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首页> 外文期刊>Journal of Cellular Physiology >Parkin potentiates ATP-induced currents due to activation of P2X receptors in PC12 cells.
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Parkin potentiates ATP-induced currents due to activation of P2X receptors in PC12 cells.

机译：由于帕金强化ATP-induced电流P2X受体在PC12细胞的激活。

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Loss-of-function mutations of the parkin gene causes an autosomal recessive juvenile-onset form of Parkinson's disease (AR-JP). Parkin was shown to function as a RING-type E3 ubiquitin protein ligase. However, the function of parkin in neuronal cells remains elusive. Here, we show that expression of parkin-potentiated adenosine triphosphate (ATP)-induced currents that result from activation of the P2X receptors which are widely distributed in the brain and involved in neurotransmission. ATP-induced inward currents were measured in mock-, wild-type or mutant (T415N)-parkin-transfected PC12 cells under the conventional whole-cell patch clamp configuration. The amplitude of ATP-induced currents was significantly greater in wild-type parkin-transfected cells. However, the immunocytochemical study showed no apparent increase in the number of P2X receptors or in ubiquitin levels. The increased currents were attenuated by inhibition of cAMP-dependent protein kinase (PKA) but not protein kinase C (PKC) or Ca2+and calmodulin-dependent protein kinase (CaMKII). ATP-induced currents were also regulated by phosphatases and cyclin-dependent protein kinase 5 (CDK5) via dopamine and cyclic AMP-regulated phosphoprotein (DARPP-32), though the phosphorylation at Thr-34 and Thr-75 were unchanged or rather attenuated. We also tried to investigate the effect of alpha-synuclein, a substrate of parkin and also forming Lysine 63-linked multiubiquitin chains. Expression of alpha-synuclein did not affect the amplitude of ATP-induced currents. Our finding provides the evidence for a relationship between parkin and a neurotransmitter receptor, suggesting that parkin may play an important role in synaptic activity.
机译：帕金丧失突变的基因一种常染色体隐性幼年发病原因帕金森病(AR-JP)。函数作为环形E3泛素蛋白连接酶。神经细胞仍然是难以捉摸的。parkin-potentiated腺苷的表达式全身的三磷酸腺苷(ATP)电流的结果从激活的P2X受体广泛分布在大脑和参与神经传递。在模拟测量,野生型和突变体(T415N) -parkin-transfected PC12细胞下传统的全细胞膜片箝配置。在野生型电流明显更大parkin-transfected细胞。采用免疫研究显示不明显P2X受体或数量的增加泛素的水平。减毒cAMP-dependent的抑制蛋白激酶(PKA)但不是蛋白激酶C(PKC)或Ca2 +和calmodulin-dependent蛋白质激酶(CaMKII)。由磷酸酯酶和细胞周期蛋白依赖性蛋白激酶5 (CDK5)通过多巴胺和循环不过,AMP-regulated磷蛋白质(DARPP-32)的磷酸化Thr-34和刺- 75不变或减毒。调查的影响α-突触核蛋白,a衬底的帕金也形成赖氨酸63 - multiubiquitin链有关。α-突触核蛋白并没有影响的振幅ATP-induced电流。帕金和之间的关系的证据神经递质受体,这表明帕金可能在突触活动起着重要的作用。

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