K. Ma

Publications9
h-index6
Citations345
Highly Influential Citations17
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Structural basis for the phosphorylation of FUNDC1 LIR as a molecular switch of mitophagy
TLDR
It is demonstrated that phosphorylation of Tyr18 of FUNDC1 serves as a molecular switch for mitophagy, and may represent a novel target for therapeutic intervention.
View on Taylor & Francis
Regulation of mATG9 trafficking by Src- and ULK1-mediated phosphorylation in basal and starvation-induced autophagy
TLDR
Two conserved classic adaptor protein sorting signals within the cytosolic N-terminus of m ATG9 mediate trafficking of mATG9 from the plasma membrane and trans-Golgi network (TGN) via interaction with the AP1/2 complex, and suggest a coordination of basal and stress-induced autophagy.
View on Nature
Dynamic PGAM5 multimers dephosphorylate BCL-xL or FUNDC1 to regulate mitochondrial and cellular fate
TLDR
PGAM5, which exists in an equilibrium between dimeric and multimeric states, dephosphorylates BCL-xL to inhibit apoptosis or FUNDC1 to activate mitofission and mitophagy in response to distinct stresses.
View on Springer
Mitophagy, Mitochondrial Homeostasis, and Cell Fate
TLDR
Recent findings on molecular pathways governing mitophagy and its coordination with other mitochondrial behaviors, which together determine cellular fate are summarized.
View on PubMed
The SIAH2-NRF1 axis spatially regulates tumor microenvironment remodeling for tumor progression
TLDR
It is shown that the E3 ligase SIAH2 degrades NRF1 in response to hypoxia to enhance pro-tumor metabolic and environmental effects, whereasNRF1 stabilization sensitizes tumor cells to apoptosis, representing that inhibition of NRF 1 degradation is a potential therapeutic strategy against cancer.
View on Springer
Monitoring Mitophagy in Mammalian Cells.
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Molecular regulation of mitochondrial autophagy and cellular fate
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Mechanism of mitophagy in cell homeostasis
TLDR
The molecular mechanism and contributions of mitophagy in physiological and pathological contexts are reviewed and emerging findings are discussed, highlighting the potential value ofMitophagy regulation and related Mitophagy molecular pathways might be exploited for the mitochondrial function.
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Loss of SDHB reprograms energy metabolisms and inhibits high fat diet induced metabolic syndromes
TLDR
The findings reveal that the unanticipated role of complex II orchestrating both lipid and glucose metabolisms, and suggest that SDHB is an ideal therapeutic target for combating obesity.
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