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首页> 外文期刊>Neuron >RNA editing at arg607 controls AMPA receptor exit from the endoplasmic reticulum.
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RNA editing at arg607 controls AMPA receptor exit from the endoplasmic reticulum.

机译：arg607处的RNA编辑控制AMPA受体从内质网退出。

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摘要

AMPA-receptor (AMPAR) transport to synapses plays a critical role in the modulation of synaptic strength. We show that the functionally critical GluR2 subunit stably resides in an intracellular pool in the endoplasmic reticulum (ER). GluR2 in this pool is extensively complexed with GluR3 but not with GluR1, which is mainly confined to the cell surface. Mutagenesis revealed that elements in the C terminus including the PDZ motif are required for GluR2 forward-transport from the ER. Surprisingly, ER retention of GluR2 is controlled by Arg607 at the Q/R-editing site. Reversion to Gln (R607Q) resulted in rapid release from the pool and elevated surface expression of GluR2 in neurons. Therefore, Arg607 is a central regulator. In addition to channel gating, it also controls ER exit and may thereby ensure the availability of GluR2 for assembly into AMPARs.
机译：AMPA受体（AMPAR）转运至突触在调节突触强度中起关键作用。我们表明，功能关键的GluR2亚基稳定地位于内质网（ER）的细胞内池中。该池中的GluR2与GluR3广泛复合，但不与GluR1广泛复合，后者主要局限于细胞表面。诱变表明，GluR2从ER向前转运需要C末端的元素（包括PDZ基序）。出乎意料的是，GluR2的ER保留是由Q / R编辑位点上的Arg607控制的。还原为Gln（R607Q）导致从池中快速释放，并且神经元中GluR2的表面表达升高。因此，Arg607是中央调节器。除了通道门控之外，它还控制ER出口，从而可以确保GluR2可用于组装成AMPAR。

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