PINK1-mediated mitochondrial fission is Drp1S616 phosphorylation dependent. Overexpression of either wild-type Drp1 or of the phosphomimetic mutant Drp1S616D , but not a dephosphorylation-mimic mutant Drp1S616A , rescues PINK1 deficiency-associated phenotypes in Drosophila. Moreover, Drp1 restores PINK1-...
本研究表明通过调节RIP1/RIP3通路加速p62自噬小体转换和破损线粒体清除可能是改善CIRI恶性循环的有效措施,而维持线粒体质量平衡和减少线粒体ROS堆积(包括减少ROS生成和增加ROS清除等)可能是从根本上改善CIRI预后的关键。 本文中Drp1 干扰腺...
本研究表明通过调节RIP1/RIP3通路加速p62自噬小体转换和破损线粒体清除可能是改善CIRI恶性循环的有效措施,而维持线粒体质量平衡和减少线粒体ROS堆积(包括减少ROS生成和增加ROS清除等)可能是从根本上改善CIRI预后的关键。 本文中Drp1 干扰腺病毒、Drp1-S616D 和 Drp1-S616A 过表达腺病毒及外泌体浓度粒径(NTA)检测...
(S616) was less in both DRP1K532Rand DRP1K532R S616Dmutants than DRP1 and DRP1S616D(Fig.6G andH). As expected, the amount of the fission protein recruited to the mitochondria was most in the presence of DRP1S616D. These results reiterate that ISGylation of DRP1 is crucial for its ...
本文中Drp1 干扰腺病毒、Drp1-S616D 和 Drp1-S616A 过表达腺病毒及外泌体浓度粒径(NTA)检测均由上海吉凯基因提供。 段晨阳,临床医学博士,博士后,重庆医学会麻醉学分会青年委员。长期从事围术期危重症多器官功能损害与保护相关临床工作和科学研究。主持国家自然科学基金青年基金1项、中国博士后面上项目1项,入选 “...
本文中Drp1 干扰腺病毒、Drp1-S616D 和 Drp1-S616A 过表达腺病毒及外泌体浓度粒径(NTA)检测均由上海吉凯基因提供。 段晨阳,临床医学博士,博士后,重庆医学会麻醉学分会青年委员。长期从事围术期危重症多器官功能损害与保护相关临床工作和科学研究。主持国家自然科学基金青年基金1项、中国博士后面上项目1项,入选 “...
N2a cells were transfected with different plasmids (Drp1-Myc, the dephosphorylation-mimic mutant Drp1S616A-Myc and the phosphorylation-mimic mutant Drp1S616D-Myc). The expression of CDK5 and its activator p35, Drp1 and phosphorylated Drp1 on S616 was determined by western blot. The morphology of...
5)PINK1通过调节Drp1 S616磷酸化影响线粒体分裂参与突触发育的调控.Drp1S616A KI小鼠组织及原代神经元中线粒体的长度异常延长.向PINK1KO神经元中过表达Drp1WT/Drp1S616D突变体可以恢复PINK1缺失导致的线粒体异常.另外,PINK1缺失引起树突内ATP的含量下降,而使用改善线粒体功能,增加ATP产生的药物Piracetam可以一定程度上...
[135] S616D → increased fission event rate [140] → no significant changes [144] → elongation [135] S616A → elongation [131] → fragmentation [56,135] → no significant changes [132,137,139,141,144] No (cerebellar granule neurons [128]) Yes [129] No (HeLa cells, HEK293 cells,...