The disordered C-terminal tail allows XRCC4-like factor (XLF) to find and bind the XRCC4-Lig4 complex, enabling DNA end synapsis and subsequent ligation during non-homologous end joining.
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.
In-silico modeling of gene and protein emergence reveals how colony-stimulating factors contributed to the evolution and functional adaptions observed in mammalian neutrophils.
Crosslinking the AAA+ protease interface does not abolish protein degradation by ClpAP, establishing that rotation of the AAA+ unfoldase with respect to its partner peptidase is not essential for activity.
A new system to genetically label and manipulate plasma cells in vivo in their microenvironment resolves current technical limitations and reveals tissue-specific homeostatic population turnover.