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目的观察阿尔茨海默病转基因小鼠海马结构NIX的变化。方法以Morris水迷宫检测野生型和突变型转基因小鼠学习记忆能力,免疫组织化学和共聚焦激光扫描显微技术观察转基因小鼠海马结构促凋亡蛋白NIX的变化结果野生型和突变型小鼠逃避潜伏期中位数分别为29.00 s和38.00 s,差异无统计学意义,P>0.05;野生型和突变型小鼠搜索策略相比,突变型较野生型使用的搜索策略减少,差异有统计学意义,P<0.05;野生型和突变型小鼠NIX免疫反应阳性物灰度值中位数分别为103.83和128.85,差异有统计学意义,P<0.05;野生型和突变型小鼠海马结构NIX平均荧光强度分别为92.18±7.81和103.07±14.94,差异有统计学意义,P<0.05;野生型和突变型小鼠海马结构NIX与线粒体共定位的数目分别为240.94±169.48和544.18±336.44,差异有统计学意义,P<0.05。结论阿尔茨海默病转基因小鼠出现学习记忆障碍,海马结构促凋亡蛋白NIX的量增多,且NIX与线粒体共定位的量增多,提示NIX在阿尔茨海默病病理改变过程中可能起到一定的作用。 相似文献
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Mitophagy is a selective form of macro‐autophagy in which mitochondria are specifically targeted for autophagic degradation. Mitophagy plays an important role in cellular homeostasis by eliminating dysfunctional mitochondria and reducing mitochondrial mass as an adaptive response to stress. Cells execute mitophagy through several non‐redundant mechanisms, including the PINK1/Parkin partnership, which modulates turnover of depolarized mitochondria, and stress‐induced BNIP3, NIX, and FUNDC1 molecular adaptors, which interact directly with LC3 to promote mitophagy. These pathways are deregulated in human diseases, including cancer, neurodegeneration, metabolic disorders, muscle atrophy, ageing, and inflammation, reflecting the importance of mitophagy as a cellular housekeeping function. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献
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目的:探讨前列腺素 E1(PGE1)对肺撞击伤后肺泡细胞凋亡的影响。方法雄性 SD大鼠分为正常对照组、伤后对照组和伤后 PGE1处理组。致伤后24 h 检测动脉氧分压、肺系数,TUNEL 染色检测肺泡细胞凋亡的整体情况。以蛋白免疫印迹试验(Western blot)检测自噬相关蛋白及自噬调节蛋白 NIX 的表达情况。结果伤后24 h 肺组织可见明显结构破坏及肺水肿。与正常对照组相比,伤后对照组动脉氧分压降低(P <0.05),肺泡细胞凋亡指数增加(P <0.05),同时肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白 NIX 表达增加(P <0.05)。伤后 PGE1处理组动脉氧分压低于正常对照组(P <0.05),但较伤后对照组显著改善(P <0.05);肺泡细胞凋亡指数高于正常对照组,但显著低于伤后对照组(P <0.05);肺组织自噬相关蛋白Beclin-1、LC3Ⅱ/LC3Ⅰ及自噬调节蛋白 NIX 的表达虽然较正常对照组增加(P <0.05),但显著低于伤后对照组(P <0.05)。结论PGE1减轻大鼠肺撞击伤后肺泡细胞凋亡,此作用可能是通过抑制 NIX 介导的细胞自噬,以及肺泡细胞自噬性凋亡实现。 相似文献
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SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy
Xingyu Li Peili Hou Wenqing Ma Xuefeng Wang Hongmei Wang Zhangping Yu Huasong Chang Tiecheng Wang Song Jin Xue Wang Wenqi Wang Yudong Zhao Yong Zhao Chunqing Xu Xiaomei Ma Yuwei Gao Hongbin He 《Cellular & molecular immunology》2022,19(1):67
The global coronavirus disease 2019(COVID-19)pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)has caused severe morbidity and mortality in humans.It is urgent to understand the function of viral genes.However,the function of open reading frame 10(ORF10),which is uniquely expressed by SARS-CoV-2,remains unclear.In this study,we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon(IFN-I)genes and IFN-stimulated genes.Then,mitochondrial antiviral signaling protein(MAVS)was identified as the target via which ORF10 suppresses the IFN-I signaling pathway,and MAVS was found to be degraded through the ORF10-induced autophagy pathway.Furthermore,overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy.Mechanistically,ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X(NIX)and induced mitophagy through its interaction with both NIX and LC3B.Moreover,knockdown of NIX expression blocked mitophagy activation,MAVS degradation,and IFN-I signaling pathway inhibition by ORF10.Consistent with our observations,in the context of SARS-CoV-2 infection,ORF10 inhibited MAVS expression and facilitated viral replication.In brief,our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response;that is,ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX. 相似文献
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