Research + Discoveries

  • Derbyshire Lab Takes Aim at Human Cell Machinery

    A team effort by the Derbyshire lab has led to the identification of human genes and pathways that facilitate the infection of liver cells by Plasmodium parasites, the causative agents of malaria. Their results suggest that this parasite co-opts the vesicular trafficking of its host cell to support its dramatic growth during the liver stage of infection. This work provides insights into the poorly understood interactions between Plasmodium parasites and the host liver cells they invade.

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  • Franz Lab Interfaces Inorganic Chemistry and Cellular Biology while Outside of Metal Comfort Zones

    Knowledge of metal-trafficking processes can be leveraged to develop small molecules that help cells regain metal homeostasis for optimal cellular function or conversely that push cells away from homeostasis and into cellular distress.

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  • Small Molecule Drug May Prevent Chemotherapy Resistance

    A team led by Professors Jiyong Hong and Pei Zhou has discovered a small molecule drug that can stop cancer cells from becoming resistant to chemotherapy. The new compound, which was tested in an animal model of melanoma, could serve as a powerful adjuvant to make current chemotherapies more effective.

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  • Malcolmson Lab Illustrates Chiral Allene Synthesis by Pd-Catalyzed Amine–Enyne Couplings

    The Malcolmson lab has demonstrated that conjugated enynes undergo efficient and selective intermolecular 1,4-hydroamination to afford chiral allenes with a variety of primary and secondary aliphatic amines as well as benzophenone imine as an ammonia surrogate. A large number of allenes are obtained in racemic form with an achiral Pd(DPEPhos) catalyst. Through the design and development of a novel PHOX ligand, the group illustrates that highly enantioenriched allenes may be obtained in several cases.

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  • Franz lab discovers relationship between copper levels and drug tolerance in fungal pathogen Candida albicans

    Lizzie Hunsaker of the Franz lab has discovered that modulating copper levels in the growth environment of Candida albicans reduces tolerance of this pathogen to widely prescribed azole antifungal drugs. Their results suggest that, even though these drugs are capable of coordinating transition metal centers, the observed copper-potentiated activity is not due to the formation of a copper complex. Instead, the data point to a broader relationship between Cu homeostasis and azole antifungals, a relationship that the lab continues to explore.

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