An approachable framework for the scalable implementation of proteome-wide thermal shift assays to assess drug mechanisms of action.

Single-molecule tracking at scale, analyzing millions of cells and thousands of compounds per day, demonstrates that measuring protein motion provides mechanistic insights relevant to drug discovery.

Genetically-encoded platforms direct kinase inhibitor drugs to organelles to reveal new dimensions of local kinase signaling.

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.

Computational reaction representations and profile hidden Markov model searches of metagenomics databases can be harnessed to accurately predict bacterial species and enzyme sequences responsible for biotransformations in the human gut microbiome.

Analysis of the mechanism of action of cystic fibrosis corrector drugs reveals signalling pathways potently controlling the proteostasis of the main disease-relevant CFTR mutant.

Motivational coupling of action to reward and inhibition to punishment is subserved by dissociable learning and choice processes, and is modulated by dopamine/noradrenaline transporter blockade.

A novel phenotypic screening platform based on immunofluorescent imaging of histone modifications enables accurate identification of cell fates and environmental perturbations.

Bactericidal/permeability-increasing protein (BPI) from the scorpionfish Sebastes schlegelii escapes detection by BPI autoantibodies derived from people with cystic fibrosis and reveals excellent anti-inflammatory potency as well as profound antimicrobial activity towards Pseudomonas aeruginosa, including multiple drug-resistant strains.

The notion that the drug-like small molecule Sephin1 protects against protein misfolding by selectively disrupting a cellular phosphatase is refuted.