Mutations in the TRIM5α retrovirus-binding interface frequently improve but rarely disrupt retroviral restriction.

Higher-order assembly enables and links pathogen recognition and downstream steps in the TRIM5-mediated anti-HIV response.

To protect mammals against retroviral infections, TRIM5 restriction factors recognize viral capsids by forming complementary hexagonal nets that can adapt to the patterns of capsid protein subunits on the viral capsid surface.

Unique biosensor design and protein-engineering enables direct visualization of the active form of Fyn kinase with high specificity, minimal perturbation and shows cellular signaling to be compartmentalized and pulsatile.

Super-resolution microscopy sets a new strategy to comprehend the membrane organization of γ-secretase at single complex resolution identifying nanodomain associations and its diffusion in situ in the living membrane.

Conformational flexibility in HIV-1 capsid, provided by cyclophilin A binding, facilitates evasion of capsid-targeting restriction factor MxB, while allowing sequence change to facilitate cytotoxic T-cell evasion.

Genomes take advantage of the gene-duplicating ability of retroelements to birth novel innate immune defense genes.

A long noncoding RNA uses viral mimicry to achieve developmental gene silencing across a chromosome.

Lymphocyte migration and autoimmunity induction rely on Formin-like 1-mediated actin network remodeling to push the lymphocyte nucleus through restrictive endothelial barriers.