Weak yet highly species-specific protein-protein interactions enhance the activity of metabolically related enzymes in bacteria at endogenous conditions, but also mean that overexpression of one partner leads to permanent non-physiological complexes and gene dosage toxicity.

Airborne PM2.5 exposure triggers oxidative stress and mitochondrial apoptosis in placental trophoblast cells via the KLF9/CYP1A1 transcriptional axis, ultimately leading to adverse pregnancy outcomes.

Genetic analysis of a CLN4 Drosophila model suggests that the disease-causing alleles act as dominant gain of function mutations that cause CSPα oligomerization and impair secretory and prelysosomal trafficking.

The transcriptomic profiles of the constituent monotherapies of synergistic drug pairs tend to be correlated and result in novel gene expression in the combinations.

A synthetic quadrastable gene network provides a synthetic biology framework to study cell fate determination.

Axon guidance genes are conserved regulators of neurodegeneration in Drosophila melanogaster and human inducible motor neuron models of UBQLN2-associated amyotrophic lateral sclerosis.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Detailed molecular profiling investigations alongside antitumor testing and tolerability studies in animals suggest caution when considering the clinical development of inhibitors of CDK8 and CDK19, since a clear therapeutic window could not be demonstrated with two structurally distinct, potent and selective prototype drugs.

Indomethacin, a nonsteroidal anti-inflammatory drug, alters the composition of the intestinal microbiota, and the intestinal microbiota affect the pharmacokinetics of indomethacin.

Genetic and proteomic screening with Wolbachia's CidB enzyme reveal the mechanisms and targets of cytoplasmic incompatibility (CI).