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.

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

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.

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.

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.

RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.

A novel and metazoan-specific protein, Tim29, is identified as a subunit of the human TIM22 complex and shown to function in the assembly of hTim22 and facilitate contacts with the TOM complex.

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.

Partial reduction of CFIm25 protein levels leads to misregulated alternative polyadenylation in neurons and learning deficits.