Analysis of the pathogenic mechanism for neuropsychiatric disease-like abnormal behavior in IRBIT knockout mouse

一种称为伊尔比特（1，4，5-三磷酸肌醇释放的IP 3 R结合蛋白）的IP 3 R结合蛋白，其与IP 3 R的IP 3结合核心结构域相互作用并调节IP 3 R的IP 3敏感性。最近，我们发现钙/钙调蛋白依赖性激酶II α（CaMK II α）作为一个伊尔比特结合蛋白。本研究通过观察伊尔比特缺失对单胺（多巴胺和去甲肾上腺素）合成和细胞内pH调节的影响，来阐明伊尔比特在中枢神经系统中的作用。我们发现伊尔比特通过CaMK Ⅱ α调节TH的磷酸化状态。此外，伊尔比特还参与了NBC 1对神经元和星形胶质细胞内pH的调节。

An IP3R binding protein termed IRBIT (IP3R binding protein released with inositol 1,4,5-trisphosphate) that interacts with the IP3 binding core domain of IP3R and regulate the IP3 sensitivity of IP3R. Recently, we identified calcium/calmodulin-dependent kinase II alpha (CaMKIIalpha) as an IRBIT binding protein. In this study, we investigated the effect of IRBIT deletion on the monoamine (dopamine and norepinephrine) synthesis and intracellular pH regulation to explain the function of IRBIT in the central nervous system. We found that IRBIT regulated the phosphoryaltion state of TH by CaMKIIalpha. In addition, IRBIT contributed the regulation of intracellular pH by NBC1 in the neuron and astrocyte.