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The level of an individual protein in cells treated with combinations of drugs is best explained by simple linear superposition of the protein levels in response to single drugs. This finding may facilitate rational design of higher order drug combinations.
The buildup of toxic intermediates during lignocellulose pretreatment limits the utility of this abundant biomass for biofuel production. A recent study on the degradation pathways of two of the most hazardous toxins, furfural and HMF, now paves the way for mechanism-based enhancements of biodetoxification efficiency.
NMR-measured order parameters of methyl groups can be used to quantify the entropy of protein conformational change associated with calmodulin–peptide ligand interactions. This conformational entropy is a major contributor to the affinity of calmodulin interactions and can now be determined experimentally on a per-atom basis.
In most archaea, the enzyme TiaS post-transcriptionally modifies a cytidine in the anticodon of tRNAIle, converting it to agmatidine (agm2C or C+). This unique nucleoside allows translation at the AUA isoleucine codon and prevents misreading of the AUG methionine codon.
The final steps in the biosynthetic pathway to the morphine alkaloids have been revealed with the characterization of two key enzymes. In addition to the widely exploited parent compound, these new O-demethylases control metabolic flux to pharmaceutically useful opioid precursors.
Many kinase inhibitors for cancer therapy are rather nonselective, and their cellular mechanisms of action are incompletely understood. A nested chemical proteomics and chemical genetics strategy reveals which cellular targets of the clinical kinase inhibitor dasatinib functionally relate to its anti-oncogenic activity.
Organic synthesis plays a leading role in the discovery of small molecules for the exploration of biological systems. Therefore, the development of efficient strategies for the preparation of these molecules is a necessary aspect of the small-molecule approach to chemical biology.
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.
