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首页> 外文期刊>EMBO Journal >Coordinated action of NSF and PKC regulates GABA(B) receptor signaling efficacy
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Coordinated action of NSF and PKC regulates GABA(B) receptor signaling efficacy

机译：协调行动的NSF和PKC调节GABA (B)受体信号功效

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The obligatory heterodimerization of the GABA(B) receptor ( GBR) raises fundamental questions about molecular mechanisms controlling its signaling efficacy. Here, we show that NEM sensitive fusion ( NSF) protein interacts directly with the GBR heterodimer both in rat brain synaptosomes and in CHO cells, forming a ternary complex that can be regulated by agonist stimulation. Inhibition of NSF binding with a peptide derived from GBR2 ( TAT-Pep-27) did not affect basal signaling activity but almost completely abolished agonist-promoted GBR desensitization in both CHO cells and hippocampal slices. Taken with the role of PKC in the desensitization process, our observation that TAT-Pep-27 prevented both agonist- promoted recruitment of PKC and receptor phosphorylation suggests that NSF is a priming factor required for GBR desensitization. Given that GBR desensitization does not involve receptor internalization, the NSF/PKC coordinated action revealed herein suggests that NSF can regulate GPCR signalling efficacy independently of its role in membrane trafficking. The functional interaction between three bona fide regulators of neurotransmitter release, such as GBR, NSF and PKC, could shed new light on the modulation of presynaptic GBR action.
机译：的义务heterodimerization GABA (B)受体(GBR)提出了根本性的问题对控制其分子机制信号的有效性。敏感的融合(NSF)相互作用的蛋白质在老鼠都直接与GBR异质二聚体大脑突触体和CHO细胞,形成三元复杂,可以由受体激动剂刺激。肽来源于GBR2 (TAT-Pep-27)没有但几乎影响基底信号活动完全废除agonist-promoted GBR在CHO细胞和海马脱敏片。脱敏治疗过程中,我们的观察TAT-Pep-27阻止受体激动剂——提升招聘的PKC和受体磷酸化表明,NSF的启动因素是必需的GBR脱敏。脱敏不涉及受体内化,NSF / PKC协调行动显示在此表明,NSF可以调节GPCR信号独立于其功效作用在膜贩运。之间的交互三个善意的监管机构神经递质释放,比如GBR, NSF和PKC,可以揭示的调制突触前GBR行动。

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