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Synaptic plasticity: ARC plays inverse tag at synapses.

机译:突触可塑性:ARC在突触中起反作用。

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摘要

Activity-regulated transcription of the immediate early gene Arc is followed by targeting of ARC protein to the synapse, where (in addition to other effects) it is thought to weaken synaptic strength by promoting the endocytosis of AMPA receptors (AMPARs). However, the mechanisms by which ARC targets particular synapses are unknown. Okuno et al. now show that ARC localizes to synapses that exhibit reduced activity by interacting with an inactive form of Ca~(2+)/calmodulin-dependent protein kinase IIbeta (CaMKlIbeta).
机译:活性早期的Arc基因的转录受活性调节,其后将ARC蛋白靶向突触,其中(除其他作用外)据认为可通过促进AMPA受体(AMPAR)的内吞作用来削弱突触强度。但是,ARC靶向特定突触的机制尚不清楚。 Okuno等。现在表明,ARC通过与非活性形式的Ca〜(2 +)/钙调蛋白依赖性蛋白激酶IIbeta(CaMK11beta)相互作用而定位于突触,突触的活性降低。

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