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从多巴胺受体信号传导角度看蛋白激酶C

PKC in the perspective of dopamine receptor signaling.

作者信息

Ma Haixiang

机构信息

School of Pharmaceutical Sciences, Guizhou University, Guiyang, China.

出版信息

Acta Biochim Pol. 2025 Jun 9;72:14488. doi: 10.3389/abp.2025.14488. eCollection 2025.

DOI:10.3389/abp.2025.14488
PMID:40552006
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12183092/
Abstract

Protein kinase C (PKC) is widely distributed in various tissues, organs, and cells. By catalyzing the phosphorylation of Ser/Thr residues on various proteins, PKC regulates the metabolism, growth, proliferation, and differentiation of multiple cells and plays a crucial role in transmembrane signal transmission. In dopamine receptor signal transduction, PKC regulates numerous physiological functions, such as dopamine release, internalization of the dopamine transporter, downregulation of dopamine receptors, etc. In disease conditions, hyperactivation of PKC can lead to disorders such as schizophrenia and Parkinson's disease, while reduced PKC signaling may be associated with Alzheimer's disease. In the past few decades, researchers have paid increasing attention to the transduction role of PKC in dopamine receptor signaling, aiming to identify and discover potential targets for dopaminergic diseases. This review, from the perspective of signal transduction between dopamine receptors and PKC, reveals the pivotal hub position of PKC in the intracellular signal transduction network and its regulation of various physiological functions, providing ideas for future research on PKC and therapeutic interventions for dopaminergic diseases.

摘要

蛋白激酶C(PKC)广泛分布于各种组织、器官和细胞中。通过催化各种蛋白质上丝氨酸/苏氨酸残基的磷酸化,PKC调节多种细胞的代谢、生长、增殖和分化,并在跨膜信号传递中起关键作用。在多巴胺受体信号转导中,PKC调节多种生理功能,如多巴胺释放、多巴胺转运体的内化、多巴胺受体的下调等。在疾病状态下,PKC的过度激活可导致精神分裂症和帕金森病等疾病,而PKC信号传导减少可能与阿尔茨海默病有关。在过去几十年中,研究人员越来越关注PKC在多巴胺受体信号传导中的转导作用,旨在识别和发现多巴胺能疾病的潜在靶点。本综述从多巴胺受体与PKC之间的信号转导角度,揭示了PKC在细胞内信号转导网络中的关键枢纽地位及其对各种生理功能的调节作用,为未来PKC研究及多巴胺能疾病的治疗干预提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/e14e02beb000/abp-72-14488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/1667910d182d/abp-72-14488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/7dc8dd17534b/abp-72-14488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/11a53283dfd8/abp-72-14488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/e14e02beb000/abp-72-14488-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/1667910d182d/abp-72-14488-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/7dc8dd17534b/abp-72-14488-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/11a53283dfd8/abp-72-14488-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa70/12183092/e14e02beb000/abp-72-14488-g004.jpg

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Cognitive impairment in schizophrenia is associated with prefrontal-striatal functional hypoconnectivity and striatal dopaminergic abnormalities.精神分裂症患者的认知障碍与前额叶-纹状体功能连接不足和纹状体多巴胺能异常有关。
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TPPB modulates PKC activity to attenuate neuroinflammation and ameliorate experimental multiple sclerosis.
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Front Cell Neurosci. 2024 May 22;18:1373557. doi: 10.3389/fncel.2024.1373557. eCollection 2024.
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Mdm2-mediated ubiquitination of PKCβII is responsible for insulin-induced heterologous desensitization of dopamine D receptor.Mdm2 介导的 PKCβII 泛素化负责胰岛素诱导的多巴胺 D 受体异源脱敏。
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