PKC γ介导的信号和精神分裂症

Fan Zhang, Q. Qu
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引用次数: 0

摘要

精神分裂症是一种复杂的精神障碍。虽然已经提出了多种假设来解释该疾病发病机制的分子机制,但关键的病理过程尚不清楚。早期临床研究提示组氨酸三联体核苷酸结合蛋白-1 (Hint1)在精神分裂症发病机制中的作用。Zhang等人最近的一项研究利用hint1敲除动物模型确定了大脑中PKC γ蛋白(PKC )的活性。他们发现,hint1缺乏导致大脑中PKC传导信号受损,这可能为精神分裂症的谷氨酸假说提供了新的线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PKC gamma-mediated signaling and schizophrenia
Schizophrenia is a complicated mental disorder. Although multiple hypotheses have been proposed to interpret the molecular mechanisms underlying the pathogenesis of the disease, the key pathological process is yet blurry. Early clinical studies have implicated a role of the histidine triad nucleotide-binding protein-1 (Hint1) in the pathogenesis of schizophrenia. A most recent investigation by Zhang et al has defined the activity of protein PKC gamma (PKC𝛾) in the brain using Hint1-knockout animal model. Their finding that Hint1-deficiency causes a compromised PKC𝛾 signaling in the brain may shed a new light on the glutamate hypothesis of schizophrenia.
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