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Ming Chen

Researcher at University of Tennessee

Publications -  29
Citations -  2413

Ming Chen is an academic researcher from University of Tennessee. The author has contributed to research in topics: Mitochondrial fission & Mitochondrion. The author has an hindex of 14, co-authored 26 publications receiving 1856 citations. Previous affiliations of Ming Chen include Baylor University & Chinese Academy of Sciences.

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Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells

TL;DR: It is reported that FUNDC1, an integral mitochondrial outer-membrane protein, is a receptor for hypoxia-induced mitophagy, and its findings offer insights into mitochondrial quality control in mammalian cells.
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Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy.

TL;DR: The data suggest that FUNDC1 regulates both mitochondrial fission or fusion and mitophagy and mediates the “coupling” across the double membrane for mitochondrial dynamics and quality control.
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NLLSS: Predicting Synergistic Drug Combinations Based on Semi-supervised Learning.

TL;DR: This study proposed similar nature of drug combinations: principal drugs which obtain synergistic effect with similar adjuvant drugs are often similar and vice versa and developed a novel algorithm termed Network-based Laplacian regularized Least Square Synergistic drug combination prediction (NLLSS) to predict potential synergistic drug combinations by integrating different kinds of information.
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Increasing occurrence of antimicrobial resistant hypervirulent (hypermucoviscous) Klebsiella pneumoniae isolates in China

TL;DR: Resistance to all the tested antimicrobials, except carbapenems and amikacin, was observed in a proportion of hvKP strains, 17% (5/29) of which expressed extended-spectrum β-lactamase, indicating an increasing propensity for the acquisition of antimicrobial resistance.
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A small natural molecule promotes mitochondrial fusion through inhibition of the deubiquitinase USP30

TL;DR: A diterpenoid derivative 15-oxospiramilactone (S3) is identified that potently induced mitochondrial fusion to restore the mitochondrial network and oxidative respiration in cells that are deficient in either Mfn1 or Mfn2.