Developmental genetic and cell culture studies indicate that the Inhibitor of DNA-binding protein Extra macrochaetae (Emc), previously thought to determine where bHLH proteins can act, is itself regulated by those bHLH dimerization partners at the level of protein stability.
SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.
Interplay between FGF-induced bHLH transcription factors and BMP-induced bHLH inhibitory id genes govern mesodermal cell fate choice along the mediolateral axis in both zebrafish and mouse.
Analysis of data on drug-gene interactions suggests that decentralized collaboration will increase the robustness of scientific findings in biomedical research.
Publication bias, in which positive results are preferentially reported by authors and published by journals, can restrict the visibility of evidence against false claims and allow such claims to be canonized inappropriately as facts.
Analysis of experiments on bacteria suggests that the dependence of cell size on growth rate is not an adaptation but a causal consequence of a regulatory mechanism that controls DNA replication.
A simulation study is used to demonstrate how mistakes in identifying the experimental unit and the unit of analysis can lead to incorrect analyses and inappropriate inferences when reporting research studies.
Key numbers about the biology of the SARS-CoV-2 virus and the infection of a single human host by the virus have been compiled from the peer-reviewed literature.
