FUNDC1 collaborates with PINK1 in regulating mitochondrial Fission and compensating for PINK1 deficiency
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS(2023)
摘要
Parkinson's disease is presently thought to have its molecular roots in the alteration of PINK1-mediated mitophagy and mitochondrial dynamics. Finding new suppressors of the pathway is essential for developing cutting-edge treatment approaches. Our study shows that FUNDC1 suppressed PINK1 mutant phenotypes in Drosophila. The restoration of PINK1-deficient phenotypes through FUNDC1 is not reliant on its LC3-binding motif Y (18)L (21) or autophagy-related pathway. Moreover, the absence of Drp1 affects the phenotypic restoration of PINK1 mediated by FUNDC1 in flies. In summary, our findings have unveiled a fresh mechanism through which FUNDC1 compensates for the loss of PINK1, operating independently of autophagy but exerting its influence via interaction with Drp1.
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关键词
PD,Ubiquitin-independent mitophagy,Autophagy receptor,Mitochondrial dynamics,Drp1
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