Loss-of-heterozygosity mutations, but not aneuploidies, are linked to the evolution of drug resistance in Candida albicans isolated from immunocompromised patients.

Combined analyses of transcriptome and chromatin accessibility elucidated the mechanisms underlying cancer cell lines response to antitumor candidates and provided a versatile perturbation-informed basal signature able to predict drug sensitivity.

Potent and low-cost Nanosota-1 drug candidates block SARS-CoV-2 infections in vitro and in animal models and act preventively and therapeutically.

Previously uncharacterized long repeat sequences are associated with significant genome variation that can increase fitness and promote antifungal drug resistance in diverse isolates of Candida albicans.

The dynamic transcription responses of the human fungal pathogen Candida glabrata during macrophage infection is revealed and a novel transcription factor important for the responses to macrophage, proliferation within macrophage, as well as anti-fungal drug resistance has been discovered.

Candida albicans cells respond in two distinct ways to fluconazole exposure where cells enter the Ribo-dominant state characterized by an upregulation of ribosomal-related proteins and processes, or cells enter the Stress-dominant state characterized by the upregulation of stress responses.

A novel neuroprotective pathway that enhances acetyl-CoA metabolism via inhibition of acetyl-CoA carboxylase 1 may prevent the contribution of the aging process in the brain to Alzheimer's disease.

The structure of the Mycobacterium smegmatis CIII₂CIV₂ respiratory supercomplex with telacebec (Q203) bound shows how this tuberculosis drug candidate blocks respiration in mycobacteria.

The three-dimensional structures of Mycobacterium tuberculosis cytochrome bcc in complex with the antituberculosis agents, Q203 and TB47, explain how these inhibitors suppress activity of the complex.

The first-in-class cell-permeant fluorescent probe provides direct and visual evidence of SARM1 activation in axonal degeneration and identified the first covalent, allosteric inhibitor of SARM1 acting on the NAD-binding pocket in the ARM domain.