的功能特性,包括通道电导和受体膜定位等。AMPA受体磷酸化的水平同时还在学习和记忆的细胞模型中发生改变,如长时程增强(LTP)和长时程抑制(LTD)。此外,AMPA受体中GIuR1亚单位的磷酸化对于各种形式的可塑性以及空间记忆的维持有重要的作用。实验室主要研究突触部位谷氨酸受体在亚细胞水平的定位和聚集的分子机制。最近,一系列可以直接或间接与AMPA和NMDA受体相互作用的蛋白质得以发现,其中包括一个新发现的蛋白家族GRIPs(glutamate receptor interacting proteins)。GRIPs可以直接和AMPA受体的GluR2/3亚单位的C端结合。GRIPs包含7个PDZ结构域,可以介导蛋白与蛋白直接的相互连接,从而把各个AMPA受体交互连接在一起并与其他蛋白相连。另外,GluR2亚单位的C端还可以和兴奋性突触中的蛋白激酶C结合蛋白(PICK1)的PDZ结构域相互作用。另外,GluR2亚单位的C端也可以与一种参与膜融合的蛋白NSF相互作用。这些与AMPA受体相互作用的蛋白质对于受体在膜上的运输以及定位有至关重要的作用。同时,受体与PICK1和GRIP的结合对于小脑运动学习中的LTD有重要作用。总体上说,该实验室发现了一系列可以调节神经递质受体功能的分子机制,这些工作提示受体功能的调节可能是突触传递可塑性发生的一个主要机制,并且可能最终导致了动物行为的改变。HUGANIR Richard L 2008生命科学2008,20,5:1
18Identification of protein kinase C phosphorylation sites within the AMPA receptor GluR2subunit显示文摘McDonald BJ Chung HJ Huganir RL 2001Neurophamacology2001,41,:1
19Identification of protein kinase C phosphorylation sites within the AMPA receptor GluR2 subunit 显示文摘Mcdonald BJ Chung HJ Huganir RL 2001Neurophamacology2001,41,:1
20Requirement of AMPA receptor GluR2 phosphorylation for cerebellar long-term depression显示文摘Chung H J Steinberg J P Huganir R L 2003Science2003,300,5626:1
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