Bacterial-encoded covalent adhesion is a new molecular principle in host-microbe interactions and may play a key role in host colonization by a wide range of Gram-positive bacteria.

Genetic susceptibility to an infectious disease is linked to competition for binding a molecule on the bacterial surface by two host proteins with opposing roles in host immunity.

Short linear motifs throughout the intrinsically disordered proteome use sequence context in diverse ways to target actin remodeler ENAH.

To avoid recognition by the immune system, bacteria use autolysins to trim fragments of peptidoglycans that are exposed on the bacterial cell wall.

Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.

Fibronectin can shift from a globular to fibrillated form when adsorbing to implant surfaces, and this shift makes it accessible to attachment by Staphylococcus epidermidis, which is the leading cause of implant-associated infections.

Precise control of the bacterial flagellar motor determines bacterial cell dispersal and bacteria-surface interactions.

A high-throughput technique to characterize the substrate specificities of tyrosine kinases identifies the key features of kinases and substrates that enforce accurate signaling from T cell receptors.

A method has been developed to characterize the expressed biochemical activities of gut microbial communities using retrievable, microscopic, fluorescent-labeled glass beads containing chemically bound surface biomolecules.