首页> 美国卫生研究院文献>Neuropsychiatric Disease and Treatment >COP9 Signalosome Subunit 3 Restricts Neuroinflammatory Responses During Cerebral Ischemia/Reperfusion Injury Through Stabilizing Suppressor of Cytokine Signaling 3 Protein
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COP9 Signalosome Subunit 3 Restricts Neuroinflammatory Responses During Cerebral Ischemia/Reperfusion Injury Through Stabilizing Suppressor of Cytokine Signaling 3 Protein

机译:COP9信号组亚单位3通过稳定细胞因子信号传导3蛋白的抑制剂限制在脑缺血/再灌注损伤期间的神经炎反应

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摘要

The suppressor of cytokine signaling 3 (SOCS3) is a specific negative regulator of signal transducer and activator of transcription 3 (STAT3) signaling, which is predominantly activated to induce neuroinflammatory response in microglia and functions essential roles during cerebral ischemia-reperfusion (I/R) injury. Constitutive photomorphogenesis 9 (COP9) signalosome (CSN) is a signaling platform controlling protein stability by remodeling of cullin-RING ubiquitin ligases, which is recently reported to specifically recognize proteins with SOCS-box domains. However, whether SOCS3 is related to COP9 signalosome in neuroinflammation during cerebral I/R injury is completely unclear.
机译:细胞因子信号3(SOCS3)的抑制剂是信号传感器和转录3(STAT3)信号传导的激活剂的特定负调节器,其主要被激活,以诱导微胶质细胞中的神经炎症反应,并且在脑缺血再灌注过程中诱导神经胶质炎症反应(I / R. ) 受伤。组成型光学发生9(COP9)信号组(CSN)是通过重塑Cullin环泛素连接酶来控制蛋白质稳定性的信号平台,其最近据报道特异性地识别具有SOCS盒结构域的蛋白质。然而,SOCS3是否与COP9炎症在脑I / R损伤期间的COP9信号组有关,完全不清楚。

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