Phosphorylation deactivates TRIM21 B Box autoinhibition to licence proinflammatory signalling by cytosolic antibodies.

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.

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

TRIM33 performs an essential function in B cell acute lymphoblastic leukemia through an association with a single cis element.

Studying the impact of natural variation on a key immune gene highlights how focusing on a single wild-type sequence overlooks that rare variants cause the most disease.

Cell biology and animal model analysis in mice shows that molecules involved in glycolytic metabolism could potentially serve as therapeutic targets for the treatment of neurological diseases.

PITAR interaction with TRIM28 mRNA, which encodes a p53 targeting E3 ubiquitin ligase, keeps p53 levels low for cancer cells to divide and attenuates the DNA damage response by p53.

Repressing the conserved pro-differentiation let-7 microRNAs through limiting Ago2 levels is critical to maintaining pluripotency in stem cells.

TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing the PPARγ protein.