Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

Tumor-growth-factor-beta signaling helps cancer cells to evolve and become resistant to drugs by down-regulating accurate DNA repair.

A single mutation in Escherichia coli connects two essential cell envelope assembly pathways and confers vancomycin resistance by displaying molecular decoys at the cell surface.

Modelling beta-amyloid deposition in bioengineered human vessels represents a notable advance to further investigate the role of the vasculature in Alzheimer's disease.

A single neonatal inflammatory event induces long-term impairments in two forms of adult respiratory motor plasticity, an important aspect of the control of breathing for compensation after injury or disease.

Genome-scale integration of transposon mutagenesis with a redox biosensor identified a hypothetical transcription factor- Rv0158 required to calibrate the growth, cytoplasmic redox potential, and respiration of Mycobacterium tuberculosis in response to metabolic switching from glucose to fatty acids.

A distinctive novel mechanism of ephrin-A/EphA signaling modulation in retinal growth cones ensures concurrent quantitative accuracy and adaptability of topographic hardwiring.

Detailed structural analysis of NPAS1-ARNT and NPAS3-ARNT complexes, and further comparisons with other bHLH-PAS protein structures, show that this family of mammalian transcription factors have distinct ligand-binding pockets within their molecular architectures.

Bulk whole genome sequencing data can be used to study the genetic variation present in pathogenic bacterial populations over the time-course of a single infection within a host.

ADeS, a novel deep learning approach for apoptosis detection, achieves 98% accuracy in vitro and in vivo while providing unprecedented insights into the spatial–temporal foundation of cell death.