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A high-throughput phenotypic screen in zebrafish embryos provides distinctive signatures by which neuroactive chemicals can be classified. These “behavioral barcodes” provide a systems approach to elucidating the mechanistic neuropharmacology of drugs and novel compounds.
A reverse genetic engineering approach identifies metabolic enzymes and their cellular pathways as potential regulators of myoblast differentiation. Targeting these metabolic nodes has provocative implications for drug discovery and therapeutic efficacy.
Reprogramming cell fates might cure or ameliorate many diseases. New results show that chemical reprogramming can be used in living animals to restore missing cell types.
A process in which peptide nucleic acids may be used for in vitro evolution has been developed. This method can offer enormous opportunities to evolve stable, non-natural molecules for therapeutic applications.
Antibiotics can break down through the action of enzymes or through non-enzymatic processes. In the case of tetracycline, this drug 'debris' can have unexpected biological activities, including selection against resistance.
Phosphoinositide 3-OH kinases (PI(3)Ks) are important lipid signaling enzymes and exciting drug targets for a number of human diseases. The first, much anticipated crystal structure of the delta isoform of PI(3)K provides surprising new insights into the selectivity of inhibitors for this versus other PI(3)K isoforms and facilitates the design of improved drugs.
Control of gene expression at the mRNA level is used extensively by cells. Now a biomimetic strategy yields a synthetic genetic switch in which an RNA-binding protein bound at the translation start site blocks progression of the ribosome.
Complete and accurate annotation of gene function is an essential starting point for genome interpretation and a host of systems and synthetic biology endeavors. Detecting errors in existing annotation now has an important new tool.
Aggregation of huntingtin protein with an expanded polyglutamine region is enhanced by its 17-residue N-terminal domain, which binds to itself and to the polyglutamine region. This enhancement is inhibited when the N-terminal domain binds to the chaperonin TRiC.
