Experiments in mice have shown than an enzyme that repairs broken DNA inside the nucleus also has a central role in the innate immune system because it is able to detect foreign DNA outside the nucleus.

A transmembrane protein uses distinct mechanisms to regulate the movement of specific toll-like receptors-key immune system components involved in detecting pathogens-to their final locations inside cells.

Proteins produced by mast cells modulate the permeability of blood vessels, and may determine whether patients infected with dengue virus develop life-threatening complications.

The eye produces a protein that inhibits the growth of blood vessels in the deep retina, which includes the photoreceptor layer, and disruption of this process can lead to blindness.

A cell-free system combined with cell-based assays elucidate the biochemical mechanism of signal transduction mediated by the mitochondrial protein MAVS and delineates the role of ubiquitin E3 ligases in antiviral innate immune responses.

Mechanisms that enable wild mice to survive infection with strains of the Toxoplasma gondii parasite virulent enough to kill laboratory mice offer an explanation for how these parasites have been able to persist in the mouse population.

TNF-α treatment induces phosphorylation and cytoplasmic translocation of the retinoblastoma protein, which regulates cytoskeletal organization in skeletal muscle cells.

RNA binding is a key input of an active chromatin complex and maintenance of stem cell fate.

A viral RNA has been identified as a specific MDA5 agonist in cells infected with encephalomyocarditis virus.

Mitochondrial anti-viral signaling proteins form three-stranded helical filaments in launching innate immune responses against RNA viruses.