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.
Multiple replicated examples of epistasis affecting gene expression in humans are identified, some explaining a substantial proportion of the variation in expression.
Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.
A combination of window-of-sensitivity, genetic, and in vitro findings illuminate mechanisms of gene–environment interaction in a multifactorial model of a common birth defect.
Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.
The Polycomb group protein SCML2 contributes to the assembly and gene silencing function of Polycomb Repressive Complex 1 (PRC1) and requires an RNA-binding region to reach chromatin targets.
A small molecule called Sm4 can disrupt interactions involving a transcription factor called Sox18, while having little impact on other members of the SoxF family.
Analysis of data on drug-gene interactions suggests that decentralized collaboration will increase the robustness of scientific findings in biomedical research.
