The activated PERK phosphorylates eIF2α, forming an inflammatory- and survival-preferred translation program. Notably, this STING–PERK–eIF2α pathway is evolutionarily primitive and physiologically critical to cellular senescence and organ fibrosis. Pharmacologically or genetically targeting this non-...
构建STING慢病毒载体转染HTR-8/SVneo细胞,利用免疫组化,免疫荧光,Western blot和q-PCR检测抑制STING基因后,内质网应激,PERK通路以及凋亡相关因子变化情况.结果:妊娠期氟氯氰菊酯暴露损害胎盘结构和发育引发不良妊娠结局;随着染毒浓度的增加胎盘细胞的增殖,迁移和侵袭能力被抑制,通过激活内质网应激介导的PERK/eIF2α/ATF4...
部分PERK激活STING-RIPK3介导海马神经元发生坏死性凋亡的分子机制研究【目的】1.明确PERK蛋白在SAE小鼠海马组织中的时空变化.2.阐明调控PERK对SAE小鼠认知功能的影响.【方法】1.采用Western blot检测CLP小鼠海马组织中葡萄糖调节蛋78(Glucose-regulated protein78,GRP78),p-PERK,PERK蛋白水平的变化;IF观察p-PERK蛋白...
此外,骨髓移植实验证实,与巨噬细胞相比,内皮细胞STING活化在动脉粥样硬化中发挥更重要的作用。本研究发现非经典STING-PERK通路介导表观遗传调控机制在炎症应答所致血管内皮功能紊乱中发挥关键作用,为临床治疗AS提供了新的干预靶点和治疗策略。南京医科大学药学院心脑血管药物重点实验室李雪松副教授为该论文第一作者。该文...
PERK-STING-RIPK3信号通路诱导海马神经元坏死性凋亡在脓毒症相关性脑病中的机制研究蛋白激酶R样内质网激酶干扰素基因刺激因子坏死性凋亡脓毒症相关性脑病认知功能障碍脓毒症相关性脑病(Sepsis associated encephalopathy,SAE)是指脓毒症发生后宿主反应失调引起的弥漫性脑功能障碍,其发病率约76%,死亡率高达60%;即使幸存,...
Overall, our study suggested that SVV infection resulted in STING degradation via PERK and ATF6-mediated reticulophagy, which may be an immune escape strategy of SVV. This finding improves the understanding of the intricate interplay between viruses and their hosts and provides a novel strategy for...