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蛋白激酶c在细胞程序性坏死中的作用探究
首发时间：2024-06-06
摘要：蛋白激酶c（protein kinase c，pkc）家族由10种结构相近的丝氨酸/苏氨酸蛋白激酶亚型组成。pkc参与调控细胞凋亡，但其对其他类型的细胞死亡，如程序性坏死和焦亡的具体作用尚不明确。本研究深入探讨了蛋白激酶c（pkc）家族在调节细胞程序性坏死中的作用。本研究采用tnfα smac-mimetic z-vad（tsz）处理的ht-29细胞模型，通过incucyte活细胞动态成像与分析系统、pi（propidium iodide）染色和western blot等技术，探究了pkc调控细胞程序性坏死的作用机制。研究发现，pkc的激活显著抑制了tsz诱导的细胞程序性坏死，而pkc的抑制则促进了细胞死亡。此外，pkc激活通过抑制ripk1、ripk3和mlkl的磷酸化，阻断了细胞程序性坏死的发生。这些发现表明pkc是细胞程序性坏死的关键调控因子，为未来针对程序性坏死相关疾病的治疗提供了新的靶点。
关键词： 细胞生物学 细胞死亡 细胞程序性坏死 蛋白激酶c 受体相互作用蛋白激酶 混合谱系激酶结构域样蛋白
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a study into the mechanism of protein kinase c in regulating necroptosis
abstract：the protein kinase c (pkc) family comprises 10 structurally similar serine/threonine protein kinase isoforms. while pkc is known to regulate apoptosis, its specific role in other types of cell death, such as necroptosis and pyroptosis, remains unclear. this study delves into the role of the pkc family in regulating necroptosis. using the ht-29 cell model treated with tnfα smac-mimetic z-vad (tsz), we investigated the mechanisms by which pkc regulates necroptosis through techniques including incucyte live-cell imaging system, propidium iodide (pi) staining, and western blot. our findings revealed that pkc activation significantly inhibited tsz-induced necroptosis, whereas pkc inhibition promoted cell death. moreover, pkc activation prevented necroptosis by inhibiting the phosphorylation of ripk1, ripk3, and mlkl. these results identify pkc as a crucial regulator of necroptosis, providing new targets for the treatment of necroptosis-related diseases.
keywords： cell biology cell death necroptosis protein kinase c receptor-interacting serine-threonine kinase mixed-lineage kinase domain-like protein
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