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Cong Ma

Researcher at Hong Kong Polytechnic University

Publications -  61
Citations -  1161

Cong Ma is an academic researcher from Hong Kong Polytechnic University. The author has contributed to research in topics: Bacterial transcription & RNA polymerase. The author has an hindex of 16, co-authored 55 publications receiving 842 citations. Previous affiliations of Cong Ma include Newcastle University & Massachusetts Institute of Technology.

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Catalytic Asymmetric C ? N Bond Formation: Phosphine-Catalyzed Intra- and Intermolecular γ-Addition of Nitrogen Nucleophiles to Allenoates and Alkynoates

TL;DR: An asymmetric version of this reaction affords enantioenriched pyrrolidines, indolines, and γ-amino-α,β-unsaturated carbonyl compounds.
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Bacterial Transcription as a Target for Antibacterial Drug Development

TL;DR: The inhibition of the bacterial transcription process with respect to structural studies of RNAP is described, recent progress toward the discovery of novel transcription inhibitors is highlighted, and additional potential antibacterial targets for rational drug design are suggested.
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Discovery of Novel Quinoline–Chalcone Derivatives as Potent Antitumor Agents with Microtubule Polymerization Inhibitory Activity

TL;DR: Compound 24d bound to the colchicine site of tubulin, arrested the cell cycle at the G2/M phase, induced apoptosis, depolarized mitochondria, and induced reactive oxidative stress generation in K562 cells, suggesting that 24d deserves to be further investigated as a potent and safe antitumor agent for cancer therapy.
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Inhibitors of Bacterial Transcription Initiation Complex Formation

TL;DR: A rational approach is taken to design a novel set of compounds that specifically target the formation of transcription initiation complexes by preventing the unique bacterial σ initiation factor from binding to RNAP.
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Design, synthesis and biological evaluation of quinoline-indole derivatives as anti-tubulin agents targeting the colchicine binding site.

TL;DR: Cellular mechanism studies elucidated that 34b disrupted cell microtubule networks, arrested the cell cycle at G2/M phase, induced apoptosis and depolarized mitochondria of K562 cells, suggesting that 27c and 34b deserve further research as potent antitumor agents for cancer therapy.