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Structural basis for the phosphorylation of FUNDC1 LIR as a molecular switch of mitophagy
ABSTRACT Mitophagy is a fundamental process that determines mitochondrial quality and homeostasis. Several mitophagy receptors, including the newly identified FUNDC1, mediate selective removal ofExpand
Regulation of mATG9 trafficking by Src- and ULK1-mediated phosphorylation in basal and starvation-induced autophagy
Autophagy requires diverse membrane sources and involves membrane trafficking of mATG9, the only membrane protein in the ATG family. However, the molecular regulation of mATG9 trafficking forExpand
The SIAH2-NRF1 axis spatially regulates tumor microenvironment remodeling for tumor progression
The interactions between tumor cells with their microenvironments, including hypoxia, acidosis and immune cells, lead to the tumor heterogeneity which promotes tumor progression. Here, we show thatExpand
Mitophagy, Mitochondrial Homeostasis, and Cell Fate
Mitochondria are highly plastic and dynamic organelles that have graded responses to the changing cellular, environmental, and developmental cues. Mitochondria undergo constant mitochondrial fissionExpand
Dynamic PGAM5 multimers dephosphorylate BCL-xL or FUNDC1 to regulate mitochondrial and cellular fate
Mitochondria are highly dynamic organelles and respond to stress by changing their fission-fusion cycle, undergoing mitophagy, or releasing apoptotic proteins to initiate cell death. The molecularExpand
Mechanism of mitophagy in cell homeostasis
Mitophagy is an evolutionally conserved mechanism to remove dysfunctional or unwanted mitochondria, thus orchestrates mitochondrial number and cell metabolism. So its molecular mechanism is a hotExpand
Monitoring Mitophagy in Mammalian Cells.
In eukaryotes, physiological cell functions rely on the preservation of the size and activity of the mitochondrial network. Mitophagy provides a key contribution in this setting by ensuring theExpand
Loss of SDHB reprograms energy metabolisms and inhibits high fat diet induced metabolic syndromes
Mitochondrial respiratory complex II utilizes succinate, key substrate of the Krebs cycle, for oxidative phosphorylation, which is essential for glucose metabolism. Mutations of complex II causeExpand