GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1
GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1
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DOI：
10.1038/nn0901-908
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发表时间：
2001-09-01
影响因子：
25
通讯作者：
Moss, SJ
中科院分区：
文献类型：
--
作者：
Bedford, FK;Kittler, JT;Moss, SJ
控制神经元膜中功能性γ-氨基丁酸A（GABA（A））受体的数量是抑制性神经传递功效的关键因素。在这里，我们描述了GABA（A）受体与泛素样蛋白Plic-1的直接相互作用。此外，PLIC-1在抑制性突触处富集，并与突触下膜相关。在功能上，Plic-1促进GABA（A）受体细胞表面表达，而不影响受体内化的速率。Plic-1还增强细胞内GABA（A）受体亚单位的稳定性，增加可插入质膜的受体数量。我们的研究确定了Plic-1以前未知的作用，即GABA（A）受体细胞表面数量的调节，这表明Plic-1促进了这些受体在树突状细胞膜中的积累。
Controlling the number of functional gamma -aminobutyric acid A (GABA(A)) receptors in neuronal membranes is a crucial factor for the efficacy of inhibitory neurotransmission. Here we describe the direct interaction of GABA(A) receptors with the ubiquitin-like protein Plic-1. Furthermore, Plic-1 is enriched at inhibitory synapses and is associated with subsynaptic membranes. Functionally, Plic-1 facilitates GABA(A) receptor cell surface expression without affecting the rate of receptor internalization. Plic-1 also enhances the stability of intracellular GABA(A) receptor subunits, increasing the number of receptors available for insertion into the plasma membrane. Our study identifies a previously unknown role for Plic-1, a modulation of GABA(A) receptor cell surface number, which suggests that Plic-1 facilitates accumulation of these receptors in dendritic membranes.