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

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.

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

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

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.

Newly identified gain-of-function variants indicate TRPM3 as the cause of a spectrum of autosomal dominant neurodevelopmental disorders with frequent cerebellar involvement in humans.

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.

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

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